A comparison of match outcomes between traditional medical degree and dual-degree applicants.

BACKGROUND: Dual degrees combining and MD with another professional degree (MPH, MBA, or PhD) are becoming more common in an attempt to increase an applicant's competitivity for a residency. OBJECTIVE: This study was designed to assess differences in MD-only and dual degree MD applicants with respect to applicant characteristics and match outcomes. METHODS: Utilizing the voluntarily-reported publicly available 2017-2019 Texas STAR database, we assessed applicants from 115 medical schools. Texas STAR indicates that over this time period, there were 18,224 responses for a response rate of 43.8%. Comparisons were made between groups using student's t-test and chi-squared analysis. RESULTS: Compared to MD only students, MD/MPH applicants had a higher propensity towards primary care specialties. MD/PhD applicants did not differ versus MD only applicants in their selection of primary care specialties, or of competitive specialties. MD/MBA applicants chose more competitive specialties and less primary care specialties. Despite all these differences, match rates were not different comparing MD only and dual-degree students. CONCLUSIONS: Despite the growing popularity of combined MD programs, such programs do not appear to increase applicant match competitivity.

Chronic Stress Exposure Suppresses Mammary Tumor Growth and Reduces Circulating Exosome TGF-ß Content via ß-Adrenergic Receptor Signaling in MMTV-PyMT Mice.

Preclinical models of breast cancer have established mechanistic links between psychological stress and cancer progression. However, epidemiological evidence linking stress and cancer is equivocal. We tested the impact of stress exposure in female mice expressing the mouse mammary tumor virus polyoma middle-T antigen (MMTV-PyMT), a spontaneous model of mammary adenocarcinoma that mimics metastatic hormone receptor-positive human breast cancer development. MMTV-PyMT mice were socially isolated at 6 to 7 weeks of age during premalignant hyperplasia. To increase the potency of the stressor, singly housed mice were exposed to acute restraint stress (2 hours per day for 3 consecutive days) at 8 to 9 weeks of age during early carcinoma. Exposure to this dual stressor activated both major stress pathways, the sympathetic nervous system and hypothalamic-pituitary-adrenal axis throughout malignant transformation. Stressor exposure reduced mammary tumor burden in association with increased tumor cleaved caspase-3 expression, indicative of increased cell apoptosis. Stress exposure transiently increased tumor vascular endothelial growth factor and reduced tumor interleukin-6, but no other significant alterations in immune/inflammation-associated chemokines and cytokines or changes in myeloid cell populations were detected in tumors. No stress-induced change in second-harmonic generation-emitting collagen, indicative of a switch to a metastasis-promoting tumor extracellular matrix, was detected. Systemic indicators of slowed tumor progression included reduced myeloid-derived suppressor cell (MDSC) frequency in lung and spleen, and decreased transforming growth factor ß (TGF-ß) content in circulating exosomes, nanometer-sized particles associated with tumor progression. Chronic ß-adrenergic receptor (ß-AR) blockade with nadolol abrogated stress-induced alterations in tumor burden and cleaved caspase-3 expression, lung MDSC frequency, and exosomal TGF-ß content. Despite the evidence for reduced tumor growth, metastatic lesions in the lung were not altered by stress exposure. Unexpectedly, ß-blockade in nonstressed mice increased lung metastatic lesions and splenic MDSC frequency, suggesting that in MMTV-PyMT mice, ß-AR activation also inhibits tumor progression in the absence of stress exposure. Together, these results suggest stress exposure can act through ß-AR signaling to slow primary tumor growth in MMTV-PyMT mice.