Evaluation of general surgery residency program websites.

Background: The purpose of this study was to evaluate the websites of general surgery residency programs in the United States and Puerto Rico.

Methods: Electronic Residency Application Service (ERAS) websites (n = 254) were accessed between October 2016 and January 2017 and evaluated for content, including: education, resident and faculty information, program environment and specific recruitment incentives.

Results: General information, such as conference information, rotations, and faculty information were available for more than 80% of programs.

Atypical Colorectal Neoplasms.

Primary colorectal lymphoma, carcinoids (neuroendocrine tumors), and gastrointestinal stromal tumors comprise a small subset of all colorectal cancers. Their features are unique, and their treatment varies from that of colorectal adenocarcinoma. Appropriate identification is key in the management of these tumors.

KSR1 is required for cell cycle reinitiation following DNA damage.

KSR1 (kinase suppressor of Ras 1) is a molecular scaffold and positive regulator of the Raf/MEK/ERK phosphorylation cascade. KSR1 is required for maximal ERK activation induced by growth factors and by some cytotoxic agents. We show here that KSR1 is also required for maximal ERK activation induced by UV light, ionizing radiation, or the DNA interstrand cross-linking agent mitomycin C (MMC).

Characterization of kinase suppressor of Ras-1 expression and anticancer drug sensitivity in human cancer cell lines.

Previous studies have indicated that the ERK1/2 MAP kinase signaling pathway plays an important role not only in cell growth, cell cycle regulation, and differentiation, but also in determining the sensitivity of cells to anticancer agents as well. Furthermore, expression of kinase suppressor of Ras-1 (KSR1), a molecular scaffold that modulates signaling through the ERK1/2 MAP kinase pathway, has been shown to influence the cellular sensitivity to the anticancer agent cisplatin. To further define the role of KSR1 expression on drug sensitivity, the expression of KSR1 was examined in the NCI60 anticancer drug screen, a panel of cancer cell lines representing nine tissue types, established by the Developmental Therapeutics Program (DTP) at the National Cancer Institute (NCI).

Expression of kinase suppressor of Ras1 enhances cisplatin-induced extracellular signal-regulated kinase activation and cisplatin sensitivity.

Kinase suppressor of Ras1 (KSR1) interacts with several mitogen-activated protein (MAP) kinase pathway components, including Raf, MAP/extracellular signal-regulated kinase (ERK) kinase (MEK), and ERK, and acts as a positive regulator of the Ras signaling cascade. Previous studies have shown that exposure of cells to the anticancer agent cisplatin (cis-diamminedichloroplatinum, CDDP) is associated with changes in multiple signal transduction pathways, including c-Jun-NH2-kinase, ERK, and p38 pathways. Moreover, ERK activation has been linked to changes in cell survival following CDDP treatment.

BRCA1-mediated G2/M cell cycle arrest requires ERK1/2 kinase activation.

Germline mutations in the BRCA1 gene are associated with an increased susceptibility to the development of breast and ovarian cancers. Evidence suggests that BRCA1 protein plays a key role in mediating DNA damage-induced checkpoint responses. Several studies have shown that ectopic expression of BRCA1 in human cells can trigger cellular responses similar to those induced by DNA damage, including G2/M cell cycle arrest and apoptosis.