Disparities in Late-Stage Breast and Colorectal Cancer Diagnosis Among Hispanic, Non-Hispanic White, and Non-Hispanic Black Patients: a Retrospective Cohort Study of Texas Medicare Beneficiaries.

BACKGROUND: Disparities in late-stage breast or colorectal cancer diagnosis in younger populations are associated with social determinants of health (SDOH; education, poverty, housing, employment). We hypothesized that, in older Medicare beneficiaries, disparities in late-stage cancer diagnosis between Hispanic, non-Hispanic Black (NHB), and non-Hispanic White (NHW) patients would be associated with SDOH, comorbidities, and primary care physician (PCP) access. METHODS: We analyzed 2005-2017 Texas Cancer Registry data linked with Medicare data for patients aged ≥ 66 (n = 86,501). Variables included age at diagnosis, sex, comorbidities, poverty level, education, PCP, and relevant cancer screening within 1 year. RESULTS: For breast cancer in women (Hispanic, n = 6380; NHW, n = 39,225; NHB, n = 4055), a fully adjusted model showed significantly higher odds of late-stage cancer diagnosis only in NHB patients (odds ratio [OR] 1.11, 95% confidence interval [CI] 1.01-1.22) compared with NHW; adjustment for comorbidities and SDOH partially decreased the odds of late-stage diagnosis relative to NHWs. Interaction terms between race-ethnicity and poverty were not significant. For colorectal cancer, a fully adjusted multivariate model showed significantly higher odds of late-stage diagnosis only among NHBs (n = 3318, OR 1.29, 95% CI 1.19-1.40) relative to NHWs (n = 27,470); adjustment for SDOH partially decreased the odds of late-stage diagnosis in NHB patients. Interaction terms between race-ethnicity and poverty were not significant. CONCLUSION: Racial disparities in late-stage breast and colorectal cancer diagnoses remain after adjustment for SDOH and clinically relevant factors, underscoring the need to optimize access to screening and timely cancer treatment in racial/ethnic minorities.

Subventricular zone cytogenesis provides trophic support for neural repair in a mouse model of stroke.

Stroke enhances proliferation of neural precursor cells within the subventricular zone (SVZ) and induces ectopic migration of newborn cells towards the site of injury. Here, we characterize the identity of cells arising from the SVZ after stroke and uncover a mechanism through which they facilitate neural repair and functional recovery. With genetic lineage tracing, we show that SVZ-derived cells that migrate towards cortical photothrombotic stroke in mice are predominantly undifferentiated precursors. We find that ablation of neural precursor cells or conditional knockout of VEGF impairs neuronal and vascular reparative responses and worsens recovery. Replacement of VEGF is sufficient to induce neural repair and recovery. We also provide evidence that CXCL12 from peri-infarct vasculature signals to CXCR4-expressing cells arising from the SVZ to direct their ectopic migration. These results support a model in which vasculature surrounding the site of injury attracts cells from the SVZ, and these cells subsequently provide trophic support that drives neural repair and recovery.