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| Bernard Friedenson. |
| Women who inherit a defective BRCA1 or BRCA2 gene have risks for breast and ovarian cancer that are so high and seem so selective that many mutation carriers choose to have prophylactic surgery. There has been much conjecture to explain such apparently striking tissue specificity. All these suggestions share the assumption that some disabled function of normal tumor suppressor genes leads to a tissue specific cancer response. Here the idea is proposed and tested that major determinants of where BRCA1/2 hereditary cancers occur are related to tissue specificity of the cancer pathogen, the agent that causes chronic inflammation or the carcinogen. The target tissue may have receptors for the pathogen, become selectively exposed to an inflammatory process... |
| Tipo: Manuscript |
Palavras-chave: Cancer; Genetics & Genomics; Immunology; Pharmacology. |
| Ano: 2010 |
URL: http://precedings.nature.com/documents/4881/version/1 |
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| Bernard Friedenson. |
| Women who inherit a defective BRCA1 or BRCA2 gene have risks for breast/ovarian cancer that are so high and apparently so selective that many mutation carriers choose to have the most likely targets for cancer surgically removed. Recent research has focused on better methods of treating such seemingly unavoidable hereditary cancers. Prevention has received much less attention so a positive test result for a cancer gene leaves carriers with very limited options. 
In order to prevent BRCA1/2 related cancers, it may be important to understand why they seem to occur only in certain characteristic organs. Results here show that mutations in a pathway depending on BRCA1/2 gene products magnify cancer risks from chronic infection and... |
| Tipo: Manuscript |
Palavras-chave: Cancer; Genetics & Genomics; Immunology; Microbiology. |
| Ano: 2010 |
URL: http://precedings.nature.com/documents/4225/version/1 |
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| Bernard Friedenson. |
| Some environmental carcinogens may be responsible for a modest increase in the numbers of cancers after years of exposure. Economic or political factors weigh against widespread bans of carcinogens. However, lists of chemicals and agents that cause cancer assume that everyone is equally susceptible to their carcinogenic effects. 
Hereditary cancer gene mutations can target specific tissues if they are exposed to a carcinogen and the hereditary deficit impairs normal protective responses. Mutation carriers should then have higher risks for specific cancers caused by specific carcinogens.
 
For example, it can be predicted that BRCA1 or BRCA2 mutation carriers should be highly susceptible to the... |
| Tipo: Manuscript |
Palavras-chave: Cancer; Genetics & Genomics; Molecular Cell Biology; Bioinformatics. |
| Ano: 2011 |
URL: http://precedings.nature.com/documents/6024/version/1 |
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| Bernard Friedenson. |
| Recently, the President’s Cancer Panel [2008-2009] protested that preventive action is not taken when uncertainty exists about potential harm from a chemical, because the US regulatory approach demands that a hazard be incontrovertibly demonstrated. It is now incontrovertible that formaldehyde increases risks for leukemias. Evidence is also strong that formaldehyde causes some types of DNA damage in humans that are known to require repairs mediated by BRCA1/2 containing pathways. Homologous recombination repairs require BRCA1/2, Fanconi and ATM proteins in these pathways. Biallelic BRCA2 mutations interfere with these repairs and are clearly associated with leukemias, especially myeloid leukemias. Fanconi anemia homozygotes have very high... |
| Tipo: Manuscript |
Palavras-chave: Cancer; Genetics & Genomics. |
| Ano: 2011 |
URL: http://precedings.nature.com/documents/5669/version/1 |
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| Bernard Friedenson. |
| Objectives
Previous studies reported inherited BRCA1/2 deficits appear to cause cancer by impairing normal protective responses to some carcinogens. Opportunistic carcinogens can exploit these deficits by causing chronic inflammation, constant cell death and replacement in a mutagenic environment, DNA crosslinking or double strand breaks. Some of the resulting cancers may be prevented if BRCA1/2 specific carcinogens are identified.
Methods
The literature was systematically searched for carcinogens capable of exploiting deficits in BRCA1/2 pathways. Search criteria were common exposure, available information, required BRCA1/2 pathway repairs, increased risks for any cancer, and effects on stem... |
| Tipo: Manuscript |
Palavras-chave: Cancer; Genetics & Genomics; Molecular Cell Biology. |
| Ano: 2011 |
URL: http://precedings.nature.com/documents/6636/version/1 |
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| Bernard Friedenson. |
| Objectives
Previous studies reported inherited BRCA1/2 deficits can cause cancer by impairing normal protective responses. Opportunistic carcinogens can exploit these deficits by causing chronic inflammation, constant cell death and replacement in a mutagenic environment, DNA crosslinking or double strand breaks. Some of the resulting cancers may be prevented if opportunistic carcinogens are identified.

Methods
The literature was systematically searched for carcinogens capable of exploiting deficits in BRCA1/2 pathways. Search criteria were common exposure, available information, required BRCA1/2 pathway repairs, increased risks for any cancer, and effects on stem... |
| Tipo: Manuscript |
Palavras-chave: Cancer; Genetics & Genomics; Molecular Cell Biology; Earth & Environment. |
| Ano: 2011 |
URL: http://precedings.nature.com/documents/6668/version/1 |
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