PubMed · 13155867
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S DE CANDIA. 1953. [Diencephalo-hypophysial cachexia].. https://pubmed.ncbi.nlm.nih.gov/13155867/
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PURPOSE: To develop and internally validate the PANTHEIA-SIRI prognostic model, which integrates log-transformed systemic inflammation response index (SIRI) with clinical predictors, to estimate overall survival (OS) in metastatic pancreatic ductal adenocarcinoma (mPDAC) treated with first-line chemotherapy. METHODS: We used data from the multicenter PANTHEIA-SEOM registry. OS was defined from chemotherapy start. The model was fitted as a Weibull accelerated failure time model in the survival-analysis population with multiple imputation. Predictors were log-transformed baseline SIRI, modeled with restricted cubic splines, ECOG, tumor burden, chemotherapy regimen, and anorexia-cachexia syndrome. Internal validation used a separate, non-overlapping cohort from the same registry; the centers contributing to each cohort are listed in a supplementary annex. TRIPOD was followed. Discrimination was assessed with Harrell´s C-index and calibration with IPCW Brier scores and IPA. RESULTS: The derivation cohort comprised 672 patients with SIRI data (593 analyzed for survival) across 22 Spanish hospitals (2015-2025); 80.1% had died after a median OS of 9.9 months. The imputation-pooled derivation C-index was 0.654 (95% CI, 0.627-0.681); optimism-corrected, 0.629. Internal validation used 62 separate patients from the same registry; 96.8% had died after a median OS of 9.2 months. The validation C-index was 0.603 (95% CI, 0.518-0.687). Calibration was adequate at 6 and 12 months. CONCLUSIONS: The PANTHEIA-SIRI model provides individualized OS estimates in mPDAC with routine clinical predictors. Its open-access calculator ( https://pantheia-siri.shinyapps.io/calc/ ) may support prognostic communication, treatment-intensity selection, and supportive-care planning. Routine clinical implementation will require further validation in larger, fully independent cohorts.
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Cancer cachexia involves the loss of weight, mainly in skeletal muscle and adipose tissue, that is not caused simply by anorexia. The syndrome includes anemia and immunosuppression along with a number of biochemical changes indicating systemic effects of the cancer. It is a major factor in morbidity and mortality from cancer. For 30 years beginning in 1948, a large number of studies reported isolation from many tumors of a heterogeneous group of small peptides, generally labeled toxohormone, that caused various correlates of cachexia shortly after injection into mice. Interest in toxohormone-like peptides then fell off for diverse reasons that had little to do with their clinical significance and was shifted to cytokines, ILs, and ectopic hormones with catabolic consequences that were sporadically found in tumors. At the same time, evidence was accumulating for an important role of pericellular proteases in driving progressive stages of neoplastic development. A central part of that evidence was the inhibition of transformation-related changes by protease inhibitors, particularly the combination present in fetal bovine serum, which fully suppressed the expression of the transformed phenotype in discrete foci of chicken embryo fibroblasts (CEF) infected by Rous sarcoma virus against a confluent background of uninfected CEF. In contrast, CEF cultures heavily infected with Rous sarcoma virus in the same medium underwent pervasive transformation, which was correlated with the release of low molecular weight cytotoxic substances. Reevaluation of all of the evidence supports a central role for proteolytically generated peptides derived from tumors in producing cancer cachexia.