ON CANCER,

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CANCER NOTES: UNDERSTANDING CANCER--jk

I have saved the old article from 2007, at the bottom, and pasted the new one written end of 2013.  There are some significant improvements and a bit more science.  Of special interest is a very effective treatment for most cancers with minimal side effects, aspirin.  It stimulates the body’s necrosis factor for destruction of abnormal cells. It is well supported by dozens of journal articles, yet it has not entered into treatment protocols—such is the power of pharma.  At the end of the article is the section on aspirin.  This article is periodically updated at http://healthfully.org/rc/id16.html and a long version is at http://healthfully.org/rl/id4.html

CANCER basics & CHEMOTHERAPY- 3pgs -- 11/23/13  http://healthfully.org/rc/id16.html & id4

It is essential to understand the inroads made upon medical science by corporate medicine.   Corporate medicine is market driven; medical science evidence driven.    These two approaches result in different explanations concerning cancer. The goal here is to understand the general basic biology of cancer and its treatment options based quality scientific evidence—without market considerations. What follows is based upon sound science with sources.  Marketing science is driven by profits, & thus promotes aggressive treatments.   Pharma’s marketing ploys confirms Harvard Prof. Dr. Marcia Angell’s  observation that we have “the worst system we could imagine.”  To learn more read Marketing Science and its links.  The goals of the tobacco companies are the same for pharma, maximization of profits, rising stock prices, and rewards for top management. 

“A benign tumor is a mass of cells (tumor) that lacks the ability to invade neighboring tissues or metastasize. These characteristics are required for a tumor to be defined as cancerous and therefore benign tumors are non-cancerous.  Also, benign tumors generally have a slower growth rate than malignant tumors and the tumor cells are usually more differentiated (cells have normal features).  Benign tumors are typically surrounded by an outer surface (fibrous sheath of connective tissue) or remain with the epithelium.  Common examples of benign tumors include moles, colon polyps,[1] and uterine fibroids.   Although benign tumors will not metastasize or locally invade tissues, some types may still produce negative health effects…. [Some types of] benign tumors can become malignant….  invade adjacent tissues or spread to distant sites by metastasizing.  For this reason, benign tumors are not classed as cancer” Wiki.  This is the first area where business has blurred the distinction between benign and malignant by calling them “carcinoma”, then aggressively treat with surgery and chemotherapy.  Critics point out in journal articles the negative consequences of treating benign (small local) tumors of the breast prostate, thyroid cancers, and others tissues with adjunct chemotherapy following excision; moreover, removing some types of benign tumors are not advisable.  Benign breast tumors, called “cancer”, when treated with chemotherapy shorten life over 4.6 years[2] (mostly from the blocking of estrogen as part of therapy).   

“Cancer (malignant neoplasm) is a broad spectrum of diseases involving improperly regulated cell growth.  For that cell growth to become life-threatening it must be capable of sufficient reproduction so as to disrupt essential bodily processes.  Over 80% of fatal cancers spread to more distant part of the body through the lymphatic or blood systems—some such as cerebral cancer often don’t.  With the exception of blood and lymphatic cancers, they form hard tumors.  One of the most important factors in classifying a tumor as benign or malignant is its invasive potential” Wiki.   A microscopic examination of a biopsy by itself is insufficient to prove that the tissue is malignant, for it doesn’t reveal the properties of being invasive and metastatic.  Lab reports often numerical grade the tissue based on shape of differentiation of tissue and this which yields a probability rating.  Lab write ups very often use terms meaning cancerous, which is misleading.  Cancerous can only be definitively determined with additional imagining, such as MRI.  Depending on lab findings,  removal often is the best choice, and but subsequent chemotherapy often isn’t necessary.

Oncogenesis (carcinogenesis): is literally the creation of cancer. It is a process by which normal cells are transformed into cancer cells. It is characterized by a progression of changes at the cellular genetic and epigenetic [regulate the expression of other genes] that ultimately reprogram a cell to undergo uncontrolled cell division, thus forming a malignant mass.  Over 98% of potential mutations and epimutations will have no bearing on cancer” Wiki  For most tissues 7 or more mutations are required to create a malignant tumor.   Less than 10% of all cancers involve inherited mutations, the remainder is a result of environmental factors and bad luck.  Over half the cancers are attributable to carcinogens.  Excluding skin cancer, only about half of all cancers prove fatal.     

Role of Stem cells:  “they are undifferentiated biological cells, that can differentiate into specialized cells and can divide through mitosis to produce more stem cells, which are found in various tissues.  In adult organisms, stem cells and progenitor cells act as a repair system for the body, replenishing adult tissues. Stem cells maintain the normal turnover of regenerative organs, such as blood, skin, or intestinal tissues.  Stem cells possess two properties:  self-renewal (to maintain through cell division the undifferentiated state) and potency (to give rise to any mature cell type).  Induced pluripotent, these are not adult stem cells, but rather adult cells (e.g. epithelial cells) reprogrammed to give rise to pluripotent capabilities of forming more than one type of tissue.  A progenitor cell is a biological cell that, like a stem cell, has a tendency to differentiate into a specific type of cell, but is already more specific than a stem cell and is pushed to differentiate into its "target" cell… and can divide only a limited number of times” Wiki.  The finding of stem cells in malignant tumors, and the heterogeneity of cells in most malignant tumors demonstrates their role.  Unfortunately given there are over 100 tissue types that can become malignant and the variation in properties between different cancers of the same tissue type, there can be no one model for the role of stem cells, pluripotent cells, and progenitor cells in the various cancers.  In most if not nearly all cases, these types of cells pay a central into turning a benign tumor, malignant; and an indolent cancer aggressive.  In most lethal cancers stem and progenitor cells play an essential role.        

The following discussion on treatment and prognosis is about the typical, common cancers, lung, colorectal, breast, & prostate.  There are a few cancers which can successfully be treated with chemotherapy, these are not typical.   These 4 cancers account for about 80% of all cancers (excluding the very common skin cancer, for which only the rare melanoma is very often lethal).

FOUR KEY FACTORS AFFECTING PROGNOSIS:    One factor is the stage I-IV, which is based upon the degree of invasiveness of the cell line and size.  How fast the cancer is invading adjacent tissue and spreading through the tissue of origin can only be determined by successive examinations months apart.   Tumor size and location give a poor approximation.  For an example with a breast cancer of > 5 cm 45% lethal and < 2 cm 96% survival, and similar results for location.  Second is the primary tissue in which it evolved.  Each tissue has its own prognosis.  Pancreas has 3 primary tissues; however, all tissues produce a high percentage of aggressive malignancies (the 5-year survival rate is 2%).  The third factor affecting prognosis is the rate of mutations; the higher the rate the greater the chance that the cancer can metastasize or will develop these abilities. This is roughly correlated with the variety of cells, and percentage of grossly abnormal cells in the tissue.  Fourth factor is the genetic mutations that created the cancer of which there are at least 7 (less for leukemia).  Most consist of a substitution of letter in a codon[3] forming a gene that makes that gene an oncogene.  Since most mutation affected only 1 codon and there are of dozens of codons on the gene, and that mutated codon could specify one of several amino acids in the protein to be formed, the biological consequences of that mutation will be different from the hundreds of other possible mutations of that gene.  The properties of the chromosomal mutations affects prognosis.  Given this complexity, the success of treatments is based on a rough statistically observational probability.     

KEY PROBLEM WITH CHEMOTHERAPY:  Ideally it should function to make long-term dormant or destroy bodily cells that are malignant without also poisoning or making dormant normal bodily cells in an essential organ or tissue type.   The difficulty arises because cancerous cells are nearly identical to normal cells.  Often the difference is inside the cell when a set of genes are turned on to produce semen, milk, etc.  A chemical which could damage cells that produces milk would have to penetrate the breast cells and be capable of disrupting an essential function of that cell in a way to make dormant or destroy it.  Such a chemical would very likely have similar effect on many other types of cells.  Most chemical are not selective and effect many tissue types.  They disrupt cell division, production of capillaries, and other functions which can only be switched off temporarily.  “Thus chemotherapy also harms normal cells that divide rapidly in the bone marrow, digestive tract, and hair follicles, and to a lesser extent slow dividing cells.  This results in the most common side-effects of chemotherapy:  myelo-suppression (decreased production of blood cells, hence also immuno-suppression),  mucositis (inflammation of the lining of the digestive tract), and  alopecia (hair loss).  Virtually all chemotherapeutic regimens can cause depression of the immune system, often by paralysing the bone marrow and leading to a decrease of white blood cells, red blood cells, and platelets Wiki.   Indolent cancers tend to respond less to chemotherapy.  Causing damage to many tissues is why most chemotherapies are given short term and thus prolongs life on average 3 months. 

SHOULD CHEMOTHERAPY BE GIVEN TO A STAGE I, II, OR III CANCER?  Typical survival rates (5 years of being free of metastatic cancer) for the common cancers are 90 for stage I, 80% for stage II, and 65 for stage III.  Higher survival for stage 1 entail treating benign tumors mislabeled malignant.  If chemotherapy is given to those who will remain cancer free, it is life shortening and affects quality of life.  This negative effect is very significant in cancers of the prostate and breast because of hormone blocking (castrating) drugs are included in the chemotherapy.  Without estrogen, total morality was double at 10 years. Using the above stats for stage III, 65% of patients must endure chemotherapy when they don’t need it.  And for the 35% who will die of cancer, they are gaining 3 months of life.  Rather than treat every one, it would be better to treat only those who have progressed to stage IV (metastatic) cancer—better for the patient but not for the oncologist, clinic, and pharma.   And given the small benefit of chemotherapy, why prolong the illness with costly treatment that lowers very significantly the quality of life?   

Hopes Hypothesis:  Chemotherapy in clinical trials rarely has a placebo group.  It is given to terminal patients, thus avoiding long-term following with its side effects.  Remission is measure instead by imaging observations of the tumors size.  Typically the tumor stops growing or shrinks for 3 months.  Suppose the average death occurs in 12 months, some patients will die in 3 months; others will live 2 years or more.  That does not prove that a few patients had an atypical positive response to the drugs.  But rather a few patients had indolent metastatic cancer and would have lived that long, minus 3 months, without the chemotherapy.   

Recommendations: Given the bias in practice of medicine and journal and textbooks, the place to start is with a search of the critical journal articles concerning the treatment and diagnosis.  For the situation of where a suspect tumor is found in a tissue go to a teach hospital for treatment, the standards are better.   Assuming that there is a significant risk the benign tumor will become malignant, have a biopsy taken.  Read carefully the results concerning the abnormality of the tissue. The term cancer, malignant, and carcinoma can only properly be applied it the tumors have spread outside the tissue of origin.  The greater the abnormality of the cells, the greater the risk,[4] and the more likely it will be called malignant though it is benign.  If the risk is substantial that the tumor will evolve into cancer, have it removed.   If cancerous cells are also found in adjacent lymph nodes the risk of it being aggressive and/or metastatic increases.  Remember that time increases risk of an indolent cancer becoming aggressive, and only time will reveal if the removed cancer was metastatic .  If chemotherapy is recommended, submit to it only when major benefits are clearly documented and deduct for bias, which is the norm.  Don’t rely upon treatment guidelines, they are based upon marketing science, so too is the advice of the oncologist whose continuing education is given by pharma.  Published articles have an average bias of 32%.  Only for a few cancers does chemotherapy save lives.  If it is one of those cancers, then see if an in vitro chemo-sensitivity testing[5] is available.  In the majority of cases aspirin is the best prophylactic and treatment because it activates necrosis factor NF-B.  Read Aspirin. Take 975 mg of aspirin daily; and for reducing risk of cancer take 325 or 650 mg daily.  JK has taken aspirin since 1992, an average of 650 mg, and this has reduced his risk over 50%.  Testosterone and natural estrogen moderately reduce risk of certain cancers .         

Aspirin:  It is more of a miracle than penicillin; what has changed is the control pharma exerts. Its major unexpected health benefits were discovered  in the 60s through 90s.  It has the highest cure rate of all chemotherapies for stage I, II, and III,  and is also best at preventing cancer.  Aspirin promotes the apoptosis (death) of abnormal cells through stimulation of various necrosis factors and inhibition of JNK which “regulates several important cellular functions including cell growth, differentiation, survival and apoptosis”  Wiki.   A large collection of journal articles are pasted at http://healthfully.org/aspirin/ & http://healthfully.org/nsaids/.  The past below is from an article prepared by JK at  http://healthfully.org/rc/id3.html; its section on cancer:

 

BREAST CANCER SURVIVAL UP 66% by stimulating necrosis factor TNF—above. Colon cancer survival increased 74%, others.  Mechanism: COX-2 which is associated with increased prostaglandin biosynthesis which correlates to metastasis and carcinogenesis, and aspirin blocks COX-2, thereby reducing risk, plus promotes death of abnormal cells (below).     

CANCERS VARIOUS TISSUES RISK: reduction of63% colon, 39% breast, 36% lung, and 39% prostate cancer. Significant risk reductions were also observed for esophageal 73%, stomach 62%, and ovarian cancer 47%” also.  Epidemiologic studies of malignant melanoma, Hodgkin's disease, and adult leukemia also found that NSAIDs are protective; melanoma 55%.  Other studies have shown that aspirin promotes the death of abnormal cells through the natural mechanism of apoptosis by stimulating tumor necrosis factor NF-B, by p38 & JNK.  Long term, but low dose is insufficient. 

 

The increased survival of breast cancer can be extended to the other glandular, blood, & epithelial cancers.

 

The lack of dissemination of information and the failure to investigate further is a result of corporate medicine and our corporatist state.  Add to that aspirin protection from & treatment of cardiovascular disease, MI, Strokes, Alzheimer’s and ALS, rheumatoid and osteoarthritis; this proves that aspirin is clearly the best of all drugs.  Everyone over the age of 25 should be taking prophylactically a 325 mg uncoated aspirin in the morning and another in the evening.  It anti-inflammatory slows atherogenesis and the resultant cardiovascular disease; that by itself justifies daily usage.  Aspirin was the standard arthritic treatment at much higher dose (3 to 7.5 gm daily, Merck Manual 1987).  The overblown concern for stomach ulcers is the working of pharma, which  ignores the role of pylori bacteria.  The 800 pound gorilla (a phrase used by Harvard Prof. Marcia Angell, MD) has too long used its tobacco ethics.      


[1] "Most hyperplastic polyps are found in the distal colon and rectum.[3] They have no malignant potential,[3] which means that they are no more likely than normal tissue to eventually become a cancer” Wiki.  See also Controversy about removing benign bowel lesions.

[2] E.g., at 10 years in a Danish study there were 16 deaths for those receiving HRT subsequent to breast cancer compared to 33 deaths without HRT.  The same study found at 5 years a 74% reduction in fore arm fractures for the HRT cohort.  

[3] A codon is the  nucleotide triplets (3 bases) that specify which amino acid will be added next during protein synthesis. There are 4 ribonucleic acids bases which can make up the triplet.   A mutation that changes 1 base will in most cases lead to the insertion of a different amino acid, from among the 21 that are used in the production of proteins.  See Wiki.

[4] In some tissues (prostate, thyroid, and colon) the removal of low-grade benign tumor often causes more harm than good.

[5] Like the testing of an antibiotic on a patient’s bacterial culture, the chemotherapy should be tested on an in vitro tumor samples. 

CANCER,  GENERAL  OVERVIEW:

 

 

From 2007 by JK

ONCOGENES:  Cancer is the result of a series of mutations that confer on one cell line (from a single cell) a number of properties for which various biological constraints have been modified.  The process is one of genetic alteration via mutations that alter the DNA of a gene or through gross alteration of chromosome (see #9 below).  A Gene that contributes to making a cell-line cancerous is called an oncogene.  The unchanged, normally functioning, version of that gene is called a proto-oncogene.   There are 12 general types of functional alterations (and thus 12 genetic changes[i]) that contribute to turning a single cell line into a life-threatening cancer; however, not all 12 must be present.  Changes: 

1.  Turning on the chemical signal which causes a cell to rapidly divide.

2.   Turning off the chemical signal which turns stops a cell from rapidly dividing. 

3.   Stimulating the formation of new capillaries to assure adequate oxygen supply for continued growth of the abnormal cells.

4.   Limitless replication of one cell line by turning off telemorase, which limits division to around 50 to 70 generation.

5.   Invade adjacent tissues:  Most organs are enveloped in a membrane (muscles and lungs).  Most cancers fairly early develop the ability to grow through the membrane and invade adjacent tissues. 

6.  Metastasize:  have microscopic colonies of the tumor relocate in other sites.  This involves sometimes a mutation affecting adhesiveness[ii] which thus permits single cells to migrate.

7.  The markers on the cell wall[iii] must change so that when the tissue migrates it does not appear as foreign to the immune system, which will destroy those cells.  Which tissues a cancer migrates to is highly dependent upon the markers.  Over ninety percent of cancer deaths are due to metastases.

8.   Being able to both enter and leave blood vessels like the way lymphocytes do by secreting a factor which allows them to enter a capillary and then at another site to pass out of the capillary again by secreting this factor, a class of compounds know as Src kinase. 

9.   Most cancers have abnormal DNA due to gross changes in the chromosome that consist of translocation, duplication, deletion, or inversion.[iv]  This type of abnormality results in the imperfect expression of genes on that chromosome.

10.  Most cancers have disabled the gene which functions in mechanism that checks during cell mitosis that accurate replication in the new chromosome of the DNA has occurred[v].  Several genes, such as P53, have been identified as essential for this replication checking process. When disabled the risk of cancer in a cell type found in that tissue will increase several fold.  If the factor has been inherited the cancer type will be common among relatives.  Also such cancer will occur earlier than the norm.  P53 is associated with breast and several other types of cancer, for it is only active in certain tissues. 

11.  Excrete growth factors which enable the cancer to attract stem cells which then help support the growth of the tumor by stimulating the growth of capillaries and other structures needed to support a large tumor.  This is a new finding, one which explains the failure of treatments for some patients.

12.  Express any of a number of genes which give stem cells their unique properties.  This is a new finding, one which explains the failure of treatments for some patients

Oncogensis:[vi]  The process in 2 occurs two ways, either by a defect in the DNA of one particular cell line or by the inheritance of a defect in a gene such as P53. 

13. The role of inheritance:  Inheritance accounts for no more than 10% of all cancers.  Such a person often acquires cancer earlier than the norm for that type of cancer by accumulating mutations more rapidly.  All the cells of a tissue with the gene that checks replication, for example that has been disabled are accumulating mutations in the DNA at an accelerated rate.  If however, instead of being inherited the P53 has through random mutation has been disable, only the progeny of that one cell are accumulating mutations at an accelerated rate, including those to the various oncogenes[vii]   This later scenario occurs in 90% of the cancers—inheritance accounts for under 10% of all cancers.

14.  Oncogenes are genes which have been mutated in a way which promotes the cancerous cells to possible become lethal. 

15. Proto-oncogene is a normal gene that can become an oncogene due to mutations or increased expression.  The resultant protein may be termed an oncoprotein.    

THERE ARE A LARGE NUMBER OF GENES WHICH CAN PLAY A ROLE IN THE PORDUCTION OF A CACEROUS CELL LINE. Scientists have identified over 100 genes that are involved in the twelve above processes.  Since a gene occurs on both strands of a chromosome, one inherited from the mother, the other from the father, normally the gene in each strand must be altered by mutation. In some cancers however, the two alleles have not been disabled, but rather their production reduced.   The gross errors in chromosome replication (aneuploidy), such as translocation, can alter the production of an oncogene.  Often for a tumor, the cells are not just aneuploidy, but also unstable, changing every few generations.  In about half of the aneuploidy cells, the mechanism involves the formation of spindles during mitosis.[viii]  Cell biology is complex, and as I pointed out over a decade ago and others still affirm, “each tumor is unique.”[ix] 

 

RATE OF MUTATION:  There are 4 scenarios for speeding up the rate of mutations.  One is a mutation in a single cell that disables one of the systems that checks to see that during mitosis the newly formed mRNA and the DNA are as proscribed by the parent strand of DNA.  With this system disabled, the rate of mutations (imperfect copies of the DNA or RNA) is increased in that cell several fold.  Second, inherited mutation in the system which check for and corrects mutations that occur during mitosis.  Under 10% of people are born with such mutations.  Such mutation confers a very high risk, typically over 90% for developing cancer in that affected tissue.  A third one is through a cancer-causing retrovirus that has “hijacked” proto-oncogenes from their host’s genome, mutating them in the process to make malfunctioning versions.   “Only 15 percent of human cancers are caused by genes introduced by viruses” (Bailey 137).  The fourth is environmental factors, namely mutagenic substances and radiation including photons (sunshine).  The primary environmental cause of cancer is in air filtered through tobacco.  Consistent with other later studies, Ravenholt (1983) found that there were 450,000 premature deaths caused by tobacco, including 50,000 from second-hand smoke—a figure that has remained constant over 3 decades.   

 

NATURAL SELECTION:  A particular mutation or set of mutations will confer upon an exposed tissue survival advantage.[x]  Cancerous cell mired in tobacco tars have a survival advantage over normal tissue.  Even when survival is not an issue, the cancerous cells have a reproductive advantage, and thus crowd out or replace normal tissue.  In fact, which aneuploid cells survive is a result of natural selection, since most of them when formed anew are still born or abnormally slow growing. A rare success case gives that cell line a selective advantage.  Gene mutations and chromosome abnormalities, in rare instances, confer numerical advantage to a cell line.[xi] 

 

NATURAL SELECTION PLAYS A ROLE IN RESISTANCE TO CHEMOTHERAPY:  A cell line with the ability to undergo genetic alterations at high rate can become resistant to chemotherapy.  Thus initial success evaporates when one of the cancerous cells undergoes a mutation that makes it, and thus the new cell line resistant to a particular chemotherapy.   

 

FOUR STAGES OF CANCER:  Four things affect cancer survival.  One is the stage of its development.  Second is the primary tissue in which it evolved.  Each tissue has its own prognosis.  Pancreas has 3 tissues; however, the prognosis is equally dismal for each tissue—the 5-year survival rate is under 2%.  The third factor is where the mutations have occurred on the sequences of codons[xii] that make up a gene, and also what letter of the codon has been substituted; or if there was aneuploidy, where that has occurred.  Not all mutations of the same gene are equal.  So too does the combination of mutations giving rise to a particular cancer affect the prognosis, including both the body’s immune response and the effects of chemo and other therapies.  These differences create the great variation of responses to treatment for a cancer in the same stage (1 through 4) of the same primary tissue in different patients.  The fourth factor is the cancerous tissues ability to becoming resistant to chemotherapy.  If the tissue posses a process which accelerates genetic diversity, such as the defective spindle formation during mitosis (described earlier), then the chances of the cancer becoming resistant to chemotherapy are greater than a similar type of cancer without the defective mitosis.  A cancer will be in remission, often for years, and then suddenly again prove life threatening, and the previous successful chemotherapy proves ineffective.  Four factors thus are relevant in making a prediction as to prognosis. 

 

EARLY DETECTION: While recommended often is not with current technology feasible because of costs per life saved.  This is especially true of people under the age of 50, whose cancer risk is lower. Moreover, most cancers do not produce early unique symptom which will cause people to go to a physician.  Rates of metastasize vary for types of cancer; for lung cancer 72%, 58% for colorectal, and 34 for breast cancer.   

 

 

WHY TREATMENT WITH CHEMOTHERAPY IS UNCERTAIN:  The fundamental cause for the difficulty in devising effective noninvasive (radiation, heat, excision, and like are all invasive and directed at the tumor) methods of treatment for cancer, viz., chemotherapy, is that of finding chemicals that are sufficiently selective as to primarily target the cancer cells and disrupts their growth while not disrupting normal cells and bodily functions.  The difficult arises because cancer cells are genetically nearly identical to normal cells.  In most cases chemotherapy does not eliminate cancer, but rather produces remission and thus prolongs life. 

 

Chemotherapy is commonly used following excision and/or radiographic treatments even when there is no clear evidence of metastasis.  Studies show an improved survival rate for those who receive chemotherapy, often only a few weeks.  This plus the issue of quality of life often entail that such treatments are often not worth their costs.

 

The three leading avoidable causes of cancer are tobacco smoke, obesity, and environmental hazards such as at the work place.  Cancer is a crapshoot; however, risk goes up with age.  A 70-year old is 100 times as likely to be diagnosed with a malignancy as a 19-year old (Gibbs 58).  There are 10 million billion cells that have cooperated in the course of an 80-year life span.  Considering this number of cell, only about 40% of the population will develop a cancer serious enough to result in medical intervention, and about half will die from cancer.  Nature has endowed us with a set of quite effective safeguards against cancer



[i] Leukemia is the exception, for it requires as few as 3 genetic events.  It doesn’t need to invade adjacent tissue, be immortal for blood cells do not have nuclei, or pass through capillaries. Being less, entails that for most Leukemia’s, the average age of development is sooner.

[ii] In most cervical cancer, for example, a mutation causes the cell-to-cell adhesive molecule E-carherin to be digested, and as a consequence the cancerous cervical cell line can spread to distant tissues.

[iii]  On the surface of cells are unique small chains of peptides that function as markers recognized by immune cells.  If that tissue with that particular type of marker is found among a tissue with a different marker, certain type of white-blood cells will recognize the migrated tissue as foreign and initiate the events which will result in the destruction of this foreign tissue.   Cancer cells that spread to a distant organ must go to a tissue type in that organ for which they do not appear foreign (breast cancer often spreads to the brain, for example).  Complex organs with many different tissues, such as the brain and the liver, are thus frequent sites for the primary cancer to metastasize to. 

[iv]  Duplication error consists of a section of the chromosome strand being made more than normal once.  Trisomy occurs when there is an extra copy of the entire strand.  If it occurs on chromosome 21, it results in Down’s syndrome.  Translocation is the shuffling of a section of one strand onto the other strand.  Deletion is where a portion of one of the strands is not replicated.  And inversion is where a section of a strand is reproduced in the opposite to normal order. 

[v]  One method is by methylation of the DNA, which primarily occurs during embyogenesis and development, has been associated with inaction of tumor suppressor genes.  This occurs when the abnormal methylation alters a gene responsible for the checking of the accuracy of the DNA replication.

 

[vi]   Ocogensis:  the origin and growth of  a neoplasm (tumor).  The can be either benign or malignant. 

[vii]  Thus for example in a study of 476 tumors of the thyroid, BRAF oncogene was altered in two-thirds of papillary thyroid cancers, but not in any other kinds of thyroid cancers.  Unfortunately generalizations have counter examples.  Thus oncogene c-fos and c-erbb3 are not disable but less active than in normal tissue.  Conversely RB is more active in colon cancer, and thus protects the tumor from the auto-destruction mechanism.   For one of the common genes which perform this checking function, P53, between one-third and one-half of the cancers have this among other mutations (Bailey 137).  Genetics and Evolution:  The Molecules of Inheritance, Jill Bailey, Oxford University Press, NY, 1995.

[viii]  German A. Pihan and colleagues found and published in March of 04 that of the 116 pre-malignant tumors removed from the tissues of the cervix, prostate, and breast, that between 30 and 72% had defective process during mitosis, Gibbs at 64.

[ix] Untangling the Roots of Cancer, W. Wayt Gibbs, Scientific American, 11/03, P. 61.

[x]  Lengauer and colleagues exposed human cell lines to toxic levels of a carcinogen in broiled meat.  Only a few cells developed resistance and survived.  And all of them were genetically unstable before exposure to the toxin, Gibbs at 64. 

[xi]  Thomas Reid of the national Cancer Institute noted that for colorectal cancer there is aneuploidy of chromosomes 7, 8, 13, or 20, and for cervical cancer of chromosome 3.  He also noted that aneuploidy happened at very early stage and seems to confer a selective advantage.  Reid noted that in the tissues examined there was a stead increase in the number of abnormal chromosomes as the stage of cancer advanced.  It went from 0.2 to 12 for metastatic colon tumors, Gibbs at 64.

[xii]  A codon is the sequence of three consecutive bases on a DNA or mRNA molecule that specify a particular amino acid to be inserted in the production of a protein.  Change a base will in most cases lead to the insertion of a different amino acid, from among the 21 that are used in the production of proteins.



[i] Leukemia is the exception, for it requires as few as 3 genetic events.  It doesn’t need to invade adjacent tissue, be immortal for blood cells do not have nuclei, or pass through capillaries. Being less, entails that for most Leukemia’s, the average age of development is sooner.

[ii]  Telomeres are specific set of codons at the end of a chromosome.  The set is repeated 50 to 70 times.  With each cell division one of the telomeres is removed by a specific enzyme called telomerase.  When the last telomere codon is removed, the cell undergoes senescence.   This is one of the mechanisms by which cell replication and thus cell reproduction is limited. 

[iii] In most cervical cancer, for example, a mutation causes the cell-to-cell adhesive molecule E-carherin to be digested, and as a consequence the cancerous cervical cell line can spread to distant tissues.

[iv]  On the surface of cells are unique small chains of peptides that function as markers recognized by immune cells.  If that tissue with that particular type of marker is found among a tissue with a different marker, certain type of white-blood cells will recognize the migrated tissue as foreign and initiate the events which will result in the destruction of this foreign tissue.   Cancer cells that spread to a distant organ must go to a tissue type in that organ for which they do not appear foreign (breast cancer often spreads to the brain, for example).  Complex organs with many different tissues, such as the brain and the liver, are thus frequent sites for the primary cancer to metastasize to. 

[v]  Duplication error consists of a section of the chromosome strand being made more than normal once.  Trisomy occurs when there is an extra copy of the entire strand.  If it occurs on chromosome 21, it results in Down’s syndrome.  Translocation is the shuffling of a section of one strand onto the other strand.  Deletion is where a portion of one of the strands is not replicated.  And inversion is where a section of a strand is reproduced in the opposite to normal order. 

[vi]   Ocogensis:  the origin and growth of  a neoplasm (tumor).  The can be either benign or malignant. 

[vii]  Thus for example in a study of 476 tumors of the thyroid, BRAF oncogene was altered in two-thirds of papillary thyroid cancers, but not in any other kinds of thyroid cancers.  Unfortunately generalizations have counter examples.  Thus oncogene c-fos and c-erbb3 are not disable but less active than in normal tissue.  Conversely RB is more active in colon cancer, and thus protects the tumor from the auto-destruction mechanism.   For one of the common genes which perform this checking function, P53, between one-third and one-half of the cancers have this among other mutations (Bailey 137).  Genetics and Evolution:  The Molecules of Inheritance, Jill Bailey, Oxford University Press, NY, 1995.

[viii]  German A. Pihan and colleagues found and published in March of 04 that of the 116 pre-malignant tumors removed from the tissues of the cervix, prostate, and breast, that between 30 and 72% had defective process during mitosis, Gibbs at 64.

[ix] Untangling the Roots of Cancer, W. Wayt Gibbs, Scientific American, 11/03, P. 61.

[x]  Lengauer and colleagues exposed human cell lines to toxic levels of a carcinogen in broiled meat.  Only a few cells developed resistance and survived.  And all of them were genetically unstable before exposure to the toxin, Gibbs at 64. 

[xi]  Thomas Reid of the national Cancer Institute noted that for colorectal cancer there is aneuploidy of chromosomes 7, 8, 13, or 20, and for cervical cancer of chromosome 3.  He also noted that aneuploidy happened at very early stage and seems to confer a selective advantage.  Reid noted that in the tissues examined there was a stead increase in the number of abnormal chromosomes as the stage of cancer advanced.  It went from 0.2 to 12 for metastatic colon tumors, Gibbs at 64.

[xii]  A codon is the sequence of three consecutive bases on a DNA or mRNA molecule that specify a particular amino acid to be inserted in the production of a protein.  Change a base will in most cases lead to the insertion of a different amino acid, from among the 21 that are used in the production of proteins.

 

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Disclaimer:  The information, facts, and opinions provided here is not a substitute for professional advice.  It only indicates what JK believes, does, or would do.  Always consult your primary care physician for medical advice, diagnosis, and treatment.