Gene mutation increases prostate cancer risk seven fold

BBC NEWS: A BRCA2 gene mutation can increase risk of prostate cancer by up to seven-fold, while a BRACA1 mutation is thought to double risk in men under 65 years old, a study shows. READ MORE>

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Prostate cancer is not simply a disease we inherit

NEW PROSTATE CANCER INFOLINK: Prostate cancer is linked to gene variations we inherit, but there are other factors involved as well, writes Mike Scott. READ MORE>

It is all too easy to want to believe that prostate cancer (and other forms of cancer) might be like one of the truly heritable diseases that are utterly dependent on one’s genetics, such as sickle cell anemia or Huntington’s disease.

Unfortunately, it just isn’t going to be that simple.

The development of prostate cancer in any specific individual is most probably a multi-stage process.

It may well be linked to the genes you are born with, but it is also quite certainly linked to other things that happen as you age.

As yet, we have minimal understanding of what those “other things” really are.

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Five new gene variations found that may be linked to prostate cancer

MSNBC: A large study in Japan into possible genetic causes for prostate cancer has uncovered five new gene variants which have never been seen in previous studies in Caucasians. READ MORE>

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Gene fusion now thought to be the cause of prostate cancer

US PROSTATE CANCER FOUNDATION: The primary cause of prostate cancer could be the fusion of two genes and the subsequent abnormal prostate cell growth that results when receptors for the hormone androgen get blocked, a new study reveals. READ MORE>

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DNA variations associated with prostate cancer outcomes

URO TODAY: Researchers have investigated associations between 29 single nucleotide polymorphisms (SNP) and biochemical recurrence, castration-resistant metastasis, and prostate cancer-specific survival, and found the SNPs are a clue to outcomes. READ MORE>

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DNA damage can trigger the development of (prostate) cancer, accelerate aging, or both

NEW ENGLAND JOURNAL OF MEDICINE: DNA damage can trigger the development of cancer, accelerate aging, or both, writes Dr Jan H.J. Hoeijmakers, Erasmus University Medical Center, Rotterdam.

When the damage is not repaired, the outcome may be cancer – or, if cell death or senescence (aging) occurs, protection from cancer – but the trade-off is acceleration of the aging process.

The development of cancer and the process of aging can be delayed by reducing the load of DNA damage — by avoiding or limiting exposure to exogenous genotoxins and by suppressing metabolism — thereby producing fewer reactive species.

However, DNA damage, like caloric (calories) restriction, can also elicit a protective survival response that promotes longevity and healthy aging.

Recently, the use of (immuno-suppressant drug) sirolimus in mice was found to extend their life span and delay the development of conditions associated with aging, including cancer. Sirolimus is one of presumably many compounds that may elicit the survival response.

The frequent derailment of DNA damage-response systems in tumours presents another possible route by which new treatments can act selectively on the tumor.

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