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An independently validated nomogram for isocitrate dehydrogenase-wild-type glioblastoma patient survival.
BackgroundIn 2016, the World Health Organization reclassified the definition of glioblastoma (GBM), dividing these tumors into isocitrate dehydrogenase (IDH)-wild-type and IDH-mutant GBM, where the vast majority of GBMs are IDH-wild-type. Nomograms are useful tools for individualized estimation of survival. This study aimed to develop and independently validate a nomogram for IDH-wild-type patients with newly diagnosed GBM.MethodsData were obtained from newly diagnosed GBM patients from the Ohio Brain Tumor Study (OBTS) and the University of California San Francisco (UCSF) for diagnosis years 2007-2017 with the following variables: age at diagnosis, sex, extent of resection, concurrent radiation/temozolomide (TMZ) status, Karnofsky Performance Status (KPS), O6-methylguanine-DNA methyltransferase (MGMT) methylation status, and IDH mutation status. Survival was assessed using Cox proportional hazards regression, random survival forests, and recursive partitioning analysis, with adjustment for known prognostic factors. The models were developed using the OBTS data and independently validated using the UCSF data. Models were internally validated using 10-fold cross-validation and externally validated by plotting calibration curves.ResultsA final nomogram was validated for IDH-wild-type newly diagnosed GBM. Factors that increased the probability of survival included younger age at diagnosis, female sex, having gross total resection, having concurrent radiation/TMZ, having a high KPS, and having MGMT methylation.ConclusionsA nomogram that calculates individualized survival probabilities for IDH-wild-type patients with newly diagnosed GBM could be useful to physicians for counseling patients regarding treatment decisions and optimizing therapeutic approaches. Free software for implementing this nomogram is provided: https://gcioffi.shinyapps.io/Nomogram_For_IDH_Wildtype_GBM_H_Gittleman/
Factors Influencing Patients’ Intention to Perform Physical Activity During Hematopoietic Cell Transplantation
A Cross-Sectional Study of KLKB1 and PRCP Polymorphisms in Patients with Cardiovascular Disease
Plasma kallikrein formed from prekallikrein (PK) produces bradykinin from kininogens and activates factor XII. Plasma PK is activated by factors XIIa, XIIa or prolylcarboxypeptidase (PRCP). A cross-sectional investigation determined if there is an association of PRCP and KLKB1 polymorphisms with cardiovascular disease. DNA was obtained from 2243 individuals from the PEACE trial. Two PRCP SNPs, rs7104980 and rs2298668 and 2 KLKB1 SNPs, rs3733402 and rs3087505, were genotyped. Logistic regression models were performed for history of diabetes, MI, stroke, angina, angiographic coronary disease, CABG, intermittent claudication, PTCA, and TIA. The PRCP SNP rs7104980 increased the odds of having a history of PTCA by 21% [OR = 1.211; 95% CI = (1.008, 1.454)]; P= 0.041, but was non significant after Bonferroni correction. Alternatively, having the G allele for rs3733402 (KLKB1 gene) decreased the odds of having a history of angiographic coronary disease by 24% [OR = 0.759; 95% CI = (0.622, 0.927)]; P = 0.007 that was statistically significant (p<0.01) after Bonferroni correction for multiple hypothesis testing. When the best-fit model based on the Akaike information criterion (AIC) controlled for age, weight, gender, hypertension, and history of angina. the G allele of KLKB1 rs3733402 that is associated with less plasma kallikrein activity correlated with reduced history of cardiovascular diseas