Gastrointestinal stromal tumors: molecular markers and genetic subtypes.

Mutation-activated signaling from the KIT and PDGFRA kinases has been successfully targeted in gastrointestinal stromal tumors (GISTs), with subtle differences between the mutations serving to refine prognosis and more precisely tailor therapy. There is a growing understanding of the molecular drivers of GISTs lacking mutations in KIT or PDGFRA, so called wild-type GISTs, further aiding in management decisions. This article provides an overview of all the known molecular subtypes of GIST and provides information about clinical correlates, treatment, and prognosis depending on the subtype.

Management of tyrosine kinase inhibitor-resistant gastrointestinal stromal tumors.

The treatment of gastrointestinal stromal tumors (GISTs) has been a model for targeted cancer therapy. The discovery of driver somatic mutations in the KIT and PDGFRA receptor tyrosine kinases led to a shift of therapy from conventional cytotoxic chemotherapy to inhibitors of these receptors. Targeted molecular therapy of GIST has markedly increased the overall survival of patients with advanced disease.

Gastrointestinal stromal tumours: origin and molecular oncology.

Gastrointestinal stromal tumours (GISTs) are a paradigm for the development of personalized treatment for cancer patients. The nearly simultaneous discovery of a biomarker that is reflective of their origin and the presence of gain-of-function kinase mutations in these tumours set the stage for more accurate diagnosis and the development of kinase inhibitor therapy. Subsequent studies of genotype and phenotype have led to a molecular classification of GIST and to treatment optimization on the basis of molecular subtype.

Prostate cancer and vitamin D: what does the evidence really suggest?

The optimal approach to vitamin D supplementation for the average healthy person is debatable. In patients with cancer, the role of vitamin D supplementation, possibly in treatment, is even less clear. Vitamin D is shown to play a role in prostate cancer biology; however, the clinical data have not consistently demonstrated a link.

Prolonged response to early docetaxel in a patient with biochemical relapse after primary therapy for prostate cancer and incomplete response to androgen suppression therapy.

Sensitivity to androgen suppression therapy (AST) is a key determinant of survival in patients with non-localized prostate cancer. While an incomplete response to AST is associated with poor survival, additional therapy is typically withheld until obvious cancer progression. It is not known if the application of additional therapy earlier can have a favorable impact on long-term outcomes.

Serum 25-OH vitamin D levels and risk of developing prostate cancer in older men.

Objective: Multiple studies have shown clear evidence of vitamin D's anti-tumor effects on prostate cancer cells in laboratory experiments, but the evidence has not been consistent in humans. We sought to examine the association between vitamin D and prostate cancer risk in a cohort of older men.

Methods: We conducted a prospective case-cohort study nested within the multicenter Osteoporotic Fractures in Men (MrOS) study.