Predicting Osteopathic Medical Student Performance on the United States Medical Licensing Examination Step 2 Clinical Knowledge From Results of the Comprehensive Osteopathic Medical Licensing Examination Level 2-Cognitive Evaluation.

Background To improve their standing in residency selection, many osteopathic medical students choose to take the United States Medical Licensing Examination (USMLE). Although scores on USMLE Step 1 and Level 1 of the Comprehensive Osteopathic Medical Licensing Examination (COMLEX-USA) are known to be highly correlated, scarce data exist on the association between COMLEX-USA Level 2-Cognitive Evaluation (CE) and USMLE Step 2 Clinical Knowledge (CK) scores. In this study, we aimed to determine the association between COMLEX-USA Level 2-CE and USMLE Step 2 CK scores and derive an equation to predict performance on USMLE Step 2 CK for applicants who have only taken COMLEX-USA.

Predicting Osteopathic Medical Students' Performance on the United States Medical Licensing Examination From Results of the Comprehensive Osteopathic Medical Licensing Examination.

Introduction The reliance on the United States Medical Licensing Examination (USMLE) Step 1 scores in residency selection creates problems for osteopathic medical students and the programs that review their applications. Although many osteopathic students take the USMLE to improve their standing for residency selection, students who score poorly may harm their candidacy. Simultaneously, programs unfamiliar with the Comprehensive Osteopathic Medical Licensing Examination (COMLEX-USA) may struggle to evaluate applicants who have not taken USMLE.

Integrin αvβ3 and fibronectin upregulate Slug in cancer cells to promote clot invasion and metastasis.

The blood clotting cascade is selectively involved in lung metastasis, but the reason for this selectivity is unclear. Here, we show that tumor cells that metastasize predominantly to the lung, such as renal cell carcinoma (RCC) and soft tissue sarcoma (STS), have an inherent capacity to generate extensive invadopodia when embedded in a blood clot. Compared with other metastatic cancer cells tested, RCC and STS cells exhibited increased levels of expression of fibronectin and an activated form of the integrin αvβ3, which coordinately supported the generation of an elaborate fibronectin matrix and actin stress fibers in fibrin-embedded tumor cells.

Association of the von Hippel-Lindau protein with AUF1 and posttranscriptional regulation of VEGFA mRNA.

The von Hippel-Lindau (VHL) tumor suppressor gene product is the recognition component of an E3 ubiquitin ligase and is inactivated in patients with VHL disease and in most sporadic clear-cell renal cell carcinomas (RCC). pVHL controls oxygen-responsive gene expression at the transcriptional and posttranscriptional levels. The VEGFA mRNA contains AU-rich elements (ARE) in the 3'-untranslated region, and mRNA stability or decay is determined through ARE-associated RNA-binding factors.

EAF2 loss enhances angiogenic effects of Von Hippel-Lindau heterozygosity on the murine liver and prostate.

Von Hippel-Lindau (VHL) disease results from the inactivation of the VHL gene and is characterized by highly vascular tumors. A consequence of VHL loss is the stabilization of hypoxia-inducible factor (HIF) alpha subunits and increased expression of HIF target genes, which include pro-angiogenic growth factors such as vascular endothelial growth factor (VEGF). In mice, homozygous deletion of VHL is embryonic lethal due to vascular abnormalities in the placenta; and, VHL(+/-) mice develop proliferative vascular lesions in several major organs, most prominently the liver.

Genotype-phenotype correlations of pheochromocytoma in two large von Hippel-Lindau (VHL) type 2A kindreds with different missense mutations.

Von Hippel-Lindau (VHL) disease type 2A is an inherited tumor syndrome characterized by predisposition to pheochromocytoma (pheo), retinal hemangioma (RA), and central nervous system hemangioblastoma (HB). Specific VHL subtypes display genotype-phenotype correlations but, unlike other familial syndromes such as MEN-2, the phenotype in VHL has not yet been stratified at the codon level. Over decades, we have managed two very large VHL type 2A regional kindreds with nearly adjacent but distinct VHL missense mutations.

Lung cancer susceptibility in Fhit-deficient mice is increased by Vhl haploinsufficiency.

The FHIT gene plays important roles in cancer development, including lung cancers, in which the Fhit protein is frequently lost. To determine if Fhit-deficient mice exhibit increased susceptibility to carcinogen-induced lung cancer, mice were treated with the pulmonary carcinogen 4-methylnitrosamino-1-3-pyridyl-1-butanone. Wild-type and Fhit-deficient animals did not exhibit significantly different frequencies of lung lesions, but Fhit-/- mice showed significantly increased average tumor volume (1.

Susceptibility to vascular neoplasms but no increased susceptibility to renal carcinogenesis in Vhl knockout mice.

The von Hippel-Lindau (VHL) tumor suppressor gene plays a prominent role in the development of renal cell carcinoma (RCC) in humans. VHL functions as a ubiquitin E3 ligase, controlling the stability of hypoxia inducible factor (HIF) and tumor angiogenesis. Alterations in this tumor suppressor gene are rarely observed in spontaneous or chemically induced RCC that arise in conventional strains of rodents and Vhl knockout mice (Vhl+/-) do not develop spontaneous RCC.

Loss of pVHL is sufficient to cause HIF dysregulation in primary cells but does not promote tumor growth.

Inactivation of the von Hippel-Lindau (VHL) gene is associated with the development of highly vascularized tumors. pVHL targets the alpha subunits of hypoxia inducible factor (HIF) for ubiquitin-mediated degradation in an oxygen-dependent manner. Although pVHL-deficient tumor cell lines demonstrate constitutive stabilization and activation of HIF, it has yet to be shown that loss of murine Vhl alone is sufficient to dysregulate HIF.

Induction of cell cycle arrest and apoptosis in human prostate carcinoma cells by a recombinant adenovirus expressing p27(Kip1).

Background: Adp27(Kip1), a recombinant adenovirus, was evaluated for expression of p27, a cyclin-dependent kinase inhibitor (CDKI) and tumor suppressor protein, in human prostate carcinoma cells. Effects of p27(Kip1) on cell cycle and apoptosis were analyzed.

Methods: We evaluated the effects of overexpression of p27(Kip1) in the human prostate carcinoma cell lines LNCaP, DU-145, and PC-3 in vitro and in vivo.

A recombinant adenovirus expressing p7(Kip1) induces cell cycle arrest and apoptosis in human 786-0 renal carcinoma cells.

Purpose: We evaluated the effects of the over expression of p27Kip1, a cyclin dependent kinase inhibitor and tumor suppressor protein, on the 786-0 human renal carcinoma cell line.

Materials And Methods: The recombinant adenovirus Adp27Kip1 was evaluated for the induction of p27 protein expression in 786-0 renal carcinoma cells. Expression time and optimal vector concentration were determined.