The Paradoxical Protective Effect of Immigration on Colorectal Cancer Survivals.

BACKGROUND: It is unknown whether the place of birth would affect colon cancer survival. METHODS: An observational study of colon cancer patient data using the SEER database from 1973 to 2010 was performed. Patients with more than one primary cancer in their lifetime or patients who were under age 18 were excluded. The primary outcome was cancer-specific survival. Cox proportional hazards analyses were performed, adjusting for patient demographics and oncological characteristics. RESULTS: A total of 262,618 colon cancer patients were analyzed, with the majority (86.0%) born in the US. The overall 5-year cancer-specific survival rate was 51.4% and was significantly lower for US-born than non-US born patients (50.4% vs 58.1%). This difference persisted in local/regional disease and in cases with distant metastasis, and across racial groups. On adjusted analysis, US-born patients had worse disease-specific survivals (HR 1.28, 95% CI 1.24-1.33), and this effect persisted in all racial groups except in Asians. CONCLUSION: US-born patients have worse survivals than non-US born patients. This is paradoxical given known disparities in quality of care delivered to immigrant populations. It may be useful to consider including geographical histories in patient interviews.

Correction: A novel epigenetic modulating agent sensitizes pancreatic cells to a chemotherapy agent.

[This corrects the article DOI: 10.1371/journal.pone.0199130.].

A novel epigenetic modulating agent sensitizes pancreatic cells to a chemotherapy agent.

Pancreatic ductal adenocarcinoma (PDAC) is expected to be the second leading cause of cancer mortality by 2030. PDAC remains resistant to the majority of systemic chemotherapies. In this paper, we explore if epigenetic sensitization can improve chemotherapy response in PDAC. Multiple PDAC cell lines were tested with serial concentrations of the epigenetic modulators 5-azacitidine (Aza) and guadecitabine (SGI-110). Guadecitabine was effective at inhibiting the expression of DNA Methyltransferase 1 (DNMT1) and in decreasing cell viability at nanomolar concentrations. We also report that guadecitabine has increased efficacy following a delay period or as we reference, a 'rest period'. Sensitization with guadecitabine improved response to the chemotherapeutic agent-Irinotecan- as measured by decreased cell viability and accompanied by an increase in caspase activity. Additional studies are needed to understand the mechanism of action.