Exercise is medicine in oncology: Engaging clinicians to help patients move through cancer

A compelling evidence base supports exercise as a safe, effective intervention to improve many cancer related health outcomes among cancer patients and survivors. Oncology clinicians play a key role in encouraging their patients to move more. Therefore, the oncology clinical care team is urged to do the following at regular intervals: ASSESS exercise levels, ADVISE patients to become more active, and REFER patients to specific exercise programming. It is recommended that a process be developed to incorporate these steps into the standard care of oncology patients. A simple, straightforward approach is recommended to discern whether patients should be referred to outpatient rehabilitation versus community based exercise programming. The exponential growth of exercise oncology research has driven the need for revised cancer exercise guidelines and a roadmap for oncology clinicians to follow to improve physical and psychological outcomes from cancer diagnosis and for the balance of life. This paper serves as a call to action and details pathways for exercise programming (clinical, community and self-directed) tailored to the different levels of support and intervention needed by a given cancer patient or survivor. Preserving activity and functional ability is integral to cancer care and oncology clinicians are key to providing these referrals

Weight gain and the risk of developing insulin resistance syndrome

http://deepblue.lib.umich.edu/bitstream/2027.42/51453/1/Everson SA, Weight Gain and the Risk of Developing Insulin Resistance Syndrome, 1998.pd

FANCD2 Facilitates Replication through Common Fragile Sites

Common fragile sites (CFSs) are genomic regions that are unstable under conditions of replicative stress. Although the characteristics of CFSs that render them vulnerable to stress are associated mainly with replication, the cellular pathways that protect CFSs during replication remain unclear. Here, we identify and describe a role for FANCD2 as a trans-acting facilitator of CFS replication, in the absence of exogenous replicative stress. In the absence of FANCD2, replication forks stall within the AT-rich fragility core of CFS, leading to dormant origin activation. Furthermore, FANCD2 deficiency is associated with DNA:RNA hybrid formation at CFS-FRA16D, and inhibition of DNA:RNA hybrid formation suppresses replication perturbation. In addition, we also found that FANCD2 reduces the number of potential sites of replication initiation. Our data demonstrate that FANCD2 protein is required to ensure efficient CFS replication and provide mechanistic insight into how FANCD2 regulates CFS stability

Histone H3K9 methylation is dispensable for Caenorhabditis elegans development but suppresses RNA:DNA hybrid-associated repeat instability

Genome Instability and Cance