Alcohol Consumption: Discussing Potential Risks for Informed Decisions in Breast Cancer Survivors.

BACKGROUND: Alcohol consumption is a known risk factor for breast cancer. Because breast cancer survivors are already at risk for recurrence, it is important to understand whether these survivors could benefit from survivor-specific recommendations for alcohol consumption. OBJECTIVES: The purpose of this article was to review primary research specific to alcohol and breast cancer survivors to see whether those who consume alcohol experience more adverse effects. METHODS: This literature review examined nine cohort studies specific to breast cancer survivors, alcohol consumption, and risks for breast cancer recurrence, breast cancer-specific mortality, and second primary breast cancers. FINDINGS: Current guideline recommendations of a safe limit of one drink per day or less may not protect breast cancer survivors from cancer- related adverse events. The authors recommend that breast cancer survivors be educated about the associated risks of alcohol consumption so that they can make informed decisions about usage.

A critical role for donor-derived IL-22 in cutaneous chronic GVHD.

Graft-versus-host disease (GVHD) is the major cause of nonrelapse morbidity and mortality after allogeneic stem cell transplantation (allo-SCT). Prevention and treatment of GVHD remain inadequate and commonly lead to end-organ dysfunction and opportunistic infection. The role of interleukin (IL)-17 and IL-22 in GVHD remains uncertain, due to an apparent lack of lineage fidelity and variable and contextually determined protective and pathogenic effects. We demonstrate that donor T cell-derived IL-22 significantly exacerbates cutaneous chronic GVHD and that IL-22 is produced by highly inflammatory donor CD4+ T cells posttransplantation. IL-22 and IL-17A derive from both independent and overlapping lineages, defined as T helper (Th)22 and IL-22+ Th17 cells. Donor Th22 and IL-22+ Th17 cells share a similar IL-6-dependent developmental pathway, and while Th22 cells arise independently of the IL-22+ Th17 lineage, IL-17 signaling to donor Th22 directly promotes their development in allo-SCT. Importantly, while both IL-22 and IL-17 mediate skin GVHD, Th17-induced chronic GVHD can be attenuated by IL-22 inhibition in preclinical systems. In the clinic, high levels of both IL-17A and IL-22 expression are present in the skin of patients with GVHD after allo-SCT. Together, these data demonstrate a key role for donor-derived IL-22 in patients with chronic skin GVHD and confirm parallel but symbiotic developmental pathways of Th22 and Th17 differentiation.