MEDIECIN
Cancer
And
Genes
2 October 2020
Authors Anna Di Lonardo, Sergio Nasi, Simonetta Pulciani authored a 2015 article (review) entitled "Cancer: We Should Not Forget The Past", published in the journal Cancer "jcancer.org" write the following:
"Cancer has been in existence longer than human beings, and man has been facing the illness ever since he made his appearance on Earth."
"Amazingly, the first human cancer gene was cloned only thirty years ago."
Source:
Review.
Cancer:
We
Should
Not
Forget
The
Past
J Cance 2015; 6(1):29-39. doi:10.7150/jca.10336
The authors note, "This, and other extraordinary scientific goals achieved by molecular cancer research in the last 30 years, seems to suggest that definitive answers and solutions to this severe disease have been finally found."
"This was not the case, as cancer still remains to be defeated. To do so, cancer must be first understood," the writers of the review add.
Source:
Review.
Cancer:
We
Should
Not
Forget
The
Past
J Cance 2015; 6(1):29-39. doi:10.7150/jca.10336
The authors address, "This review highlights how cancer onset and progression has been tackled from ancient times to present day."
They explain, "Old theories and achievements have provided the pillars of cancer understanding, in laying the basis of 'modern era' cancer research, are discussed."
The authors address, "The review highlights the discovery of oncogenes and suppressor tumor genes, underlining the crucial role of these achievements in cancer diagnosis and therapies."
"Finally, an overview of how the modern technologies have given impetuous to expedite these goals is also considered," the writers add.
Anna Di Lonardo, Sergio Nasi, Simonetta Pulciani in introduction address, "The scientific path taken to understand cancer is paved with thousands of theories and scientific findings, from the time of Hippocrates to genomics today."
"Many of these are fundamental in our modern approaches to the disease."
The authors in the conclusion write, "Still cancer is an unresolved problem, and researchers must work harder to get to the root of all these open ended questions."
The writers address, "Confucio said, 'Study the past if you would define the future'."
They write, "Past scientific achievements could represent the milestones for building future bridges along the path of cancer research understanding, 'we should not forget the past'."
Source:
Review.
Cancer:
We
Should
Not
Forget
The
Past
J Cance 2015; 6(1):29-39. doi:10.7150/jca.10336
The website "dana-farber.org" introduces Dr. David M. Livingston, MD
(Charles A. Dana Chair in Human Cancer Genetics, A Distinguished Professor of Medicine, Harvard Medical School) and writes:
"Dr. Livingston is an internationally recognized expert on genes that regulate cell growth in the body - genes that, when they go awry, can lead to cancer."
The website informs:
"These genes are called oncogenes and tumor suppressor genes."
According to the website, "Through his research, Dr. Livingston has uncovered detailed biochemical steps required to initiate and maintain the transformation of these cells into tumor cells."
David
M.
Livingston,
MD
The March 2017 issue of Annual Review of Cancer Biology published an article entitled "How Tumor Virology Evolved into Cancer Biology and Transformed Oncology" authored by Harold Varmus of Meyer Cancer Center, Weill Cornell Medicine, New York, NY.
First published online as a Review in Advance on September 28, 2016
The author writes, "Animal viruses appeared to be the only feasible means to seek definitive evidence about whether cancers could be caused by genetic changes, in large part because they might reveal the specific kinds of genes that could drive cancerous changes in cells."
Source:
How
Tumor
Virology
Evolved
into
Cancer
Biology
and
Transformed
Oncology
Annual Review of Cancer Biology
Vol. 1:1-18 (Volume publication date March 2017)
Annual Review of Cancer Biology
Vol. 1:1-18 (Volume publication date March 2017)
https://doi.org/10.1146/annurev-cancerbio-050216-034315
Dr. Varmus points out, "Spurred on by these thoughts, I wanted to look for cancer genes by becoming a tumor virologist."
He addresses, "I also had little or nothing to say about how the studies I envisioned conducting with cancer-causing viruses of animals could help with the diagnosis, prevention, or treatment of human cancers—unless, of course, the viruses themselves proved to be closely related to viruses that caused human cancer."
"But, unlike some tumor virologists, I was not convinced that most human cancers had an infectious origin," the author notes.
The writer explains, "As early as 1980, a mere five years after the discovery of c-src, enough cellular proto-oncogenes had been discovered by tracking retroviral oncogenes to their sources to require a new nomenclature that might bring clarity to a rapidly expanding field."
Source:
How
Tumor
Virology
Evolved
into
Cancer
Biology
and
Transformed
Oncology
Annual Review of Cancer Biology
Vol. 1:1-18 (Volume publication date March 2017)
Annual Review of Cancer Biology
Vol. 1:1-18 (Volume publication date March 2017)
Dr. Varmus of Cornell University writes, "Today, the “oncogene wave” is a virtual tsunami."
He addresses, "Literally hundreds of genes, most of which have never appeared in retroviral genomes, are associated with human tumorigenesis because new genomic methods can rapidly compare tumor DNAs with germ line DNA from the same individual to identify recurrent somatic changes [Catalogue of Somatic Mutations in Cancer (http://cancer.sanger.ac.uk/cosmic) and The Cancer Genome Atlas (http://cancergenome.nih.gov)].
The author explains, "The repetitive sighting of such mutations implies that the changes confer a selective advantage on the cells in which they occur."
"But studies to ascertain the biological consequence of most of these alterations—are they “drivers” of neoplasia or merely coincidental “passengers”?—are required before pursuing them in greater scientific depth or before using them for therapeutic or diagnostic purposes," adds the writer.
Dr. Varmus points out, "I have emphasized how retroviruses have enriched biology in many ways, most obviously by leading us to proto-oncogenes."
"But it goes almost without saying that tumor virology, similar to all fields, has benefited from advances in many other disciplines," the author notes.
Source:
How
Tumor
Virology
Evolved
into
Cancer
Biology
and
Transformed
Oncology
Annual Review of Cancer Biology
Vol. 1:1-18 (Volume publication date March 2017)
Annual Review of Cancer Biology
Vol. 1:1-18 (Volume publication date March 2017)
The writer addresses, "I have already mentioned “imported” methods—such as molecular hybridization, recombinant DNA technology, and DNA sequencing—that allowed progress in tumor virology; cancer biology is now dependent on many others, including genetically engineered mice, inhibitory RNAs, and (most recently) efficient DNA editing. The routes to discovery in all fields of science are two-way streets."
The author writes, "The Oncogene Meeting brought DNA tumor virologists back into contact with RNA tumor virologists—in part because, by the late 1980s, it was becoming clear that the mechanisms used by RNA and DNA
tumor viruses to transform cells are not, after all, so far apart."
Dr. Varmus addresses, "For both classes of viruses, transformation is dependent on instructive relationships between host and viral genes."
The author writes, "For instance, several UCSF faculty, ranging from yeast geneticists to full-time clinicians, gathered monthly, lured by free pizza, to hear how oncologists conduct clinical trials and how molecular biologists implicate cellular genes and proteins in human cancers."
"Still, the cultures remained quite far apart, and the discussions were halting, requiring translations," the writer notes.
Source:
How
Tumor
Virology
Evolved
into
Cancer
Biology
and
Transformed
Oncology
Annual Review of Cancer Biology
Vol. 1:1-18 (Volume publication date March 2017)
Annual Review of Cancer Biology
Vol. 1:1-18 (Volume publication date March 2017)
Matt Ridley, in chapter 17 of his 1999 book "Genome:The Authobiography of A Species in 23 Chaprers" (New York, Harper Collins Publishers) writes the following:
"In 1909, Peyton Rous had proved that a chicken with a form of cancer called sarcoma could pass the disease to a healthy chicken."(p.234)
The author points out, "His work was largely ignored, since there seemed so little evidence that cancer was contagious."(p.234)
The writer adds, "But in the 1960s, a whole string of animal cancer viruses, or oncoviruses, were discovered, beginning with the Rous Sarcoma virus itself."
"Rous was eventually given the Nobel prize at the age of eighty-six in recognition of his prescience." (p.234)
The author cites the book of W. Cookson (1994) with a title "The gene hunters: adventures in the genome jungle" (Aurun Press, London) as saying, " Human oncoviruses soon followed and it became apparent that the whole classes of cancer, such as cervical cancer, were indewd causwd partly by viral infection."(p.234)
The writer addresses, "Putting the Rous sarcoma virus through the gene-sequencer revealed that it carried a special cancer-causing gene, now known as src."(p.234)
"Other such 'oncogenes' soon followed from other oncoviruses."(p.234)
The author explains, "Like Ames, the virologists were beginning to realise that cancer was a disease of genes."(p.234)
Science
Technology
Daily
(20
April
2021):
Strange
New
Genetic
Disease
Discovered
That
Causes
Children's
Brains
To
Develop
Abnormally
All
Therapeutic
Cancer
Treatment
Works
Only
Because
It
Induces
Apoptosis
1 October 2020
Matt Ridley, in chapter 17 of his 1999 book "Genome:The Authobiography of A Species in 23 Chaprers" (New York, Harper Collins Publishers) writes the following:
"Indeed, so important is apoptosis that it is gradually becoming clear that almost all therapeutic cancer treatment works only because it induces apoptosis by alerting p53 and its colleagues."(p.238)
The author addresses, "It used to be thought that radiation therapy and chemotherapy worked because they preferentially killed dividing cells by damaging their DNA as it was being copied."(p.238)
"But if that is the case, why do some tumours respond so poorly to treatment," the author questions.(p.238)
The writer notes, "There comes a point in the progression of fatal cancer when the treatment no longer works-the tumour no longer shrinks under chemical or radiation attack."(p.238)
"Why should this be? If the treatment kills the dividing cells, it should continue to work all times," the writer addresses.(p.238)
The writer points out, "Scott Lowe, working at Cold Spring Harbor Laboratory, has an ingenious answer."(p.238)
The author quotes Scott Lowe as saying, "These treatments do indeed cause a little DNA damage."(p.238)
"But not enough to kill the cells," adds Lowe.
"Instead, the DNA damage is just sufficient to alert p53, which tells the cells to commit suicide.So chemotherapy and radiation therapy are actually, like vaccination, trwatments that work by helping the body to help itself,"explains Lowe from the Cold Spring Harbor Laboratory.(pp.238-239)
Author Matt Ridley in his 1999 book "Genome" writes, "The evidence for Lowe's theory is good."(p.239)
"Radiation, or treatment with 5-fluorouracil, etopside or adrimycine- three chemical cancer treatments-all encourage apoptosis in laboratory cells infected with a viral oncogene."(p.239)
The writer addresses, "And when hitherto tractable tumours relapse and suddenly fail to respond to treatment, the change correlates closely with a mutation knocking out T53."(p.239)
"Likewise, the most intractable tumours- melanoma, lung, colorectal, bladder and prostate- are the ones in which T53 is usually mutated already," notes the author.(p.239)
The writer points out, "Certain kinds of breast cancer resist treatment:the ones in which T53 is broken."(p.239)
What
is
biotechnology?
Inside
A
Growing
Ball of
Cancer
Cells
1 October 2020
Matt Ridley, in chapter 17 of his 1999 book "Genome:The Authobiography of A Species in 23 Chaprers" (New York, Harper Collins Publishers) writes the following:
"Inside a growing ball of cancer cells, the blood supply can run short, so the cells begin to suffocate."(p.238)
The author adds, "Malignant cancers get over this problem by sending out a signal to the body to grow new arteries into the tumour-the characteristic, crab-craw-like arteries that first gave cancer its Greek name."(p.238)
"Some of the most promising new cancer drugs block this process of 'angiogenesis', or blood-vessel formation," the writer notes.(p.238)
The author addresses,"But p53 sometimes realises what is happening and kills the tumour cells before the blood supply arrives."(p.238)
The writer cites an article in the journal Cell (88:313-31) entitled "P53, the cellular gatekeeper for growth and division" written by A. J. Lavine as saying:
"Cancers in tissues with poor blood supply, such as skin cancers, therefore, must disable TP53 early in their development or fail to grow. That is why melanomas are so dangerous."(p.238)
The author addresses, "Little wonder that p53 has earned the nickname 'Guardian of the Genome', or even 'Guardian Angel of the Genome'."(p.238)
"T53 seems to encode the greater good, like a suicide pill in the mouth of a soldier that disolves only when it detects evidence that he is about to mutiny," the writer notes.(p.238)
The author writes, "The suicide of cells in this way is known as apoptosis, from the Greek for the fall of autumn leaves."(p.238)
"It is the most important of the body's weapons against cancer, the last line of defence."(p.238)
In the website "a-star.edu.sg" (WELCOME TO THE P53LAB) it reads:
"11 Million people living with cancer have specific mutations in the p53 gene leading to the production of a faulty p53 protein."
Source:
WELCOME
TO
THE
P53
LAB
(David
Lane"
The website "a-star.edu.sg" (David Lane's p53-Lab) addresses, "This is half the cases of human cancer."
The information in the website of David Lane's p53-Lab says, "In those that have an apparently normal p53 gene we believe that there are faults in the p53 pathway."
"We are using a variety of approaches to translate this extraordinary finding into clinical benefit," the website informs.
According to the information in the website of the p53-Lab (David Lane),
"This is half the cases of human cancer."
The same website addresses, "In those that have an apparently normal p53 gene we believe that there are faults in the p53 pathway."
"We are using a variety of approaches to translate this extraordinary finding into clinical benefit," the website adds.
The website (Wikipwdia) addresses,
"The p53 gene is the most frequently altered gene in human cancer with more than half of all cancers having mutant p53."
In Wikipedia it reads:
"He is co-author with Ed Harlow of the most successful practical guide to the use of immunochemical methods. The "Antibodies" manual has sold over 40,000 copies."
Source:
p53
& David
Lane
The Wikipedia informs, " Sir David is currently Chief Scientist of Singapore's Agency for Science, Technology and Research (A*STAR, Singapore) heading the p53 laboratory."
"He is also Professor of Tumour Suppressor Biology at the Department of Microbiology,Tumor and Cell Biology at the Karolinska Institute."
Source:
p53
& David
Lane
isna
.ir|
چهارشنبه /
۲۸
مهر
۱۴۰۰ :
تحولات
نوین
درحوزه
ژنتیک
و
بیو
تکنولوژی؛
نتایج
امیدبخش
درمان
سرطان
و کرونا
با
روش
کریسپر
پایه
/پیشنهاد
محققان
برای
توسعه
کریسپر
در
کشور
ir.sputnik
news
.com|14
Feb
2022:
نشانه
های
بالا
بودن
سطح
کلسترول
در
پاها
کدامند؟
Source:
Review.
Cancer:
We
Should
Not
Forget
The
Past
J Cance 2015; 6(1):29-39. doi:10.7150/jca.10336
The authors note, "This, and other extraordinary scientific goals achieved by molecular cancer research in the last 30 years, seems to suggest that definitive answers and solutions to this severe disease have been finally found."
"This was not the case, as cancer still remains to be defeated. To do so, cancer must be first understood," the writers of the review add.
Source:
Review.
Cancer:
We
Should
Not
Forget
The
Past
J Cance 2015; 6(1):29-39. doi:10.7150/jca.10336
The authors address, "This review highlights how cancer onset and progression has been tackled from ancient times to present day."
They explain, "Old theories and achievements have provided the pillars of cancer understanding, in laying the basis of 'modern era' cancer research, are discussed."
The authors address, "The review highlights the discovery of oncogenes and suppressor tumor genes, underlining the crucial role of these achievements in cancer diagnosis and therapies."
"Finally, an overview of how the modern technologies have given impetuous to expedite these goals is also considered," the writers add.
Anna Di Lonardo, Sergio Nasi, Simonetta Pulciani in introduction address, "The scientific path taken to understand cancer is paved with thousands of theories and scientific findings, from the time of Hippocrates to genomics today."
"Many of these are fundamental in our modern approaches to the disease."
The authors in the conclusion write, "Still cancer is an unresolved problem, and researchers must work harder to get to the root of all these open ended questions."
The writers address, "Confucio said, 'Study the past if you would define the future'."
They write, "Past scientific achievements could represent the milestones for building future bridges along the path of cancer research understanding, 'we should not forget the past'."
Source:
Review.
Cancer:
We
Should
Not
Forget
The
Past
J Cance 2015; 6(1):29-39. doi:10.7150/jca.10336
The website "dana-farber.org" introduces Dr. David M. Livingston, MD
(Charles A. Dana Chair in Human Cancer Genetics, A Distinguished Professor of Medicine, Harvard Medical School) and writes:
"Dr. Livingston is an internationally recognized expert on genes that regulate cell growth in the body - genes that, when they go awry, can lead to cancer."
The website informs:
"These genes are called oncogenes and tumor suppressor genes."
According to the website, "Through his research, Dr. Livingston has uncovered detailed biochemical steps required to initiate and maintain the transformation of these cells into tumor cells."
David
M.
Livingston,
MD
The March 2017 issue of Annual Review of Cancer Biology published an article entitled "How Tumor Virology Evolved into Cancer Biology and Transformed Oncology" authored by Harold Varmus of Meyer Cancer Center, Weill Cornell Medicine, New York, NY.
First published online as a Review in Advance on September 28, 2016
The author writes, "Animal viruses appeared to be the only feasible means to seek definitive evidence about whether cancers could be caused by genetic changes, in large part because they might reveal the specific kinds of genes that could drive cancerous changes in cells."
Source:
How
Tumor
Virology
Evolved
into
Cancer
Biology
and
Transformed
Oncology
Annual Review of Cancer Biology
Vol. 1:1-18 (Volume publication date March 2017)
Annual Review of Cancer Biology
Vol. 1:1-18 (Volume publication date March 2017)
https://doi.org/10.1146/annurev-cancerbio-050216-034315
Dr. Varmus points out, "Spurred on by these thoughts, I wanted to look for cancer genes by becoming a tumor virologist."
He addresses, "I also had little or nothing to say about how the studies I envisioned conducting with cancer-causing viruses of animals could help with the diagnosis, prevention, or treatment of human cancers—unless, of course, the viruses themselves proved to be closely related to viruses that caused human cancer."
"But, unlike some tumor virologists, I was not convinced that most human cancers had an infectious origin," the author notes.
The writer explains, "As early as 1980, a mere five years after the discovery of c-src, enough cellular proto-oncogenes had been discovered by tracking retroviral oncogenes to their sources to require a new nomenclature that might bring clarity to a rapidly expanding field."
Source:
How
Tumor
Virology
Evolved
into
Cancer
Biology
and
Transformed
Oncology
Annual Review of Cancer Biology
Vol. 1:1-18 (Volume publication date March 2017)
Annual Review of Cancer Biology
Vol. 1:1-18 (Volume publication date March 2017)
Dr. Varmus of Cornell University writes, "Today, the “oncogene wave” is a virtual tsunami."
He addresses, "Literally hundreds of genes, most of which have never appeared in retroviral genomes, are associated with human tumorigenesis because new genomic methods can rapidly compare tumor DNAs with germ line DNA from the same individual to identify recurrent somatic changes [Catalogue of Somatic Mutations in Cancer (http://cancer.sanger.ac.uk/cosmic) and The Cancer Genome Atlas (http://cancergenome.nih.gov)].
The author explains, "The repetitive sighting of such mutations implies that the changes confer a selective advantage on the cells in which they occur."
"But studies to ascertain the biological consequence of most of these alterations—are they “drivers” of neoplasia or merely coincidental “passengers”?—are required before pursuing them in greater scientific depth or before using them for therapeutic or diagnostic purposes," adds the writer.
Dr. Varmus points out, "I have emphasized how retroviruses have enriched biology in many ways, most obviously by leading us to proto-oncogenes."
"But it goes almost without saying that tumor virology, similar to all fields, has benefited from advances in many other disciplines," the author notes.
Source:
How
Tumor
Virology
Evolved
into
Cancer
Biology
and
Transformed
Oncology
Annual Review of Cancer Biology
Vol. 1:1-18 (Volume publication date March 2017)
Annual Review of Cancer Biology
Vol. 1:1-18 (Volume publication date March 2017)
The writer addresses, "I have already mentioned “imported” methods—such as molecular hybridization, recombinant DNA technology, and DNA sequencing—that allowed progress in tumor virology; cancer biology is now dependent on many others, including genetically engineered mice, inhibitory RNAs, and (most recently) efficient DNA editing. The routes to discovery in all fields of science are two-way streets."
The author writes, "The Oncogene Meeting brought DNA tumor virologists back into contact with RNA tumor virologists—in part because, by the late 1980s, it was becoming clear that the mechanisms used by RNA and DNA
tumor viruses to transform cells are not, after all, so far apart."
Dr. Varmus addresses, "For both classes of viruses, transformation is dependent on instructive relationships between host and viral genes."
The author writes, "For instance, several UCSF faculty, ranging from yeast geneticists to full-time clinicians, gathered monthly, lured by free pizza, to hear how oncologists conduct clinical trials and how molecular biologists implicate cellular genes and proteins in human cancers."
"Still, the cultures remained quite far apart, and the discussions were halting, requiring translations," the writer notes.
Source:
How
Tumor
Virology
Evolved
into
Cancer
Biology
and
Transformed
Oncology
Science
Technology
Daily
(20
April
2021):
Strange
New
Genetic
Disease
Discovered
That
Causes
Children's
Brains
To
Develop
Abnormally
What
is
biotechnology?
Source:
How
Tumor
Virology
Evolved
into
Cancer
Biology
and
Transformed
Oncology
Annual Review of Cancer Biology
Vol. 1:1-18 (Volume publication date March 2017)
Annual Review of Cancer Biology
Vol. 1:1-18 (Volume publication date March 2017)
Matt Ridley, in chapter 17 of his 1999 book "Genome:The Authobiography of A Species in 23 Chaprers" (New York, Harper Collins Publishers) writes the following:
"In 1909, Peyton Rous had proved that a chicken with a form of cancer called sarcoma could pass the disease to a healthy chicken."(p.234)
The author points out, "His work was largely ignored, since there seemed so little evidence that cancer was contagious."(p.234)
The writer adds, "But in the 1960s, a whole string of animal cancer viruses, or oncoviruses, were discovered, beginning with the Rous Sarcoma virus itself."
"Rous was eventually given the Nobel prize at the age of eighty-six in recognition of his prescience." (p.234)
The author cites the book of W. Cookson (1994) with a title "The gene hunters: adventures in the genome jungle" (Aurun Press, London) as saying, " Human oncoviruses soon followed and it became apparent that the whole classes of cancer, such as cervical cancer, were indewd causwd partly by viral infection."(p.234)
The writer addresses, "Putting the Rous sarcoma virus through the gene-sequencer revealed that it carried a special cancer-causing gene, now known as src."(p.234)
"Other such 'oncogenes' soon followed from other oncoviruses."(p.234)
The author explains, "Like Ames, the virologists were beginning to realise that cancer was a disease of genes."(p.234)
Science
Technology
Daily
(20
April
2021):
Strange
New
Genetic
Disease
Discovered
That
Causes
Children's
Brains
To
Develop
Abnormally
All
Therapeutic
Cancer
Treatment
Works
Only
Because
It
Induces
Apoptosis
1 October 2020
Matt Ridley, in chapter 17 of his 1999 book "Genome:The Authobiography of A Species in 23 Chaprers" (New York, Harper Collins Publishers) writes the following:
"Indeed, so important is apoptosis that it is gradually becoming clear that almost all therapeutic cancer treatment works only because it induces apoptosis by alerting p53 and its colleagues."(p.238)
The author addresses, "It used to be thought that radiation therapy and chemotherapy worked because they preferentially killed dividing cells by damaging their DNA as it was being copied."(p.238)
"But if that is the case, why do some tumours respond so poorly to treatment," the author questions.(p.238)
The writer notes, "There comes a point in the progression of fatal cancer when the treatment no longer works-the tumour no longer shrinks under chemical or radiation attack."(p.238)
"Why should this be? If the treatment kills the dividing cells, it should continue to work all times," the writer addresses.(p.238)
The writer points out, "Scott Lowe, working at Cold Spring Harbor Laboratory, has an ingenious answer."(p.238)
The author quotes Scott Lowe as saying, "These treatments do indeed cause a little DNA damage."(p.238)
"But not enough to kill the cells," adds Lowe.
"Instead, the DNA damage is just sufficient to alert p53, which tells the cells to commit suicide.So chemotherapy and radiation therapy are actually, like vaccination, trwatments that work by helping the body to help itself,"explains Lowe from the Cold Spring Harbor Laboratory.(pp.238-239)
Author Matt Ridley in his 1999 book "Genome" writes, "The evidence for Lowe's theory is good."(p.239)
"Radiation, or treatment with 5-fluorouracil, etopside or adrimycine- three chemical cancer treatments-all encourage apoptosis in laboratory cells infected with a viral oncogene."(p.239)
The writer addresses, "And when hitherto tractable tumours relapse and suddenly fail to respond to treatment, the change correlates closely with a mutation knocking out T53."(p.239)
"Likewise, the most intractable tumours- melanoma, lung, colorectal, bladder and prostate- are the ones in which T53 is usually mutated already," notes the author.(p.239)
The writer points out, "Certain kinds of breast cancer resist treatment:the ones in which T53 is broken."(p.239)
What
is
biotechnology?
