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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,
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
(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
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,
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
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
of “63% 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.
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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
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what JK believes, does, or would do. Always
consult your primary care physician for medical advice, diagnosis, and
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