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Krzysztof Safranow

Publications and source records attributed to Krzysztof Safranow.

2 recordsLinked to original sources

Kruskal-Wallis Power Studies Utilizing Bernstein Distributions; preliminary empirical studies using simulations/medical studies

Bernstein fits implemented into R allow another route for Kruskal-Wallis power-study tool development. Monte-Carlo Kruskal-Wallis power studies were compared with measured power, with Monte-Carlo ANOVA equivalent and with an analytical method, with or without normalization, using four simulated runs each with 60-100 populations (each population with N=30000 from a set of Pearson-type ranges): random selection gave 6300 samples analysed for predictive power. Three medical-study datasets (Dialysis/systolic blood pressure; Diabetes/sleep-hours; Marital-status/high-density-lipoprotein cholesterol) were also analysed. In three from four simulated runs (run_one, run_one_relaxed, and run_three) with Pearson types pooled, Monte-Carlo Kruskal-Wallis gave predicted sample sizes significantly slightly lower than measured but more accurate than with ANOVA methods; the latter gave high sample-size predictions. Populations (run_one_relaxed) with ANOVA assumptions invalid gave Kruskal-Wallis predictions similar to those measured. In two from three medical studies, Kruskal-Wallis predictions (Dialysis: similar predictions; Marital: higher than measured) were more accurate than ANOVA (both higher than measured) but in one (Diabetes) the reverse was found (Kruskal-Wallis: lower; Monte-Carlo ANOVA: similar to measured). These preliminary studies appear to show that Monte-Carlo Kruskal-Wallis power studies based on Bernstein fits might perform better than ANOVA equivalents in many settings (and provide reasonable results when ANOVA cannot be used); and both Monte-Carlo methods appeared considerably more accurate than the analysed analytical version.

q-bio.QM↗

Colorectal cancers differ in respect of PARP-1 protein expression

Recent findings raise the possibility of PARP inhibitor therapy in colorectal cancers(CRCs). However, the extent of PARP-1 protein expression in clinical specimens of CRC is not known. Using immunohistochemistry we assessed PARP-1 protein expression in tissue microarrays of 151 CRCs and its association with the patient's age, sex, Astler-Coller stage, grade and site of the tumor. High PARP nuclear immunoreactivity was found in 68.2% (103/151) of all cases. In turn, 31.8% (48/151)of tumors showed low PARP expression, including 9 (6%) PARP-1 negative CRCs. There was a significant association of PARP-1 expression with the site of CRC and Astler-Coller stage. A high PARP expression was noted in 79.1% of colon vs. 53.9% of rectal tumors (p = 0.001). The mean PARP-1 score was 1.27 times higher in colon vs. rectal cancers (p = 0.009) and it was higher in stage B2 vs. stage C of CRCs (p = 0.018). In conclusion, the level of PARP-1 protein nuclear expression is associated with the tumor site and heterogeneous across clinical specimens of CRC, with the majority of CRCs expressing a high level but minority - low or no PARP-1 expression. These findings may have a clinical significance because the assessment of PARP-1 expression in tumor samples may improve selection of patients with CRC for PARP inhibitor therapy.

q-bio.SC↗