Prognostic nutritional index (PNI), which is calculated using the albumin level reflecting nutritional status and lymphocyte count reflecting immune status, is useful in showing nutritional and immunological status related to survival and prognosis in many cancers. In this study, we aimed to evaluate the biomarker potential and effect of PNI in determining the prognosis of metastatic castration-sensitive prostate cancer (mCSPC). This retrospective observational study included the complete data of 108 patients with mCPSC who were treated for at least three months between 1 January 2010, and 1 June 2021. The relationships between cancer-specific survival (CSS), overall survival (OS), progression-free survival (PFS), and PNI were evaluated. The Kaplan–Meier method for OS, PFS, and CSS, as well as univariate and multivariate Cox regression models, were used for the statistical analyses. The median age of 108 patients included in the study was 68.54 (61.05–74.19) years. A value of 49.75 was determined to be the best cut-off point for the PNI. OS (months) was found to be significantly lower in patients with low PNI (median: 34.93, 95% CI: 21.52–48.34) than in patients with high PNI (median: 65.60, 95% CI: 39.36–91.83) (p = 0.016). Patients with high PNI (median: 48.20, 95% CI: 34.66–61.73) had significantly better CSS (months) than patients with low PNI (median: 27.86, 95% CI: 24.16–31.57) (p = 0.001). There was no statistically significant difference in PFS between patients with high PNI values (median: 24.60, 95% CI: 10.15–39.05) and patients with low PNI values (median: 20.03, 95% CI: 11.06–29.03) (p = 0.092). The PNI is a good predictor of OS and CSS in patients with mCSPC. The prediction of PFS, albeit showing a trend towards significance, was not statistically significant, probably due to the small number of cases.
Background: The purpose of our study was to investigate the immunohistochemical expression of TGF-β1 and p27 in pancreatic adenocarcinomas and to compare the findings with the clinicopathological features and survival. We also aimed to evaluate the expression of TGF-β1 and p27 in the context of other cell cycle and proliferation markers such as cyclin D1 and Ki-67. Methods: We examined TGF-β1 and p27 expression immunohistochemically in 63 cases of invasive ductal adenocarcinoma of the pancreas. Standard streptavidin-biotin immunperoxidase method was used for immunostaining and the stained slides were examined microscopically using semiquantitative criteria. Results: TGF-β1 stained the cytoplasms of the tumor cells in 43 cases [68.3%]. There was a statistically significant difference among TGF-β1 staining scores in terms of clinicopathologic factors such as blood vessel invasion, stage and distant metastasis [p < 0.05]. Of the 63 tumors evaluated 23 [36.5%] were positive for p27 within the nucleus. An inverse correlation was found between p27 immunoreactivity and grade [p < 0.05]. But no significant correlation was found between p27 and other parameters. Among the patients with survival data 27 patients had RO resections and these cases were considered in survival analysis. In the univariate analysis, neither TGF-β1 nor p27 expression was related with patient survival. Conclusion: Our findings suggest that in pancreatic carcinoma, TGF-β1 expression is related to tumor growth and metastasis. But it is not associated with cell cycle proteins. p27 expression is reduced in pancreatic adenocarcinomas and decreased protein levels of p27 may play a role in the differentiation of pancreatic cancer.
Tumor lysis syndrome is a potentially fatal complication of anticancer therapy that is usually seen in patients with bulky, rapidly proliferating, treatment-sensitive tumors such as hematological malignancies, but it rarely occurs in a variety of solid tumors such as colorectal carcinoma. Combination chemotherapy with infusional 5-fluorouracil/leucoverin and irinotecan has been recently accepted as the first treatment option for metastatic colorectal cancer. We present a case of tumor lysis syndrome in a patient with metastatic colon carcinoma that occurred 72 hrs after the initial course of a combination chemotherapy with irinotecan and 5-fluorouracil/leucoverin. Despite the immediate treatment with aggressive hydration by a sodium bicarbonate infusion, followed by forced diuresis and uricolytic therapy, he died of a sudden cardiac arrest complicated by acute renal failure. Our case indicates that administration of 5-fluorouracil/leucoverin and irinotecan for bulky tumors of colorectal origin with a rapid doubling time may induce an acute tumor lysis syndrome, which necessitates frequent laboratory monitoring and a close follow-up of the patient as well as prompt initiation of appropriate therapeutic measures.
Fluoropyrimidine-based chemotherapy is extensively used for the treatment of solid cancers, including colorectal cancer. However, fluoropyrimidine-driven toxicities are a major problem in the management of the disease. The grade and type of the toxicities depend on demographic factors, but substantial inter-individual variation in fluoropyrimidine-related toxicity is partly explained by genetic factors. The aim of this study was to investigate the effect of dihydropyrimidine dehydrogenase (DPYD), thymidylate synthase (TYMS), and methylenetetrahydrofolate reductase (MTHFR) polymorphisms in colorectal cancer patients. Eighty-five patients who were administered fluoropyrimidine-based treatment were included in the study. The DPYD, TYMS and MTHFR polymorphisms were scanned by a next generation Sequenom MassARRAY. Fluoropyrimidine toxicities were observed in 92% of all patients. The following polymorphisms were detected: DPYD 85T>C (29.4% heterozygote mutants, 7.1% homozygote mutants), DPYD IVS 14+1G>A (1.2% heterozygote mutants), TYMS 1494del TTAAAG (38.4% heterozygote mutants, 24.7% homozygote mutants), MTHFR 677C>T (43.5% heterozygote mutants, 9.4% homozygote mutants) and MTHFR 1298A>C (8.2% heterozygote mutants, 2.4% homozygote mutants). A statistically significant association was demonstrated between MTHFR 677C>T and fluoropyrimidine-related toxicity (p value = 0.007). Furthermore, MTHFR 1298A>C was associated with hematopoietic toxicity (p value = 0.008). MTHFR polymorphisms may be considered as related factors of fluoropyrimidine toxicity and may be useful as predictive biomarkers for the determination of the colorectal cancer patients who can receive the greatest benefit from fluoropyrimidine-based treatments.
29 November 2013 in Journal of Cancer Research and Clinical Oncology
Exercise capacity is a significant determinant of mortality for cancer patients, so knowing the possible determinants of exercise capacity will produce physical and psychological benefits for individuals with cancer cachexia. To investigate the relationship between exercise capacity on peripheric and respiratory muscle strength, physical activity, fatigue and quality of life in subjects with cancer cachexia. The study included 31 patients diagnosed with cancer cachexia. Functional capacity was assessed by 6-Minute Walk Test, hand grip strength and proximal muscle mass by hand dynamometer, respiratory muscle strength by the Maximum Expiratory Pressure and Maximum Inspiratory Pressure measurements, physical activity by International Physical Activity Questionnaire Short Form, fatigue by Brief Fatigue Inventory, and quality of life by EORT-QLQ-C30. The relationship between functional capacity and continuous independent variables was determined using Spearman's or Pearson's tests. A strong positive correlation was observed between exercise capacity and expiratory muscle strength (r = 0.75, p < 0.001), activity level (r = 0.68, p < 0.001), and quality of life global health status (r = 0.74, p < 0.001). Conversely, a strong negative correlation was found between exercise capacity and fatigue severity (r = -0.64, p < 0.001). Higher exercise capacity in cancer cachexia patients is linked to reduced fatigue, improved respiratory muscle strength, increased physical activity levels, and enhanced quality of life. When designing rehabilitation programs or exercise interventions for individuals with cancer cachexia, it is crucial to assess their exercise capacity and tailor the programs accordingly.