The Eggplant Cancer Cure A Treatment for Skin Cancer
And New Hope for Other Cancers
From Natures Pharmacy Dr. Bill E. Cham, PH.D.
The Eggplant Cancer Cure Dr Bill E. Cham PH.D.
All rights reserved. No part of this book may be reproduced ortransmitted in any form or by means, electronic or mechanical,including photography, recording or by any information storage andretrieval system, without written permission from the author exceptdor the inclusion of brief quotes in a review.
2007 by Bill E. Cham
Publish in the United States of America First Edition, 2007Library of Congress Control Number: 2007933714
This book is dedicated to my family: Anita, Tania, Kai, Aruba,Karim, Georgie, Lane and Jessica.
Special thanks to Tania for her incredible dedication to
finding relevant research papers and typing this manuscript andto Aruba for creating the artwork.
Also thanks to my co-investigators and all the patients
who have encouraged the execution of the research and made itall worthwhile.
FOREWARD Perfection or near-perfection is rare in any area ofmedicine. Dr. Bill Cham has achieved it in the treatment of twocommon cancers, basal cell carcinoma and squamous cell carcinoma.Dr. Chams treatment also eliminates actinic keratosis, a usuallybenign (but potentially malignant) skin condition of middle agesand older. Whats near-perfection? A treatment that:
Works nearly every time Is incredibly simple to use Has noadverse side effects Is inexpensive compared with othertreatments
Even better, for those who want to know how does it work, thisbook tells us exactly how. The explanation is simple, easy tounderstand, and yet scientifically elegant, a molecular ballet.Heres the explanation in one line of simple English: Dr. Cham hasfound substances which can penetrate and kill skin cancer cells butcant penetrate normal skin cells, so normal skin cells areuntouched and unhurt while the skin cancer cells die! (Those whowant the full technical explanation will find itagain, in simpleEnglishin the following pages.) What youre about to read and thepictures youre about to see are absolutely breath-taking. Youllread about and see relatively small squamous and basal cell cancersdisappearing in just 12 to 16 weeks. Youll see large, neglectedcancers as large as 2 by 3 inches first get bigger as cancer cellsbeneath the surface die, and then reverse course and slowly healover the next few months. Surgical treatment of such large skincancers is almost always disfiguring, and sometimes not correctablewith plastic surgery. Dr. Chams treatment enables healing of eventhe largest cancers with minimal if any disfigurement.
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So wheres this treatment been? Why havent you heard about itfrom your doctor? Its been used for years in Australia, where itsimultaneously cured approximately 70,000 Australians of their skincancers and incurred the wrath of the Australasian College ofDermatologists and the (Australian) Therapeutic GoodsAdministration, neither of whom favor freedom of choice in healthcare, and have a special disinterest in un-approved therapies. Butenough about that fans of the Food and Drug Administration in theseUnited States are more than familiar with this situation. Alwayswork with a physician skilled and knowledgeable in naturalmedicine. Ask him or her where to find Dr. Chams skin cancer cure.In a wired world, you can also enter curadermglobal.com, Curadermor BEC-5 into your search engine, and proceed accordingly.Remember, Dr. Chams treatment can cure squamous cell cancer, basalcell cancer, and actinic keratosis but not melanoma. Also, it maynot work on skin cancers that have already undergone surgery. Butgiven these precautions, Dr. Cham has discovered, and thenthoroughly researched and developed a near-perfect treatment fortwo common skin cancers. If anyone deserves a Nobel Prize inMedicine, its Dr. Bill E. Cham.
Jonathan V. Wright m.d.
Medical director, Tahoma Clinic Renton, Washington, USA
www.tahomaclinic.com www.wrightnewsletter.com
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PROLOGUE The The Mutilated Man Sometime ago, in the 1990s, therewas a knock on my door. Come in, I said. The door opened slowly, anelderly couple entered. The male had a veil covering his face andhat on his head. The lady said, Sorry doctor but can we see you fora moment? I agreed and both sat down. The lady said, We saw you andsome patients you treated for skin cancer on TV several weeks ago.In particular we were impressed by the segment, which showed howyour treatment saved the nose of the patient who had skin cancer.We are here to encourage you and support your work. I would like toshow you why we are so interested in helping you and others. Thisis my husband. She then asked him to remove his veil and hat. Icould not believe my eyes. His head was disfigured. He had no nose,both ears were gone, one eye was half closed, there were largeindented areas with transplanted skin on his head and half his chinwas gone. I felt so sorry for the man. Choked, I attempted to say,How did this happen? It is all skin cancer, the man said. Over theyears I have had skin cancers that were treated by radiotherapy andsurgery and this is the end result. I have been mutilated. He wasquick to point out that he did not blame the radiotherapist orsurgeon for his afflictions, but he felt it was time that a bettertreatment was made available for the general public. The lady youtreated as shown on the TV would have probably ended up like me inseveral years time. Although it is too late for me, I want to helpother people by not having to go through what I am going through.One of my latest treated skin cancers has now traveled through mybody and cannot be treated. So, we are here to stimulate you tocontinue your work and to congratulate you on your achievements. Ifelt so humble and grateful. This showed unselfishness, andcompassion beyond expression. The conversation ended soon after.Several weeks later I had a telephone call from the lady whoinformed me that her husband
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had passed away. I have never forgotten this experience andthis, amongst other events, has inspired me to ensure that myattention was directed to continue my tireless quest for a bettertreatment for skin cancers.
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Table of Contents Forward i Prologue - The Mutilated Man iiiCHAPTER 1:
Introduction 1. Cancer 4. Lesions of the Skin
- Actinic Keratosis and Other Precancers 6. Skin Cancer 9.Symptoms of Skin Cancer 11. Different Types of Skin Cancer 11.Basal Cell Carcinoma 12. Types of Basal Cell Carcinoma 14. SquamousCell Carcinoma 15. Types of Squamous Cell Carcinoma 15. LikelyPlaces Where Skin Cancer Develop 16.
CHAPTER 2:
What Causes Skin Cancer 19. CHAPTER 3:
Previous Accepted Treatments 27. - Actinic Keratosis 27. -Non-Melanoma skin cancers 29.
Skin Cancer Prevention 33. CHAPTER 4:
From the Past to a New Era 35. Research 36.
BEC Solasodine Glycosides 36. Pre-Clinical Phase 37. Phase 1Clinical Trials 39. Mechanism of Action of BEC is Unique 41. PhaseII Clinical Trials 44.
Specific Indications Studied 45. Results of Phase II ClinicalTrials with BEC 45. Phase III Clinical Trials 49. Phase IV orPost-Marketing Studies 51. CHAPTER 5: Comparative AvailableTreatment Regime vs. Curaderm BEC5 55.
- Various forms of Surgery vs. Curaderm BEC5 55. -5-fluorouracil (5-FU) vs. Curaderm BEC5 65. - Photo-dynamic Therapy(PDT) vs. Curaderm BEC5 66. - Imiquimod vs. Curaderm BEC5 67.
CHAPTER 6:
Recommended Curaderm BEC5 Treatment Procedure 71.
Schematic Representation of the Sequential Events of Skin CancerTreatment with Curaderm BEC5 73. Clinical Representation of theSequential Events of Skin Cancer Treatment with Curaderm BEC5 75.CHAPTER 7: Will Consuming Eggplant Result in Removal of InternalCancer? 78. CHAPTER 8: Counterfeit Products 81. Conclusion 82.Bibliography 84. Glossary 90. About the Author 95.
Chapter 1
Introduction The inspiration of the Mutilated Man, in part, hasguided me to present this book that describes results of over aquarter of a centurys research. The main theme is focused on theexecution of research that meets the world standard for producing adrug for a specific indication. In this case the indications wereactinic keratoses and true malignant non-melanoma skin cancers,basal cell carcinoma (BCC) and squamous cell carcinoma (SCC). Thefruit of the Devils Apple plant (Solanum linnaeanum) has long beensuspected in stockmans folklore as a treatment of eye cancer inHereford cattle. It was this folklore that brought the plant to myattention. I then set out to identify the possible active compoundsof the plant. My discoveries led to the patenting of a purifiedglycoalkaloid mixture, which is now known as BEC. I subsequentlyestablished that BEC was also present in edible fruit such as theeggplant or aubergine (Solanum melongena). Eggplants are members ofthe Solanaceae (Night shade) family, classing them as relatives totomato, green pepper and tobacco. The species name melongena meanssoothing mad apple, as it once had a reputation, wrongly so, ofinducing insanity. It has been reported that eating eggplant lowersblood cholesterol, helps counteract detrimental blood effects offatty foods and clears toxic heat from the body. Eggplant is usedto relieve pain, hypertension, stomach ulcers, colitis,constipation, bleeding hemorrhoids, swellings, and tumours.Eggplant is reported to have an adverse effect on people sufferingwith rheumatoid arthritis and osteoarthritis. No controlled studieshave been done to substantiate the above claims of theeggplant.
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This book is the first to describe, substantiated by many yearsof studies, that the eggplant contains Solasodine glycosides thatare now used for the treatment of skin cancers. Twenty five yearsof basic research, pre-clinical research and clinical research haveestablished that BEC, at lower concentrations than is present inthe eggplant, in a cream formulation now available to the publicknown as Curaderm BEC5, is effective for treating non melanoma skincancers. The glycoalkaloids in BEC are currently undergoingclinical trials in humans suffering from terminal internal cancers.The objective of this book is to describe the scientificdevelopment of an anticancer drug that is extracted from an ediblefruit, the eggplant. In this book the words cancer cure has themedical definition of a cancer is considered to be cured if itdisappears and does not recur within five years. As you will read,patients were made healthy again by the eggplant treatment and werefollowed-up for over a decade after they were healed of theircancer and there were no recurrences. When reading this book youwill appreciate that no experimental short cuts were taken and thedevelopment of Curaderm BEC5 followed the necessary stringentpathways and time requirements which are essential before any newdrug, natural or synthetic, can be safely marketed for certainindications. This communication briefly describes in summarizedform only, the essence of the 25 years of investigations. For moreelaborate published scientific information please see thebibliography section in this book. The photographic figures oftreated lesions have not been modified or tampered with. They areall original.
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Before the research and new treatments are described, a guide tocancer in general and skin cancer in particular are presented.
3.
Cancer Cancer develops when cells in a part of the body begin togrow out of control. Although there are many kinds of cancer, theyall start because of out-of-control growth of abnormal cells, whichdevelop into malignant growths or tumours. Normal body cells grow,divide, and die in an orderly fashion. During the early years oflife, normal cells divide more rapidly until adulthood. After that,cells in most parts of the body divide only to replace worn-out ordying cells and to repair injuries. Because cancer cells continueto grow and divide, they are different from normal cells. Insteadof dying, they outlive normal cells and continue to form newabnormal cells. Cancer cells often travel to other parts of thebody where they begin to grow and replace normal tissue. Thisprocess, called metastasis, occurs as the cancer cells get into thebloodstream or lymph vessels of our body. Cancer cells developbecause of damage to DNA. This substance is in every cell anddirects all its activities. Most of the time when DNA becomesdamaged the body is able to repair it. In cancer cells, the damagedDNA is not repaired. People can inherit damaged DNA, which accountsfor inherited cancers. Many times though, a persons DNA becomesdamaged by exposure to something in the environment, like smokingor over-exposure of UV radiation. Cancer usually forms as a tumour.Some cancers, like leukemia, do not form tumours. Instead, thesecancer cells involve the blood and blood-forming organs, andcirculate through other tissues where they grow. Not all tumoursare cancerous. Benign (noncancerous) tumours do not spread to otherparts of the body (metastasize) and, with very rare exceptions, arenot life threatening.
4.
Different types of cancer can behave very differently. Forexample, lung cancer and skin cancer are very different diseases.They grow at different rates and respond to different treatments.That is why people with cancer need treatment that is aimed attheir particular kind of cancer. Cancer is the second leading causeof death in the United States. Half of all men and one-third of allwomen in the US will develop cancer during their lifetimes. Today,millions of people are living with cancer or have had cancer. Therisk of developing most types of cancer can be reduced by changesin a person's lifestyle, for example, by quitting smoking,protecting against UV damage and eating a better diet. The sooner acancer is found and treatment begins, the better are the chancesfor living for many years.
5.
Lesions of the Skin Actinic Keratosis and Other Precancers Anumber of abnormal but relatively harmless skin growths constitutethe early warning signs of skin cancer. These may be precancerouslesions, benign tumours that mask or mimic more serious ones, ormalignant tumours that are at the moment just on the topmost layerof the skin. They are important to recognize, because they are awarning sign of potential skin cancer. Precancerous Growths Skin ina precancerous state is abnormal but not malignant. The term"precancerous" is used because these abnormal areas of skin aremore likely to turn malignant than healthy skin. Precancerousgrowths are visible to the naked eye, and they look different fromnormal cells when they are examined under a microscope. EarlyCancer When malignant changes occur to the skin, but haven't spreadbeyond the top layer of the skin, they are called early cancers, orcancers in situ. A barrier called the basem*nt membrane helps delayinvasion by malignant cells deeper into the skin. Types ofPrecancer Actinic Keratosis Actinic keratosis (AK), also known assolar keratosis, is the result of prolonged exposure to sunlight.It is a small crusty, scaly or crumbly bump or horn that arises onthe skin surface. The base may be light or dark, tan, pink, red, ora combination of these lesions or the same colour as your skin. Thescale or crust is horny, dry, and rough, and is often recognized bytouch rather
6.
than sight. Occasionally it itches or produces a pricking ortender sensation. It can also become inflamed and surrounded byredness. In rare instances, actinic keratoses can bleed. The skinabnormality or lesion develops slowly and usually reaches a sizefrom an eighth to a quarter of an inch (2mm to 4mm) but cansometimes be as large as one inch. Early on, it may disappear onlyto reappear later. It is not unusual to see several AKs at a time.AKs most likely appear on the face, lips, ears, scalp, neck, backsof the hands and forearms, shoulders and back - the parts of thebody most often exposed to sunshine. The growths may be flat andpink or raised and rough.
Fig.1-1: Actinic Keratoses Actinic Cheilitis Actinic cheilitisis a type of actinic keratosis occurring on the lips. It causesthem to become dry, cracked, scaly and pale or white. It mainlyaffects the lower lip, which typically receives more sun exposurethan the upper lip. Arsenical Keratosis Far less common, arsenicalkeratosis is an accumulation of keratinized tissue that at firstresembles numerous small, yellowish corns. These arise most oftenon the palms, soles, and inner surfaces of the finger and toes, andthen enlarge and thicken,
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sometimes increasing in number. Although rarely seen today,arsenical keratoses usually occur on patients who were at some timein their lives exposed to arsenic, either contained in medicationor from an industrial or environmental source. LeukoplakiaLeukoplakia is a disease of the mucous membrane. White patches orplaques develop on the tongue or inside of the mouth, and have theability to develop into SCC. It is caused by sources of continuousirritation, including smoking or other tobacco use, rough teeth orrough edges on dentures and fillings. Leukoplakia on the lips ismainly caused by sun damage. Bowen's Disease This is generallyconsidered to be a superficial SCC that has not yet spread. Itappears as a persistent redbrown, scaly patch which may resemblepsoriasis or eczema. If untreated, it may invade deeperstructures.
8.
Skin Cancer Skin cancer is a disease in which skin cells losethe ability to divide and grow normally. Healthy skin cellsnormally divide in an orderly way to replace dead cells and grownew skin. Abnormal cells can grow out of control and form a mass or'tumour'. When abnormal cells originate in the skin, the mass iscalled a skin tumour. A skin tumour is considered benign if it islimited to a few cell layers and does not invade surroundingtissues or organs. But if the tumour spreads to surrounding tissuesit is considered malignant or cancerous. Cancer cells crowd out anddestroy nearby healthy cells forming growths called malignanttumours. Most skin growths, however, are non-malignant, benign (notharmful) tumours.
Some forms of skin cancer also metastasize. That is, they spreadto other parts of the body and start new tumours.
Skin cancer that spreads to vital organs like the brain or livercan be life threatening.
The skin, which is the human body's largest organ, has severalfunctions. It prevents the body from losing water and other fluids,stores fat, cools the body when sweat evaporates, and makes vitaminD. The skin also protects the body from infection, light, andinjury. There are three layers of skin:
1. Epidermis - the outer layer of skin 2. Dermis - the middlelayer of the skin; contains nerves,
blood vessels, sweat glands, hair follicles, and oil- 9.
3. producing cells that keep the skin from drying out 4. Fattylayer - the deep layer of skin
Fig1-2: Cut-away view of the skin Skin cancer begins in theepidermis, the outer layer of skin. The epidermis has three kindsof cells.
Squamous cells are cells that progressively flatten and fillwith protective keratin (a tough, insoluble protein that makes skinalmost completely waterproof) to form the outmost surface of theskin.
Basal cells are small cells located at the base of the epidermisthat serve as a reservoir for squamous cells shed from theskin.
Melanocytes are cells that produce a dark material, or pigment,that gives the skin its colour.
Each of these cells can suddenly start to divide abnormally andbecome cancerous. The main types of skin cancer are named afterthese cells.
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Symptoms of Skin Cancer Skin cancer first appears as a growth,or abnormal accumulation of cells. It sometimes takes the form of asore or pimple that does not heal. The sore may bleed or oozefluid, crust or scab over, and then ooze or bleed again. Cancer canoccur on almost any area of the skin, but is most common on areasoften exposed to the sun. Skin cancer usually is painless. The mostcommon symptoms are:
A new growth on the skin. A change in an existing skin growth. Asore that does not heal.
Not all changes in the skin are symptoms of skin cancer.
Different Types of Skin Cancer There are a number of differenttypes of skin cancers depending on the type of skin cell from whichthey arise. Each kind of skin cancer has its own distinctiveappearance. Certain skin cancers also tend to develop in specificareas of the body.
Basal cell carcinoma. Squamous cell carcinoma. A third type,malignant melanoma, is relatively rare but
can be very dangerous.
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Basal Cell Carcinoma Basal cell carcinoma (BCC) is the mostcommon form of cancer, with more than one million new casesestimated in the US each year. Basal cells are cells that line thedeepest layer of the epidermis. An abnormal growth a tumour of thislayer is known as basal cell carcinoma. Basal cell carcinoma canusually be diagnosed with a simple biopsy and is fairly easy totreat when detected early. However, 5 to 10 percent of BCCs can beresistant to treatment or locally aggressive, eating away at theskin around them, sometimes even into bone and cartilage. When nottreated quickly, they can be difficult to eliminate. Fortunately,however, this is a cancer that has an extremely low rate ofmetastasis, and although it can result in scars and disfigurement,it is not usually life-threatening. There are five most typicalcharacteristics of basal cell carcinoma which are shown below.Frequently, two or more features are present in one tumour. Inaddition, BCC sometimes resembles non-cancerous skin conditionssuch as psoriasis or eczema.
An Open Sore that bleeds, oozes, or crusts and remains open forthree or more weeks. A persistent, non-healing sore is a verycommon sign of an early basal cell carcinoma. A Reddish Patch orirritated area, frequently occurring on the chest, shoulders, arms,or legs. Sometimes the patch crusts. It may also itch or hurt. Atother times, it persists with no noticeable discomfort.
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A Shiny Bump or nodule that is pearly or translucent and isoften pink, red, or white. The bump can also be tan, black, orbrown, especially in dark-haired people, and can be confused with amole. A Pink Growth with a slightly elevated rolled border and acrusted indentation in the center. As the growth slowly enlarges,tiny blood vessels may develop on the surface. A Scar-like Areawhich is white, yellow or waxy, and often has poorly definedborders. The skin itself appears shiny and taut. This warning signcan indicate the presence of an aggressive tumour.
Fig. 1-3: Various BCCs
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Types of Basal Cell Carcinoma Nodular. Nodular basal cellcarcinoma is the most common type. This tumour usually resembles asmooth, round, waxy pimple, pale yellow or pearl gray, and may varyin size from a few millimeters to 1 centimeter. Often, the skincovering the nodule is so thin that the slightest injury will causeit to bleed. These tumours are often depressed in the middle andshow ulceration. As the tumour grows, it destroys healthystructures in its path, including nerves, muscles, and bloodvessels. Large tumours are easily diagnosed, but smaller ones areoften difficult to tell from benign skin conditions, such as warts,seborrheic keratoses, moles, psoriasis, or fever sores.Superficial. This is a less common type of BCC. It is aprogressively spreading, slow growing cancer that differs greatlyfrom other types of this disease. The tumour is red, with aslightly raised ulcerated or crusted surface, often bordered withpearly or threadlike formations. Tumours usually appear as patcheson the torso, but can develop more extensively on the face andneck. This is often mistaken for other skin conditions such asfungal infections, eczema, or psoriasis. Morpheoic, Sclerosing orFibrosing. Fibrosing basal cell carcinoma is also calledmorphea-like carcinoma. This fibrosing type of tumour begins as aflat or slightly depressed, shiny, hard, yellow-white patch with anirregular border. Sometimes, it may be present for years withoutgrowing or changing or being recognized. Usually, though, thelesion grows quickly, reaching a diameter of several centimeterswithin a few months. This is a fairly uncommon type of skin cancer,and can be difficult to eradicate because of root-like extensionsof the tumour that reach into the underlying tissue. Pigmented.Pigmented basal cell carcinoma is similar to nodular basal cellcarcinoma, but is more likely to appear in people with
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dark hair or dark eyes. As its name implies, this growth isalmost black and can easily be mistaken for the more aggressivemalignant melanoma.
Squamous Cell Carcinoma Squamous cell carcinoma is the secondmost common form of skin cancer, with over 200,000 new cases per ayear estimated in the United States, and about 1,900 deaths fromthis type of cancer. Squamous cells are cells that compose most ofthe epidermis. An abnormal growth of these cells is known as asquamous cell carcinoma. Types of Squamous Cell Carcinoma
A wart-like growth that crusts and occasionally bleeds. Apersistent, scaly red patch with irregular borders that sometimescrusts or bleeds. An open sore that bleeds and crusts and persistsfor weeks.
15.
An elevated growth with a central depression that occasionallybleeds. A growth of this type may rapidly increase in size.
A persistent, scaly red patch with irregular borders thatsometimes crusts or bleeds. An open sore that bleeds and crusts andpersists for weeks.
Fig. 1-4: Various SCCs
Likely Places Where Skin Cancers Develop Basal cell carcinomasusually occur on parts of the body that are often exposed to thesun. These are the face, neck, V-shaped area of the chest, andupper back. They occur less often on the top sides of the arms andhands.
These tumours sometimes look like a sore or pimple that does notheal.
They may ooze yellowish fluid, crust over with a scab, and thenbreak down and ooze again.
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When the surrounding skin is stretched, a basal cell
carcinoma has a pearly gray look, with tiny blood vessels oftenvisible inside the tumour.
Squamous cell carcinomas also appear most often on the face andneck, V-shaped area of the chest, and upper back. They are morelikely than basal cell carcinomas to form on the top of the armsand hands.
Squamous cell carcinomas look like an inflamed (pinkish orreddish), scaly growth that feels sore or tender.
Some may repeatedly break open, bleed, and crust - never fullyhealing.
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Chapter 2
What Causes Skin Cancer There is convincing evidence thatsunlight causes skin cancer. The types of sun radiationinclude:
visible light, which gives us the colours we see, infraredradiation which gives us the warmth we feel, and ultraviolet (UV)radiation.
Ultraviolet (UV) radiation can cause harmful effects to theskin. There are three basic types of ultraviolet radiation:
UVA (long-wave UV), UVB (sunburn UV), and UVC (short-waveUV).
Table 2-1 summarizes the general features of each type.
Table 2-1 Types of Ultraviolet Radiation and their features
Ultraviolet Radiation Type General Features Ultraviolet Aradiation (UVA, longwave UV)
notfilteredoutintheatmosphere
passesthroughglass producessometanningonceconsideredharmless
butnowbelievedharmfuloverlongterm
levelsremainrelativelyconstantthroughouttheday
causesagingoftheskinandwrinkling 19.
Ultraviolet Radiation Type General Features
Ultraviolet B radiation (UVB, sunburn radiation)
somefilteredoutintheatmospherebytheozonelayer
doesnotpassthroughglass
causessunburn,tanning,wrinkling,ageingoftheskinandskincancer
highestintensityatnoontime
Ultraviolet C radiation (UVC, short-wave UV)
filteredoutintheatmospherebytheozone
layerbeforereachingearthmajorartificialsourcesaregermicidallamps
burnstheskinandcausesskincancer
Table 2-1 The effects of sunlight on the skin When ultravioletradiation reaches the skin, some radiation is reflected away fromthe surface. The remaining radiation is scattered into the tissuesjust beneath the skin's surface. A fraction of this radiation isabsorbed by the skin's living cells. Ultraviolet radiation absorbedby living cells damages sensitive substances that influence theskin's normal growth and appearance. Damage can result in:
sunburn, increased rate of ageing of the skin, and
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skin cancer. Sunburn Sunburn is the most familiar and immediateeffect of ultraviolet radiation on the skin. It is an inflammationcaused by an increase in blood-flow beneath the skin. The reactionis not normally instantaneous, but reaches a bright red colourwithin 15 to 20 hours. The condition can be very painful andsometimes causes peeling of the skin. Brief intense exposure cancause severe sunburn in people who are not accustomed to strongsunlight. There is evidence that this type of exposure, as well aslong-term exposures, might be linked to serious forms of skincancer later in life. Usually five sunburns over a period of timewill cause skin cancer. Increased Rate of Ageing of the SkinRepeated exposure to the sun's ultraviolet radiation eventuallycauses skin damage similar to the ageing process. Patches of skinbecome thin and less elastic, and develop blemishes, sun freckles,and wrinkles. These changes may take many years of exposure butwhen they occur, the damage is irreversible. Skin Cancer Ifexposure to sunlight continues for several years, the damaged skinhas an increased chance of developing one of the forms of skincancer. Exposure to ultraviolet radiation increases the risk ofdeveloping these cancers (although it may not be the only cause ofthe disease). While the exact relationship is not entirely defined,it appears that intermittent (occasional) exposure and exposureduring childhood and adolescence are likely important predictorsfor basal cell carcinoma and cutaneous malignant melanoma. Highlevels of chronic exposure, such as working outdoors, is more oftenassociated with squamous cell tumours.
21.
The following facts also link sunlight exposure to skincancer:
Most skin cancer occurs in areas of skin most heavily exposed tosunlight (ears, forehead, arms, etc).
Skin cancer among people who are sensitive to sunlight is morecommon in regions with stronger sunlight.
People with genetic diseases that make them more sensitive tosunlight have a greater chance of developing skin cancer.
Studies show that ultraviolet radiation similar to sunlightcauses skin cancer in animals.
UV radiation from tanning beds, or from sun lamps may cause skincancer. While skin cancer has been associated with sunburn,moderate tanning may also produce the same effect. UV radiation canalso have a damaging effect on the immune system and causepremature ageing of the skin, giving it a wrinkled, leatheryappearance.
Types of skin cancer linked to sunlight exposure Three differenttypes of skin cancer are linked to sunlight exposure:
basal cell cancer, squamous cell cancer, and malignantmelanoma.
Factors affecting risks of developing skin cancer Five mainfactors influence the risk of skin cancer:
skin pigment and ability to tan, heredity, exposure tochemicals, amount of exposure to sunlight, and people who have hadorgan transplants and are on
immuno-suppressive drugs are prone to developing squamous cellcarcinoma.
Skin Pigment and Ability to Tan Ultraviolet radiation fromsunlight affects everybody's skin to some extent, but the skin'sresponse varies widely from person to person. People's sensitivityto the sun varies according to the amount of pigment in the skinand the skin's ability to tan. Ultraviolet radiation causes tanningin two different ways: by immediate tanning and by delayed tanning.Immediate tanning causes the skin to darken in response to UVA.This darkening begins during the period of exposure, but fadeswithin a few hours or days. The amount of tanning increasesaccording to the skin's natural darkness and previous amount oftanning. Delayed tanning occurs two to three days after exposure toeither UVA or UVB. It lasts from several weeks to months, and ismaintained by repeated exposure to sunlight. With delayed tanning,the skin increases its production and distribution of dark pigment.The skin also becomes thicker. These changes can follow sunburningor develop gradually over a long period of repeated brief exposuresto sunlight. Some people burn easily after the first hour of sunexposure following winter or any period away from the sun. Otherpeople, especially those with dark skin, never burn. Thisdifference in reaction makes it possible to classify skin into oneof six different types (see Table 2-2).
Table 2-2 Classification of Skin Types
Skin Type Hair Complexion Freckles Sun Reaction Tanning
I Red or Blonde Very Fair +++ Always burns Never tans
II Blonde Fair ++ Often burns Tans lightly
III
Blonde or Light Brown
Fair to Medium + - 0
Sometimes burns
Tans progressiv-ely
23.22.
IV Brown Olive 0 Rarely burns Tans easily
V Brown to Black
Dark 0 Rarely burns Tans deeply
VI Black Very dark 0 Never burns Tans deeply The risk of skincancer from the sun generally follows the same pattern. Darkerskinned people have lower risk of sun-induced skin cancer. Theperson most prone to skin cancer caused by sunlight tans poorly andsuffers sunburn easily. Frequent and/or intense sunburn in childrenwith fair skin and freckles has been linked to malignant melanomalater in life. Heredity For reasons not completely understood,people with Celtic heritage (Irish, Scottish or Northern European)have increased risk of skin cancer from the sun. Genetic diseasesthat affect the skin can also increase the risk. For example,albinism, a genetic condition which prevents the production ofnormal skin pigments, makes the skin sensitive to ultravioletlight. Exposure to Chemicals Exposure to certain chemicals canincrease the skin's sensitivity to ultraviolet light through aprocess called photosensitization. Examples of such chemicalsinclude:
coal tar pitch and petroleum products containing polycyclicaromatic hydrocarbons (PAHs),
certain printing chemicals used in photosensitive printingprocesses,
certain drugs and antibiotics such as tetracyclines,sulfonamides, thiazide diuretics, chlorpromazine, oralcontraceptives, and
24.
chemicals called psoralens found naturally in certain plants,fruits and vegetables.
Antibiotics must be taken internally before the skin becomessensitive to sunlight. However, simple skin contact with psoralens,which are found in figs, parsnips, citrus plants, or moldy celery,can make the skin more susceptible to sunburns in some individuals.Immuno-Compromised Organ Transplant Patients Organ transplantpatients usually take immuno-suppressive drugs to reduce the bodysrejection of the transplanted organ. Suppression of the immunesystem by heavy doses of drugs after transplant surgery contributeto the incidence of skin cancer. Approximately 35 to 70 percent oforgan transplant patients develop skin cancer within 20 yearsfollowing transplant surgery, depending on geographic location.Some transplant recipients have more than 100 squamous cellcarcinomas a year. More alarmingly, some long-term transplantpatients actually die from skin cancer.
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Chapter 3
Previous Accepted Treatments ACTINIC KERATOSIS There is no onebest method to treat all skin cancers and precancers. The choice isdetermined by many factors, including the location, type, size,whether it is a primary tumour or a recurrent one, and also healthand preference of the patient. For example, a treatment that has ahigh cure rate and is painless but leaves a large scar might not bepreferred for a tumour on the face. Almost all treatments areperformed in the physicians office or in special surgicalfacilities. Most skin cancer removal can be done using a localanaesthetic. Rarely, extensive tumours may require generalanaesthesia and hospital admission. There are many methods foreliminating AKs. All cause a certain amount of reddening, and somemay cause scarring, while other approaches are less likely to doso. Cryosurgery The most common treatment for AKs, it is especiallyeffective when a limited number of lesions exist. Liquid nitrogenis applied to the growths with a spray device or cotton-tippedapplicator to freeze them. They subsequently shrink or becomecrusted and fall off, without requiring any cutting or anaesthesia.Some temporary redness and swelling may occur after treatment, andin dark-skinned patients, some pigment may be lost. Curettage andDesiccation This procedure is for lesions suspected to be earlycancers. To test for malignancy, the physician takes a biopsyspecimen, either by shaving off the top of the lesion with ascalpel or scraping it off with a curette. Then the curette is usedto remove the base of the
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lesion. Bleeding is stopped with an electrocautery needle, andlocal anaesthesia is required. Topical Medications Medicated creamsand solutions are used to remove both visible and invisible AKswhen the lesions are numerous. The patient applies the medicationaccording to a schedule. After treatment, some discomfort mayresult from skin breakdown. 5-fluorouracil (5-FU) cream orsolution, in concentrations from 0.5 to 5 percent, is the mostwidely used topical treatment for AK. It is used on the face, ears,and neck. Some redness, swelling, and crusting may occur. Anotherpreparation, imiquimod cream, is used for multiple keratoses. Itcauses cells to produce interferon, a chemical that destroyscancerous and precancerous cells. An alternative treatment, a gelcombining hyaluronic acid and the anti-inflammatory drugdiclofenac, is also used. Chemical Peeling This method makes use oftrichloroacetic acid (TCA) or a similar agent applied directly tothe skin. The top skin layers slough off, usually replaced withinseven days by new epidermis (the skins outermost layer). Thistechnique requires local anaesthesia and can cause temporarydiscolouration and irritation. Laser Surgery A carbon dioxide orerbium YAG laser is focused onto the lesion, removing epidermis anddifferent amounts of deeper skin. This finely controlled treatmentis an option for lesions in small or
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narrow areas; it can be effective for keratoses on the face andscalp, as well as actinic cheilitis on the lips. Laser surgery isuseful for people with bleeding disorders and is also used as asecondary therapy when other techniques are unsuccessful. However,local anaesthesia is usually necessary, and some scarring andpigment loss can occur. Photodynamic Therapy (PDT) PDT may be usedto treat lesions on the face and scalp. Topical 5-aminolevulinicacid (5-ALA) is applied to the lesions by the physician. Within thenext 24 hours, the medicated areas are exposed to strong light,which activates the 5-ALA. The treatment selectively destroysactinic keratoses, causing little damage to surrounding normalskin, although some swelling and redness often occur. NON MELANOMASKIN CANCERS Treatment depends on the:
type of skin cancer, its stage and location and the,individual's age and overall health.
People with small basal cell carcinomas, for instance, may needonly simple treatment. That's because basal cell cancers rarelyspread to other parts of the body and seldom are fatal. Squamouscell carcinomas have a greater tendency to spread, and may requiremore treatment. Skin cancers are usually treated by adermatologist, a doctor who specializes in skin diseases. Treatmentoften can be done in the doctor's office. Most require a localanaesthetic. Some tiny skin cancers are completely removed duringthe biopsy.
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No more treatment is needed. However, most require additionaltreatment to eliminate all of the cancer cells. Three kinds oftreatment are used for most skin cancers. They are:
Surgery: Taking out or destroying the cancer. Chemotherapy:Giving drugs to kill the cancer cells. Radiation therapy: Usingpowerful energy from x-rays or
other sources to destroy the cancer cells. In addition to these,there are other treatment options. Surgery Surgery is the mostcommon treatment. Any of several surgical methods may be used:
Simple excision involves cutting out the tumour with a margin ofsurrounding normal skin to be sure it is completely removed.
Cryosurgery (cryo = "cold") freezes and kills the cancer cells.It uses liquid nitrogen, which has a temperature of 196 degreesbelow zero Celcius. The extreme cold instantly kills the tumour,which falls off like a scab after the area thaws. Cryosurgeryitself is painless. However, the treated area may become swollenand painful after it thaws. Cryosurgery is used mainly for small orsuperficial skin cancers, and to remove precancerous growths.
Curettage and electrodessication combines two methods. In one,the doctor uses a curette, a sharp, spoon-shaped instrument, toscoop out the tumour. The area is then treated withelectrodessication, applying electrical current produced by aspecial machine. It controls bleeding, and dehydrates and killscancer cells remaining near the edge of tumour area.
Micrographic surgery (or Mohs surgery) attempts to
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remove all of the tumour and as little surrounding normal tissueas possible. One layer of tumour is removed and examined with amicroscope. If cancer cells are present another layer is removedand examined. The process continues until all cancer cells havebeen removed.
Laser surgery uses the highly focused beam of light from a laserto destroy cancer cells. It is seldom used for cancers that havenot grown beyond the outer layer of the skin.
Skin cancer surgery will leave a visible scar. Its size usuallydepends on the size of the cancer and the amount of tissue removedduring surgery.
Cryosurgery for a small tumour usually leaves a faint, whitescar.
Treatment of large cancers may require a skin graft to close thedefect. Grafting involves removing skin from another part of thebody and moving it to the area where the cancer was removed.
Chemotherapy Chemotherapy means treatment with anti-cancerdrugs. The treatment for skin cancer often uses anti-cancer drugsin a lotion or cream applied to the skin. This localized, ortopical, chemotherapy is for superficial tumours that have notadvanced beyond the top layer of the skin. Systemic chemotherapyalso may be given in a pill, injected into a muscle, orintravenously through a needle in a vein. This body-wide, orsystemic, chemotherapy can kill cancer cells that have spreadoutside the skin. It may cause nausea and other side effects insome individuals. Side effects are common. This treatment isgenerally used for metastatic cancer.
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Radiation Therapy Radiation therapy, or radiotherapy, uses aspecial kind of energy carried by invisible rays or particles tokill cancer cells, or keep them from growing. X-rays are the kindof radiation often used to kill skin cancer. The amounts are muchhigher than those used in an ordinary mammogram or chest x-ray.This therapy often is used for cancers that occur in areasdifficult to treat with surgery, especially in the very elderly,who may be unable to safely undergo surgery. These include cancerson the ears, eyelids, and tip of the nose. Radiation therapy maycause:
Rash, redness, or dryness in the area. Other changes in skintexture or colour may develop after
radiation therapy. They may become more noticeable yearslater.
Other Treatments Several other treatments may be used for skincancer, including:
Photodynamic therapy uses drugs that collect inside a tumour. Aspecial light is then focused on the tumour. The light triggers achemical reaction in the drug that destroys tumour cells, but doesnot harm surrounding normal tissue.
Biological therapy tries to use the body's own natural defensesto attack and destroy cancer cells. Cells are grown in a laboratoryand exposed to substances that boost their disease-fightingability. The activated cells then are injected back into the bodyto attack the tumour. Biological therapy is used mainly foradvanced forms of cancer that cannot be treated with other methods.It is available in clinical trials, studies conducted in medicalcentres to determine its safety and effectiveness.
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Skin Cancer Prevention The most important preventive measure isto avoid excessive exposure to the sun. Ultraviolet (UV) radiationin sunlight damages the genetic material DNA in skin cell genes.This increases the risk that a normal cell will start growingabnormally and become cancerous. UV rays also damage the structureof the skin in ways that cause premature skin ageing and wrinkling.Prevention must begin in childhood. That's because most people getabout 50% of their lifetime sun exposure before age 18 1-4.
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Chapter 4
From the Past to a New Era
NOW, WITH THE KNOWLEDGE OF THE ABOVE INFORMATION, WE TURN TO ANEW ERA OF A NOVEL,
SAFE, EFFECTIVE TREATMENT FOR PRECANCERS AND MALIGNANT NONMELANOMA SKIN CANCERS
EGGPLANT HAS THE SOLUTIONS FOR THE
TREATMENT OF SKIN CANCERS
Fig. 4-1: Eggplant produces glycoalkaloids which are extractedand purified then incorporated into the cream, Curaderm BEC5, whichis applied to a skin cancer resulting in the complete removal ofall cancer cells without affecting normal cells and healing of thetreated lesion with exceptional cosmetic results.
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Research Research is the first step in biopharmaceutical productdevelopment. Initially this involves optimization of chemicalstructures into leading compounds. Once a leading compound has beenidentified, the pre-clinical phase commences. BEC - SolasodineGlycosides Our research has resulted in the identification andcharacterization of a mixture of solasodine glycosides consistingmainly of solasonine and solamargine from various plant sourcesincluding edible fruit such as the eggplant. The actives weretermed BEC which is a standardized mixture of the twotriglycosides, solasonine, solamargine and their correspondingdi-and monoglycosides 5-15. Fig. 4-2: BEC is a standardized mixtureof sugar-bound Solasodine. The two main glycoalkaloids areSolasonine and Solamargine. All of the glycoalkaloids are made upof the steroid (aglycone meaning without sugar) Solasodine and oneor more of the sugars rhamnose, glucose or galactose.
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Pre-Clinical Phase In the pre-clinical phase, we evaluated BECfor possible therapeutic potential by conducting Ex vivo and Invivo studies. Ex Vivo studies have demonstrated that BEC waseffective against a wide spectrum of human cancers and that BEC wasselectively killing cancer cells without harming normal cells16-27.
Fig. 4-3: Effect of BEC on various primary cell lines and cellcultures. This figure shows that at a concentration of 6 ug/ml ofBEC, all Ovarian cancer cells are killed but no Bone Marrow cellsare effected. In Vivo studies of BEC with terminal tumours in mice,rats and large animals (horses) clearly established that BEC curedterminal tumours in animals. The safety of BEC administration wasalso shown 15, 19, 28-36.
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Fig. 4-4: This shows that two doses of BEC cured 42% whereasthree and four doses cured 92% of the mice that originally hadterminal cancer. All untreated mice with the cancer died at day20.
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Phase I Clinical Trials
Here we have to distinguish between the topical application(cream) as opposed to internal use such as oral or intravenousadministration. Phase I clinical trials tested BEC for safety(adverse effects) dosage tolerance, metabolism, excretion andpharmacodynamics in a small group of subjects. BEC, at variousconcentrations up to 50% in a cream formulation, was shown to bevery safe 15, 17-20, 37-43. BEC when used as Curaderm BEC5 fortreating non melanoma skin cancers could not be detected in theblood when analyzed for, by a very sensitive procedure, using GCMS.So, when Curaderm BEC5 is used, no systemic absorption occurs, thisis not surprising since Curaderm BEC5 contains much less BEC thanis found in the eggplant. Hence, Curaderm BEC5 is extremely saferegarding BEC content! BEC when used in our studies in creamformulations established that these preparations were welltolerated and safe. Analyses of blood and urine samples duringtreatment with Curaderm BEC5 showed no side effects 15, 17-20,37-43. Haematological (Table 4-1), biochemical (Table 4-2) andurinalytical parameters obtained from 62 patients prior to, duringand after Curaderm BEC5 treatment indicated that the parametersremained within the population normal range. Table 4-1: BloodHaematological constituents monitored before, during and afterCuraderm BEC5 treatment.
White blood cells Red cell distribution width
Red blood cells Platelet count
Haemoglobin Mean platelet volume 39.
Haematocrit Heterophils
Mean corpuscular volume Lymphocytes
Mean corpuscular Haemoglobin concentration Basophils
Mean corpuscular Haemoglobin Monocytes
There were no significant differences between before, during andafter treatment in any of these parameters. Table 4-2: PlasmaBiochemical constituents monitored before, during and afterCuraderm BEC5 treatment.
Sodiumion Potassiumion Chlorideion TotalCO2 Creatinine UricAcidUreanitrogen Inorganicphosphate CalciumLDHASTGGTALTAPGlucoseGlobulinsAlbuminTotalProtein
There were no significant differences between before, during andafter treatment in any of these parameters. It was established thatwhen a 1:1 mixture of solasonine and
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solamargine (the major components of BEC) was administeredintravenously at a dose of 1.5 mg/kg/day over 4 hours the analysesof the pharmaco*kinetic data revealed that the biological half-lifeof solasonine was 5.57 1.27 h and for solamargine this was 8.4 2h.The clearance was 5.6 1.6 L/h for solasonine and 3.0 0.7 L/h forsolamargine 44. Unlike many other new drugs that meet the marketplace, we have established the mode of action of BEC. That is, weknow how and why BEC selectively kills cancer cells but not normalcells. We have established that cell death occurs by apoptosis.Very interestingly, cancer cell death caused by BEC occurs whilethe cancer cells are resting and while they are dividing. Thisobservation is in stark contrast to the other anticancer drugs thatonly kill cancer cells while they are dividing, they also killnormal cells when they too are dividing.
Mechanism of Action of BEC is Unique We have now establishedthat cancer cell death through interaction with BEC involves abiochemical process not exploited by the industry at the time.Unlike established anticancer drugs, BEC is not anti-mitotic in itsaction. That is, it does not merely interfere with the celldivision process. Rather the cell itself is killed through theinteraction. Importantly, the mechanism of action incorporates celllysis through disruption of the membrane of the lysosome thusreleasing the contents of the lysosome within the cell which thenkills the cell through a system similar to apoptosis. Unlike otherspecific anticancer treatment such as matrix metalloproteinaseinhibitors, BEC is toxic to cancer cells and the tumours areeradicated as opposed to merely being constrained. Unlikeanti-angiogenics, cell death from BEC is rapid and not dependentupon starving the cancer cell.
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Apart from the obvious advantage of providing a different lineof attack against cancer (and the concomitant implications formulti-drug resistance), we have shown and now confirmed byindependent other investigators, that BEC acts preferentially upondifferentiated cells (cells transformed to cancer). This may becompared to traditional untargeted cytotoxics (anticancer drugs)which equally affect normal cells, resulting in severe toxicreactions in fast growing tissues and associated adverse reactionssuch as nausea, infection (as a result of bone marrow suppression),hair loss, severe skin reaction and ulceration. Importantly,traditional antineoplastic (anticancer drugs) are only effective atproliferating stages of cancer growth (when the cancer cells aredividing) whereas, BEC is effective at both proliferating andresting (non dividing) cancer cells. Pharmacodynamic studies havedetermined that cancer cells have a specific receptor thatrecognizes and binds BEC. Normal cells do not have this receptor,or if so, in only minor quantities. So BEC does not attach itselfsignificantly to normal cells. BEC is then internalized into thecancer cells and kills the cancer cells as shown in figures 4-5 and4-6. The receptor on the cancer cells have been characterized as acell membrane glycoprotein 16, 18, 20-30, 34, 45-47.
Fig. 4-5: The results of cell culture and whole animal studiesindicate that the mechanism of action of BEC involves the specificrecognition of the sugar parts (in particular the sugar rhamnose)of the glycoalkaloids by specific receptors, lectins, located inthe plasma membrane. Binding to these receptors, forming a complexof receptor-BEC results in endocytosis of the complex. Once insidethe cell, the complex is taken up by the lysosomes (stomach ofcell). The lysosome breaks up BEC and the alkaloid Solasodine isgenerated. Solasodine in turn causes the lysosome to rupture. Thecontents of the lysosome is spilt into the cell. The contents ofthe lysosome consists of many hydrolytic enzymes that can digestfats, proteins and carbohydrates. These enzymes then break down anddigest the contents of the living cell which leads to sudden deathof these affected cells. Malignant cells have greater abundance ofthese sugar receptors (lectins) than normal cells resulting inkilling of cancer cells relative to normal cells. Fig. 4-6: Theglycoalkaloids causes the cytoplasm of the cancer cells to undergodissolution, the nuclei contract and become dark staining (a),nuclei then enlarge (b), the chromatin (contents of nucleus) clumps(c), and finally the nuclei 42. 43.
disintegrate (d). Only cellular debris is left after theinteraction of the cancer cells with BEC (e). This cell death ischaracteristic of apoptosis which is also known as programmedcancer cell death. An analogy of the unique mechanism of action ofBEC is herewith explained in simple English. The BEC components arejoined together as a sugar (glyco) part with an alkaloid(solasodine) part. Imagine that cells are represented by rooms withdoors containing particular locks. A cancer cell is a room with aspecific door lock which is different than the door lock that is onthe normal (cell) room. The sugar (rhamnose) part of BEC may beconsidered as a specific key and the alkaloid is a bomb. The key ofBEC only fits the lock and can open and enter the cancer cells. Thekey of BEC does not fit and cannot unlock the door and thus can notopen or enter the normal cells. Once BEC has entered the cancercell, something in the cell causes the bomb (solasodine alkaloid)to explode and the cancer cell is immediately killed. Because thebomb does not get into the normal cells it cannot do harm to thesecells. Thus the uniqueness of BEC as opposed to all otheranti-cancer drugs is that BEC specifically only kills cancer cellswithout harming normal cells!
Phase II Clinical Trials A Phase II study marks the beginning ofclinical trials on a specific, statistically determined number ofpatients to:
determine the efficacy of the compound for specificindications,
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determine dosage tolerance and optimal dosage for future trialsand
identify possible adverse effects and safety risks.
Specific Indications Studied Precancer
Actinic Keratosis Malignant Skin Cancer
Basal Cell Carcinoma (BCC) Squamous Cell Carcinoma (SCC)
Results of Phase II Clinical Trials with BEC In all the clinicalstudies biopsies were taken before and after treatment with BECformulations. This was done to ensure, not only clinically, butalso histologically (microscopicaly) what skin cancer was treated,and to determine the effectiveness of BEC after the treatment wascompleted. On some occasions biopsies were taken during BEC therapyto determine by what methods BEC was killing the cancer cells. Theresults of the Phase II clinical studies with 129 patients revealedthat BEC in cream formulations was very effective for the chosenspecific indications AK, BCC and SCC. Patients tolerated high dosesof BEC and it was determined that very low doses of BEC in thepresence of keratolytic agents were optimal for treating the nonmelanoma skin cancers.
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Fig. 4-7: Clinical and histological diagnosis of an SCC on a legof a patient before treatment (lane A); during therapy (lane B);and site of treated SCC after completion of therapy (lane C). 1.clinical diagnosis; 2. histological diagnosis. Arrows indicatecancer cells dying during Curaderm BEC5 treatment (lane B; 2). Theobservation of this type of cell death caused by Curaderm BEC5 issimilar to those obtained in cell culture studies. The systemicadverse effects were non existent when blood chemistry, haematologyand urine analysis were tested and compared before, during andafter BEC therapy. No safety risks could be identified.
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Fig. 4-8: Clinical diagnosis of a BCC on the nose of a patientbefore treatment with Curaderm BEC5 (1a), during therapy (1b) andsite of treated BCC after completion of therapy (1c). Clinicalprogress of a BCC close to the eye of the patient before treatment(2a), during therapy (2b), and site of treated BCC after completionof therapy with Curaderm BEC5 (2c). Local adverse effects werelimited to local skin irritation and erythema (reddening of theskin). Some patients experienced some pain at the site ofapplication for a short duration 15, 17-20,37-43.
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Fig. 4-9: Histological analysis of a BCC before Curaderm BEC5therapy showing the deep infiltrated cancer cells well within thedermis (a); after Curaderm BEC5 therapy no cancer cells are present(b).
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Phase III Clinical Trials The results of Phase III trialsdetermined that BEC in cream formulations were effective and thesafety profile was very acceptable. Curaderm BEC5 and Phase IIIClinical Studies (232 patients) BEC was now ready to undergo a moreextensive clinical trial. Curaderm BEC5 was chosen for the PhaseIII trials. Single and randomized double-blind placebo controlledstudies were done on patients with lesions as described with thePhase II studies. A placebo is an inactive cream (in our case thesame cream formulation but without the BEC) that has no treatmentvalue. Experimental treatments are compared with placebos to assessthe experimental treatments effectiveness. The Phase III studieswere done in Australia and independent multi-centre hospitals inthe United Kingdom. Before the clinical studies commencedappropriate protocols were assessed to determine the appropriateexecution of the clinical trials. In the United Kingdom theprotocol was approved by the Medical Control Agency (MCA) for themulti-centre studies. A protocol is a carefully designed study planto safeguard the health of the participants as well as answerspecific research questions. The results of the Phase III trialsdetermined that Curaderm BEC5 produced success rates of 78% whenCuraderm BEC5 was applied twice daily under occlusive dressing for8 weeks. If the treatment regime was extended to 12 weeks thesuccess rates were virtually 100%. Only local skin irritation anderythema were observed as adverse reactions. Therefore thetreatment with Curaderm BEC5 was considered to be a safe therapy.Success was defined as zero presence of non melanoma skin cancersafter histological examination of samples extracted from the lesionsite by punch biopsy. In addition, treated patients were
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followed up for over 5 years post treatment and it wasdetermined that there were no recurrences of the treated lesions!18-20, 41- 43, 48-53 Figures 4-7 to 4-11 show cases which have beenfollowed up 5 years post treatment.
Fig. 4-10: Large BCC on the temple of a woman (a). This BCC hadbeen surgically removed and skin grafts applied on two previousoccasions only to return. Four weeks treatment with Curadermresulted in full regression (b). Note the cosmetic result. Theclinical diagnosis was confirmed histologically by punch biopsy(c). After completion of the therapy histopathology determined thatno residual cancer was present (d). Clinical assessment 5 yearspost treatment revealed that there was no recurrence.
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Fig. 4-11: SCC on the nose of a patient before (a), during (b)and after Curaderm treatment (c). Curaderm was applied for 5 weeks.Note the depth of the cancer as cartilage was exposed duringtreatment. The clinical diagnosis was confirmed histologically bypunch biopsy (d). After completion of the therapy histopathologydetermined that no residual cancer was present (e). Clinicalassessment 5 years post treatment revealed that there was norecurrence.
Phase IV or Post-Marketing Studies These studies are done tofurther confirm and describe clinical benefit of Curaderm BEC5 andyield additional information including risks and optimal use.Post-launch safety surveillance is designed to detect any rare orlong-term adverse effects over a much larger patient population andtimescale than was possible during the initial clinical trials.Phase IV trials are important as they detect any rare or long-termadverse effects. Such adverse effects have resulted in the
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withdrawal or restriction of a drug, recent examples includecerivastatin (Baycol, Lipobay), troglithzone (Rezulin) androfecobix (Vioxx). Registration of adverse effects when 50,000patients had used Curaderm BEC5 resulted in only two adverseeffects documented over a ten year period with the TherapeuticGoods Administration (TGA) in Australia. Both documented adverseeffects were dermatitis at the site of Curaderm BEC5 application.Cessation of Curaderm BEC5 application resulted in remission of thedermatitis. These observations secure Curaderm BEC5 treatments ashaving an exceptional safety profile 50, 54. Following are somepatient cases (figures 4-12 and 4-13) that have been treated withCuraderm BEC5 at the Phase IV clinical stages. Fig. 4-12: Large BCCon the leg (a). Note how rapid the cancer was being destroyed byCuraderm during treatment (b - d) and how rapid the wound healedafter 5 weeks of Curaderm therapy (e). The clinical diagnosis wasconfirmed histologically by punch biopsy (f). After completion ofthe therapy histopathology determined that no residual cancer waspresent (g). Clinical assessment 5 years post treatment revealedthat there was no recurrence.
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It can therefore be concluded that Curaderm BEC5 has beencritically evaluated, and when compared to many drugs that arecurrently marketed, is far superior in safety and efficacy.Curaderm BEC5 has met all the requirements regarding, research,pre-clinical, and clinical studies to enable its rightful placeacceptance by health professionals and public as an excellenttreatment for non melanoma skin cancers. Curaderm BEC5 is thetreatment of choice for non melanoma skin cancers. Fig. 4-13: Alarge SCC (approximately 8cm x 6cm) on the shoulder of a patientbefore (a), during (b) and after (c) treatment with Curaderm. After10 weeks the tumour was completely healed. The clinical diagnosiswas confirmed histologically by punch biopsy (d). After completionof the therapy histopathology determined that no residual cancerwas present (e). Clinical assessment 5 years post treatmentrevealed that there was no recurrence.
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Chapter 5
Comparative Available Treatment Regimes vs. Curaderm BEC5
Various forms of Surgery vs. Curaderm BEC5 BCCs can be difficultto eliminate by other widely used procedures and 5 to 10 percent ofBCCs can be resistant to treatment or locally aggressive, damagingthe skin around them, and sometimes invading bone and cartilage.SCCs are more difficult to treat than BCCs and like BCCs, can causedisfigurement. A small proportion (3-5 percent) can spread todistant organs and become life-threatening. Surgery is the mostcommon treatment for these non-melanoma skin cancers. Unfortunatelyrecurrence rates when surgical methods are used are very high(30-67 percent) for non-melanoma skin cancers55. Surgical excisionis invasive with the attendant risks of infection and is expensive.Where surgical excision is adopted, reconstructive surgery may alsobe required to address residual scarring. Tens of thousands ofpatients have now used Curaderm BEC5 successfully. Most patientshave treated small to medium sized skin cancers. It has alreadybeen shown in Chapter 4 that large skin cancers can also be treatedwith Curaderm BEC5. In this Chapter it is now shown further thatnot only large, but also difficult to treat areas with skin cancersare also treated effectively with Curaderm BEC5. Surgicalprocedures for these skin cancers would have most likely resultedin disfigurement, skin grafting and other reconstructive surgerywith the likelihood of loss of parts of the body. Figures 5-1 to5-14 show clearly that skin cancers which are either large,invasive or positioned in areas where surgery or any othertreatment procedures would have resulted in highly compromisingresults. The results with Curaderm BEC5, as can be seen, areexceptional. In particular one case is shown whereby the
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patient is an own internal control, meaning that the differencebetween Curaderm BEC5 therapy and surgery are directly comparable.This patient who was treated with Curaderm BEC5 for an SCC on thehead visited his dermatologist after Curaderm BEC5 treatmentbecause he had bumped his head accidentally. During theconsultation his dermatologist questioned the patientsparticipation in a Curaderm study and convinced the patient thatCuraderm was unproven and that surgery was now necessary involvinga skin graft on the Curaderm treated site. The patient wasintimidated and scared and agreed to the surgery but requested thehistological evidence after surgery that the SCC was still presentfollowing Curaderm therapy. After the surgery was completed, sixareas of the surgically removed tissue representing the entire areaof the surgically excised skin were analyzed histologically. Therewere no traces of cancer whatsoever in the surgically removedtissue. Thus, Curaderm had already removed the cancer altogether.Table 5-1 shows the histopathological report of the largesurgically removed tissue. No traces of cancer could be found. Thisis a unique case, because it shows the end result of surgery andskin graft (Fig. 5-15) albeit from a suspected SCC lesion (alreadysuccessfully removed by Curaderm BEC5 therapy) and the end resultof the Curaderm BEC5 successful treatment (Figure 5-12) of the truelesion on the same patient at the same lesion site. Theseobservations have now been published in a scientific journal 56.This is truly a case of Surgery vs. Curaderm BEC5. Thus, it can beconcluded that Curaderm BEC5 is advantageous over surgical excisionby demonstrating largely scar-free healing and complete removal ofthe cancer cells. Curaderm BEC5 treatment is efficacious convenientand inexpensive, being a patient administered therapy withexcellent cosmetic results.
56.
Fig. 5-1: BCC on the arm. Note initially how small the lesionappeared before Curaderm therapy (a). During therapy it is clearthat Curaderm was attacking and killing all the cancerous cells(b), which prior to Curaderm treatment were not apparent. Curadermexposes the clinically unnoticed cancer cells and eliminates them(c). Treatment period for this patient was 8 weeks. The clinicaldiagnosis was confirmed histologically by punch biopsy (d). Aftercompletion of the therapy histopathology determined that noresidual cancer was present (e). Clinical assessment 5 years posttreatment revealed that there was no recurrence. Fig. 5-2: Aclinically diagnosed BCC before treatment which appears to be twodistinct lesions (a). During treatment Curaderm shows that it isone large BCC (3cm x 4cm) (b). After treatment the lesion iscompletely ablated and some scar tissue can be seen (c). Treatmentperiod was 16 weeks. Histological analysis before Curaderm therapyshows characteristic infiltrated cancer cells well within thedermis (d); after Curaderm therapy there are no cancer cells (e).Clinical assessment 5 years post treatment revealed that there wasno recurrence.
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Fig. 5-3: BCC before treatment (a) and after 8 weeks of Curadermtreatment (b). The clinical diagnosis was confirmed histologicallyby punch biopsy (c). After completion of the therapy histopathologydetermined that no residual cancer was present (d). Clinicalassessment 5 years post treatment revealed that there was norecurrence. Fig. 5-4: BCC over the left eye of a patient before(a), during (b) and after Curaderm treatment (c). Carefulapplication of Curaderm was required to ensure that the cream didnot enter the eye. During Curaderm therapy the distinct tumour canbe seen surrounded by some inflammation. After treatment there wasno trace of the BCC. Confirmation by histological analysis of theBCC before treatment (d) and after treatment (e) are shown. Thetotal treatment period was 9 weeks. Clinical assessment 5 yearspost treatment revealed that there was no recurrence.
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Fig. 5-5: Clinical (a) and histological (c) diagnosed BCC beforeCuraderm treatment. The diameter of the lesion was 5cm. Clinical(b) and histological (d) analyses after treatment. Duration oftreatment was 8 weeks. Clinical assessment 5 years post treatmentrevealed that there was no recurrence. Fig. 5-6: Clinical (a) andhistological (c) diagnosed BCC in the ear of a patient beforeCuraderm treatment. Clinical (b) and histological (d) analysesafter treatment. Duration of treatment was 10 weeks. Clinicalassessment 5 years post treatment revealed that there was norecurrence.
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Fig. 5-7: This patient had a deep seated SCC under the chin (a).After 6 weeks treatment with Curaderm the cancer cleared up (b).The clinical diagnosis was confirmed histologically by punch biopsy(c). After completion of the therapy histopathology determined thatno residual cancer was present (d). Clinical assessment 5 yearspost treatment revealed that there was no recurrence. Fig. 5-8: SCCunder the right eye of a patient before (a) and after Curadermtreatment (b). Careful application of Curaderm was required toensure that the cream did not enter the eye. After treatment therewas no trace of the SCC. Confirmation by histological analysis ofthe SCC before treatment (c) and after treatment (d) are shown. Thetotal treatment period was 14 weeks. Clinical assessment 5 yearspost treatment revealed that there was no recurrence.
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Fig. 5-9: SCC on the nose of a patient before (a), during (b)and after treatment with Curaderm (c). Treatment duration was 16weeks. The clinical diagnosis was confirmed histologically by punchbiopsy (d). After completion of the therapy histopathologydetermined that no residual cancer was present (e). Clinicalassessment 5 years post treatment revealed that there was norecurrence. Fig. 5-10: SCC on the head of a patient before (a),during (b) and after Curaderm treatment (c). Treatment duration was6 weeks. The clinical diagnosis was confirmed histologically bypunch biopsy (d). After completion of the therapy histopathologydetermined that no residual cancer was present (e). Clinicalassessment 5 years post treatment revealed that there was norecurrence.
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Fig. 5-11: A protruding SCC before (a, b) and after Curadermtherapy (c). Treatment duration was 8 weeks. The clinical diagnosiswas confirmed histologically by punch biopsy (d). After completionof the therapy histopathology determined that no residual cancerwas present (e). Clinical assessment 5 years post treatmentrevealed that there was no recurrence. Fig. 5-12: SCC showing theeffectiveness of Curaderm to specifically target cancer cellswithout affecting normal cells. Before Curaderm treatment (a),during Curaderm treatment (b) and after treatment (c). Treatmentduration was 8 weeks. The clinical diagnosis was confirmedhistologically by punch biopsy (d). After completion of the therapyhistopathology determined that no residual cancer was present(e).
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Fig. 5-13: SCC on the nose close to the eye (a). This SCC wasstarting to impair the vision of the patient. After Curadermtherapy the lesion was ablated (b). After completion on treatmentthe vision was restored. Treatment duration was 10 weeks. Theclinical diagnosis was confirmed histologically by punch biopsy(c). After completion of the therapy histopathology determined thatno residual cancer was present (d). Clinical assessment 5 yearspost treatment revealed that there was no recurrence. Fig. 5-14: Anintra-epithelial SCC on the penis of a patient before (a), during(b) and after Curaderm therapy (c). The prognosis of this patientbefore treatment with Curaderm was amputation. Treatment period was6 weeks. The clinical diagnosis was confirmed histologically bybiopsy (d). After completion of the therapy histopathologydetermined that no residual cancer was present (e). Clinicalassessment 5 years post treatment revealed that there was norecurrence.
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Table 5-1: Histopathology report of the patient described infigures 5-12 and 5-15.
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Fig. 5-15: Skin graft of a surgically removed area which thedermatologist assumed had residual cancer after Curaderm therapy.This patient is represented by Fig. 5-12. Analysis of thesurgically removed area of the skin revealed that there was noresidual cancer present (see Table 5-1), thus this patientunderwent unnecessary surgery and skin grafting. Curaderm hadalready successfully removed all cancer cells prior to skin graftsurgery.
5-Fluorouracil (5-FU) vs. Curaderm BEC5 Of the establishedtreatment regimes, 5-FU has been used extensively as an alternativeto surgery and cryotherapy in respect of actinic keratoses. The useof 5-FU for the treatment of superficial BCC was established afterit was prescribed on an off-label basis. Efficacy rate of 5-FU isvery low against superficial BCC. Additionally, 5-FU is aconventional cytotoxic compound with a corresponding inherenttoxicity profile and so should be used sparingly. Consequentlyphysicians are reluctant to prescribe 5-FU for use on BCCs that arenot located on low risk sites such as limbs or trunk area.
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By comparison, Curaderm BEC5 has an exceptional safety profile.It has been established that neither the active glycoalkaloids(BEC) ingredients of this natural drug nor their breakdown productsenter the blood stream in quantities detectable by a very sensitiveprocedure (Mass spectrometry). Local effects of use are limited toslight inflammation, erythema (reddening of the skin) and stinging.Moreover, Curaderm BEC5 preferentially seeks out and destroyscancer cells and can be used upon substantial and sub-cutaneous(deep within the skin) cancers, rendering it a far superior option.Contrast the position with 5-FU which does not differentiate inkilling dividing cells, whether they are normal or cancerous.Curaderm BEC5 preferentially kills cancer cells only and not normalcells. In addition Curaderm BEC5 kills cancer cells whether theyare dividing or whether they are resting. Finally, Curaderm BEC5has a clinically proven very high efficacy rate.
Photo-Dynamic Therapy (PDT) vs. Curaderm BEC5
In some authorities PDT has been approved for the treatment ofBCC. PDT has significant limitations. The efficacy of PDT in thetreatment of BCCs is low and is limited to superficial BCCs. Sideeffects can prove disproportionate to the disease and may includelocal swelling and inflammation in and around the oesaphagus andlungs. All PDT patients experience photosensitivity forapproximately 30 days due to the continued presence of the drug inthe body, and exposure to bright light or direct sunlight should beavoided to prevent sunburn, redness and swelling. Other reportedside effects include nausea, fever and/or constipation. Thepatients are advised to avoid direct sunlight and bright indoorlight for at least six weeks after treatment.
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PDT centres are capital intensive and so access is limited.Moreover, not every centre incorporates a light source suitable forthe treatment of all possible PDT treatable cancers. In addition,cost, lack of safety and limited efficacy are significantdeterrents for PDT compared to Curaderm BEC5. For all these reasonsPDT is not used much.
Imiquimod vs. Curaderm BEC5
Imiquimod (as Aldara) is presently available as a treatment forexternal anogenital warts. Unlike Curaderm BEC5, topical Aldarademonstrates systemic toxicity and reported adverse drug reactionsinclude fever and general malaise. When used to treat BCCs a rangeof very serious adverse effects have been reported. Table 5-2 showscomparative profiles of the various treatment types: Treatment TypeCost Efficiency Safety
Superficial and Morphoeic
Selectivity Cosmetic Appearance
Surgery High High Moderate Both High Variable5-FU Low Low LowSuperficial None Good
PDT Very High Limited Side Effects Superficial High Good
Aldara Low Limited Side Effects Superficial ModerateVariable
Curaderm BEC5 Low High High Both High Very Good
Table 5-2: The above Table refers to BCCs. Only surgery andCuraderm BEC5 have proven to be effective in the treatment of SCCs.It is important to note that the clinico-physical health benefitsgo
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hand-in-hand with mental benefits resulting in improvedlifestyles. Herewith, a letter received from a patient togetherwith photographs of before, during and after Curaderm BEC5 therapyof a large SCC on the head. I have been a candidate for skin cancerfor many years. Some 6 years ago I was in and out of hospital withovernight stays (at least 3 times a year) having several skincancers surgically removed each time. These skin cancers lesionswere removed from my upper body, upper arms, face, head & agraft on my ear. During this time I would have had over 300stitches, no fun I can assure you. Many of these skin cancerslesions had been previously removed with Liquid Nitrogen butreoccurred at a later date. As I thought it was now time forSurgery to end once and for all. How wrong was I. Not only was Ileft with surgical scars but the lesions reoccurred once again.Then some 2 - 3 years ago I was introduced to a wonderful naturalproduct called Curaderm. After investigations I found that Curadermhad been clinically proven. This cream is made from an activeingredient extract from Egg Plant. I have been using this productever since, it is easy to use in my own home, can carry theCuraderm in my pocket, do not have to travel vast distances forsurgery, no anesthetic, no stitches to be removed and works out tobe an inexpensive medication to have in my medicine chest. Curadermhas now advanced to Curaderm BEC 5. During this time my wife hastreated over 50 BCCs on my head & back and a large SCC on myhead. I am able to treat the rest of these lesions. As my familyhas a history of skin cancers and my brother passed away due to theignorance of skin cancer I have made myself become very aware ofall types of products available for cures.
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Curaderm definitely comes up on the top of my list. Please referto photographs. [Fig. 5-16] Figure 5-16. SCC on the head of apatient before (a), during (b, c) and after (d) Curaderm BEC5treatment. The arrow indicates where the lesion was prior totreatment. It is difficult to distinguish where the cancer oncewas. This SCC is similar to the one described earlier (Figures5-12, 5-15). Again it is shown that the cosmetic result isexcellent. Although Curaderm BEC5 treats large skin cancer lesions,it is extremely important that patients in consultation with theirhealth professionals treat skin cancers in their early stages. Thesmaller the lesion, the shorter the treatment duration and the lesstroublesome for the patient.
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Chapter 6
Recommended Curaderm BEC5 Treatment Procedure
Before applying Curaderm BEC5 cream, patients are instructed towash the lesion and the surrounding area with a mild,non-irritating soap, to rinse with water, and allow the area to drythoroughly. Curaderm BEC5 is to be applied to the lesions insufficient quantity to cover each lesion. The cream is not toextend more than 0.5cm onto the apparently normal skin surroundingthe edge of the lesion. Each lesion is to be covered with anocclusive dressing (paper tape) until the next application ofCuraderm BEC5. The cream is to be applied to each lesion using thedropper lid on the plastic container by gently squeezing thecontainer at least twice daily, ie, at least every 12 hours upuntil the lesion has been completely ablated and replaced withnormal skin. Patients are to wash their hands after application ofCuraderm BEC5 and avoid contact of the cream with their eyes.Cosmetics are not to be used on the affected areas and patients arecautioned to avoid sun exposure. If the dressing becomes detachedbefore the next scheduled dosing, the patient is instructed toreapply new cream and a new dressing. The affected area is to bekept covered at all times during the treatment period. CuradermBEC5 is stored below 25C and maintained under adequate security. Ifthe cream is exposed to higher temperatures and the cream separatesto a liquid form then the separated cream cannot be used further.The patient is explained to expect that, initially duringtreatment, the lesion diameter will increase significantly and thenas treatment progresses the diameter of the lesion will decreaseuntil all cancer cells are replaced with normal cells.
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Figure 6-1 illustrates observable lesion changes in diameterduring Curaderm BEC5 therapy up to week 6 and after cessation ofCuraderm BEC5 therapy. In these studies Curaderm BEC5 was stoppedafter 8 weeks therapy. Form week 2 to 6, Curaderm BEC5 treatmentresulted in significant increases in lesions diameter. After 6weeks of treatment the lesion size was reduced. Follow-up studiesfor 6 months and 1 year show clearly that all lesions hadcompletely resolved. The number of patients studied here were 31 to57. The reason of the initial increase in lesion size is theCuraderm BEC5 is seeking and destroying the cancer cells that areinitially not viable to the bare eye. Fig. 6-1: Changes in lesiondiameter during and after Curaderm BEC5 treatment.
The correlation between the diameter (mm) of the lesion andweeks of treatment with Curaderm BEC 5. The symbol * illustratessignificant differences (Mann-Whitney U-test) from the time priorto treatment. The symbol denotes the end of Curaderm BEC 5therapy.
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Schematic Representation of the Sequential Events of Skin CancerTreatment with
Curaderm BEC5
Before Curaderm BEC5 treatment. The lesion protrudes from theskin. Start Curaderm BEC5 treatment.
During Curaderm BEC5 treatment.
Lesion diameter is larger than before treatment. Curaderm BEC5seeks out and destroys cancer cells well within the apparentlynormal margin and exposes and kills the hidden cancer cells.
Continue to treat lesion with Curaderm BEC5.
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During Curaderm BEC5 treatment. Curaderm BEC5 continues to killthe cancer cells that are well
within the epidermis and dermis, causing an apparent hole in theskin.
Continue to treat lesion with Curaderm BEC5.
During Curaderm BEC5 treatment.
Most of the cancer cells have been killed. The killed cancercells are replaced by normal cells. The diameter of the cancer isnow smaller.
Continue to treat lesion with Curaderm BEC5.
Conclusion of Curaderm BEC5 treatment. No more cancer cells arepresent, only normal cells.
Stop Curaderm BEC5 treatment.
Fig. 6-2: Schematic Representation of the Sequential Events ofSkin Cancer Treatment with Curaderm BEC5.
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Clinical Representation of the Sequential Events of Skin CancerTreatment with Curaderm BEC5
Fig. 6-3: A very large SCC, 6cm in diameter, before (a), during(b d), and after (e) treatment with Curaderm. The treatment periodwas for 12 weeks. Note the specificity of Curaderm for the cancercells and the regrowth of normal cells during Curaderm therapy. Theclinical diagnosis was confirmed histologically by punch biopsy(f). After completion of the therapy histopathology determined thatno residual cancer was present (g). Clinical assessment 5 yearspost treatment revealed that there was no recurrence
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Chapter 7
Will Consuming Eggplant Result in Removal of InternalCancer?
A reasonable question to ask. Before this question is answeredlet us summarize what reports are available on the therapeuticeffects of the eggplant. Eggplant juice significantly reducesweight, plasma cholesterol levels and has beneficial effects on thearterial wall of rabbits that have high blood cholesterol levels.It has also been reported that in humans eggplant is capable ofreducing plasma cholesterol levels up to 30% 57. Eggplant isconsumed extensively in Brazil. It is believed that infusion of apowdered preparation of the fruit reduces blood cholesterol. Onestudy has shown that infusion of the eggplant extract for fiveweeks had a modest and transitory effect of the LDL-cholesterol(bad cholesterol) 58. However, in another study, eggplant did notexhibit a therapeutic effect in lowering plasma cholesterol levelsin humans 59. Further studies should determine whether eggplant canbe truly considered as an alternative to drug therapy for reducingexcessive cholesterol levels. There are many more suggested usesfor eggplant as a therapeutic agent, but most have not beenevaluated under controlled scientific conditions. Now back to thequestion, WILL CONSUMING EGGPLANT RESULT IN REMOVAL OF INTERNALCANCER? I wish I c
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