Aim:This case–control study examined the impact of diabetes mellitus (DM) on survival in lung cancer patients and lung cancer on glycemic control in DM.Materials & methods:Patients with a new lung cancer diagnosis and DM (n = 124) were matched to 124 lung cancer patients without DM. Laboratory results and DM and cancer therapies were obtained from electronic records.Results:Five-year overall survival for lung cancer patients with and without DM was 20 versus 29% (p = .12). Glycemic control among DM patients did not change significantly with time.Conclusion:DM does not cause adverse impact on lung cancer survival. Lung cancer does not affect glycemic control.

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Aim:We aimed to determine the effect of diabetes mellitus (DM) on survival in pancreatic cancer and effects of pancreatic cancer on glycemic control in DM.Materials & methods:Patients with pancreatic cancer from 2007 to 2015, with and without DM, were matched 1:1. We compared characteristics between the groups and assessed 2-year survival with Kaplan–Meier analysis.Results:In patients with DM, hemoglobin A1c decreased significantly over time (p = 0.01). In survival analysis, 2-year overall survival estimates were 15% (95% CI: 8–24%) for DM patients versus 26% (95% CI: 17–36%) for non-DM patients (p = 0.55). The hazard ratio for matched pairs was 1.15 (95% CI: 0.75–1.77; p = 0.51).Conclusion:DM did not decrease survival in pancreatic cancer. Pancreatic cancer did not affect glycemic control.

The impact of diabetes mellitus (DM) on survival in patients with colorectal cancer and the impact of colorectal cancer on glycemic control were examined. Materials & methods: Patients with colorectal cancer with and without DM were matched 1:1 (2007-2015). Characteristics were compared between the two groups and survival assessed with the Kaplan-Meier method. Mixed models compared hemoglobin A 1c and glucose levels over time. Results: In both groups, glucose values decreased during the year following cancer diagnosis (p < 0.001). 5-year overall survival was 56% (95% CI: 42-68%) for DM patients versus 57% (95% CI: 43-69%) for non-DM patients (p = 0.62). Conclusion: DM did not adversely impact survival of patients with colorectal cancer. Colorectal cancer did not affect glycemic control.

Aim:The impact of diabetes mellitus (DM) on survival in patients with colorectal cancer and the impact of colorectal cancer on glycemic control were examined.Materials & methods:Patients with colorectal cancer with and without DM were matched 1:1 (2007–2015). Characteristics were compared between the two groups and survival assessed with the Kaplan–Meier method. Mixed models compared hemoglobin A1c and glucose levels over time.Results:In both groups, glucose values decreased during the year following cancer diagnosis (p < 0.001). 5-year overall survival was 56% (95% CI: 42–68%) for DM patients versus 57% (95% CI: 43–69%) for non-DM patients (p = 0.62).Conclusion:DM did not adversely impact survival of patients with colorectal cancer. Colorectal cancer did not affect glycemic control.

Aim:Given the lack of data in the literature, we examined the impact of diabetes mellitus (DM) on melanoma survival and the impact of melanoma on glycemic control.Materials & methods:Patients with melanoma with and without DM were matched 1:1 (2005–2016). Kaplan–Meier analysis was used to estimate overall survival and progression-free survival (PFS). Mixed models compared hemoglobin A1c (HbA1c) and glucose measures over time.Results:Mean HbA1c during the year after cancer diagnosis was 6.7%. The 5-year PFS rate was 89% (95% CI: 81–99%) for patients with DM and 63% (95% CI: 51–79%) for patients without DM (p = 0.02).Conclusion:Melanoma did not adversely impact glycemic control. The DM did not adversely impact survival of patients with melanoma, although increased PFS for melanoma was seen in individuals with DM.

Aim: We examined the effect of diabetes on survival in patients with lymphoma and the effect of lymphoma on glycemic control. Patients & methods: Patients with lymphoma with and without diabetes (2005–2016) were retrospectively identified and matched 1:1. Overall survival and progression-free survival were estimated by the Kaplan–Meier method. Hemoglobin A1c (HbA1c) and glucose levels during the year after cancer diagnosis were compared by mixed models. Results: For patients with diabetes, mean HbA1c during the year after lymphoma diagnosis was 6.7%. Estimated 5-year progression-free survival for patients with versus without diabetes was 63% (95% CI: 53–76%) versus 58% (95% CI: 46–71%) (p = 0.42). Conclusion: Lymphoma and its treatment did not affect glycemic control. Diabetes did not decrease lymphoma-specific survival.

Background: Diffuse gliomas are highly aggressive brain tumors that invariably relapse despite treatment with chemo-and radiotherapy. Treatment with alkylating chemotherapy can drive tumors to develop a hypermutator phenotype. In contrast, the genomic effects of radiotherapy (RT) remain unknown.Methods: We analyzed the mutational spectra following treatment with RT in whole genome or exome sequencing data from over > 4,000 samples, including 190 paired primary-recurrent gliomas from the Glioma Longitudinal Analysis (GLASS) dataset and 3693 post-treatment metastatic tumors from the Hartwig Medical Foundation.Results: We identified a significant increase in the burden of small deletions following radiation therapy that was independent of other factors (P¼3e-03, log-linear regression model). These novel deletions demonstrated distinct characteristics when compared to pre-existing deletions present prior to RT-treatment and deletions in RTuntreated tumors. Radiation therapy-acquired deletions were characterized by a larger deletion size (GLASS and HMF, P¼1.5e-04 and P¼6e-16, respectively; Mann-Whitney U test), an increased distance to repetitive DNA elements (P<2.2e-16, Kolmogorov-Smirnov test) and a lack of microhomology at breakpoints (P ¼ 6.6e-05, paired Wilcoxon signed-rank test). These observations suggested that canonical non-homologous end joining (c-NHEJ) was the preferred pathway for DNA double strand break repair of RT-induced DNA damage. Furthermore, radiotherapy resulted in frequent chromosomal deletions and significantly increased frequencies of CDKN2A homozygous deletions in IDHmut glioma (P¼1.9e-05, Fisher's exact test). Finally, a high burden of RT-associated deletions was associated with worse clinical outcomes (GLASS and HMF, P¼3.4e-02 and P<1e-04, respectively; log-rank test).