Fitness May Lower Breast Cancer Risk

In a new study, rats with low natural fitness were about four times as likely to develop breast cancer as those with high fitness.

New Study Offers Support for Prostate Testing

A new analysis of earlier studies found prostate screening can reduce cancer deaths, but routine screening carries risks.

Hormone Treatment for Prostate Cancer Tied to Heart Risks

Androgen deprivation therapy for prostate cancer was associated with an increased risk of heart failure and heart rhythm disorders.

The Weekly Health Quiz: Breakfast, Toxins and Marijuana

Test your knowledge of this week’s health news.

Loss of the tumor suppressor STAG2 promotes telomere recombination and extends the replicative lifespan of normal human cells

Sister chromatids are held together by cohesin, a tripartite ring with a peripheral SA1/2 subunit, where SA1 is required for telomere cohesion and SA2 for centromere cohesion. The STAG2 gene encoding SA2 is often inactivated in human cancer, but not in in a manner associated with aneuploidy. Thus, how these tumors maintain chromosomal cohesion and how STAG2 loss contributes to tumorigenesis remain open questions. Here we show that, despite a loss in centromere cohesion, sister chromatids in STAG2 mutant tumor cells maintain cohesion in mitosis at chromosome arms and telomeres. Telomere maintenance in STAG2 mutant tumor cells occurred by either telomere recombination or telomerase activation mechanisms. Notably, these cells were refractory to telomerase inhibitors, indicating recombination can provide an alternative means of telomere maintenance. STAG2 silencing in normal human cells which lack telomerase led to increased recombination at telomeres, delayed telomere shortening and postponed senescence onset. Insofar as telomere shortening and replicative senescence prevent genomic instability and cancer by limiting the number of cell divisions, our findings suggest that extending the lifespan of normal human cells due to inactivation of STAG2 could promote tumorigenesis by extending the period during which tumor-driving mutations occur.