Background: Age- and cancer-related sarcopenia and malnutrition are common in older patients with colorectal cancer (CRC) and may negatively influence treatment tolerance and prognosis. However, the comparative prognostic value of post-chemotherapy changes in CT-based body composition parameters at the third lumbar vertebra (L3) and the twelfth thoracic vertebra (T12) levels, and their associations with nutritional indices, remain unclear. This study aimed to examine and compare the prognostic relevance of post-chemotherapy body composition changes at L3 and T12 and to assess their relationship with nutritional indices in older patients with metastatic CRC (mCRC). Methods: This retrospective study included 87 older patients with mCRC. Baseline and ~3-month follow-up CT scans were analyzed at L3 and T12 using 3D Slicer to quantify skeletal muscle index (SMI), subcutaneous adipose tissue index (SATI), visceral adipose tissue index (VATI), visceral-to-subcutaneous fat ratio (VSR), and intramuscular adipose tissue index (IMATI). Changes (Δ) in CT-derived body composition after chemotherapy were calculated as percentage change using ((follow-up − baseline)/baseline) × 100. Prognostic Nutritional Index (PNI) and Geriatric Nutritional Index (GNRI), which are established nutritional assessment tools, were calculated from baseline laboratory/anthropometric data. Agreement between T12 and L3 was assessed, and associations with grade ≥ 3 toxicity, progression-free survival (PFS), and overall survival (OS) were evaluated using multivariable models and ROC analyses. Results: Mean age was 69.0 ± 4.5 years (59 male/28 female), and 26.4% developed grade ≥ 3 adverse events. Over 3 months, mean SMI declined significantly at both L3 (46.7 ± 8.8 → 42.8 ± 9.8 cm²/m²) and T12 (34.6 ± 8.2 → 31.6 ± 8.1 cm²/m²) (p < 0.001 for both), accompanied by decreases in VATI and VSR; T12-IMATI increased significantly. Baseline PNI showed a weak positive correlation with L3-SMI (r = 0.302, p = 0.033), whereas GNRI showed moderate correlations with SMI at L3 (r = 0.502, p < 0.001) and T12 (r = 0.317, p = 0.025) and was associated with longitudinal changes in muscle metrics. T12-SMI consistently yielded lower values than L3-SMI, and agreement varied by compartment (best for SATI; weakest for VSR). Lower GNRI and greater L3-SMI loss were independently associated with grade ≥ 3 toxicity; ΔL3-SMI showed the highest discrimination (AUC = 0.79, 95% CI = 0.69–0.87, p < 0.001; cut-off >5.1% loss). All patients progressed (median PFS 7.6 months); mortality was 82.8% (median follow-up: 25 months). In multivariable analysis, PFS, CRP, GNRI, and ΔL3-SMI remained independently associated with OS. ΔL3-SMI provided the strongest mortality discrimination (AUC = 0.85, 95% CI = 0.74–0.94, p < 0.001; cut-off >10.4% loss), while ΔIMATI was also informative (AUC = 0.71, 95% CI = 0.59–0.82, p = 0.023). Conclusions: In older patients with mCRC, early post-chemotherapy skeletal muscle loss—particularly at the L3 level—showed the strongest prognostic association with severe toxicity and mortality. GNRI provided complementary prognostic information as a marker of baseline immunonutritional reserve. Although T12-derived measurements were correlated with L3-derived values, systematic bias suggests that they should not be interpreted interchangeably for longitudinal risk stratification.

Background/Objectives: Neoadjuvant dual HER2 blockade is standard for HER2-positive breast cancer, yet response rates vary based on tumor biology. This multicenter study aimed to identify clinicopathological predictors of pathological complete response (pCR), focusing on quantitative hormone receptor (HR) expression and HER2 staining intensity, and to evaluate their impact on survival. Methods: This multicenter retrospective study included 290 female patients diagnosed with HER2-positive early or locally advanced breast cancer treated with neoadjuvant trastuzumab and pertuzumab-based regimens (anthracycline-based [AC-THP] or non-anthracycline [TCHP]) across six centers. HR expression was stratified into low (<50%) and high (≥50%) categories. Multivariable regression analyses identified predictors of pCR, Disease-Free Survival (DFS), and Overall Survival (OS). Results: The pCR rate was 51.4%. Multivariate analysis identified HR negativity (OR = 2.80; p < 0.001) and strong HER2 overexpression (IHC Score 3) (OR = 2.20; p = 0.037) as primary predictors. Uniquely, patients with low HR expression (<50%) achieved significantly higher pCR rates (65.9%) than strongly positive cases (36.6%; p = 0.001), biologically mimicking hormone-negative disease. The non-anthracycline TCHP regimen showed a strong trend toward superior efficacy (OR = 2.22; p = 0.054). pCR was the sole independent predictor of OS (HR = 0.134; p = 0.009). Crucially, adjusting for pCR unmasked hormone-negative status as a significant risk factor for recurrence (HR = 2.49; p = 0.028), highlighting its dual nature: high chemosensitivity but inherent biological aggression. Conclusions: “Strong” HER2 positivity and “weak” HR expression (<50%) are the primary determinants of pCR. pCR remains the strongest surrogate for survival, neutralizing initial risk factors. These findings support using quantitative biomarker thresholds for personalization and reinforce the efficacy of non-anthracycline regimens.

Background/Objectives: ABO/Rh blood groups and systemic inflammation are each linked to cancer biology and prognosis, yet their combined and interactive prognostic value has not been clarified in small-cell lung cancer (SCLC). We investigated the distribution of ABO/Rh blood groups in SCLC, their association with baseline complete blood count (CBC)–derived inflammatory indices, and the prognostic significance of blood group–inflammation interactions for treatment response and survival outcomes. Methods: This retrospective study included 158 patients with SCLC with available ABO/Rh typing and pretreatment CBC data. Neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), systemic immune–inflammation index (SII), and systemic inflammation response index (SIRI) were calculated using standard formulas. Treatment response was assessed according to RECIST v1.1 and categorized as response (CR/PR) versus non-response (SD/PD). Progression-free survival (PFS) and overall survival (OS) were analyzed using Cox regression models incorporating interaction terms. Results: Patients with blood group O exhibited consistently lower baseline inflammatory indices compared with non-O blood groups. Non-O blood group status and higher SIRI independently predicted chemoradiotherapy non-response. Among the evaluated indices, SIRI demonstrated superior diagnostic performance compared with SII, NLR, and PLR. Similarly, non-O blood group status and higher SIRI were independently associated with increased risks of progression and mortality. In joint analyses, compared with blood group O and low SIRI (reference), the highest risk of progression was observed in patients with blood group AB × high SIRI (HR 14.67), followed by blood groups A × high SIRI (HR 10.38) and B × high SIRI (HR 7.95). A similar pattern was observed for mortality, with the highest risk in patients with blood group AB × high SIRI (HR 22.76), followed by blood groups A × high SIRI (HR 13.93) and B × high SIRI (HR 12.41). Conclusions: ABO blood group is associated with distinct inflammatory profiles in SCLC. Elevated SIRI independently predicts treatment non-response and adverse survival, and its prognostic effect varies by blood group, underscoring the role of host biology in modulating systemic inflammation.

To investigate whether pretreatment serum endocan, platelet-derived growth factor (PDGF)-CC, and -DD levels are elevated in metastatic colorectal cancer (mCRC) patients compared to healthy controls, and to assess their independent associations with chemotherapy response and survival, along with their comparative predictive performance. Adult patients with mCRC receiving systemic chemotherapy combined with an anti-angiogenic agent (bevacizumab or aflibercept) were prospectively enrolled, along with healthy controls. Pretreatment serum samples were collected prior to therapy initiation. Endocan, PDGF-CC, and PDGF-DD levels were measured in duplicate using enzyme-linked immunosorbent assay. Treatment response was evaluated according to Response Evaluation Criteria in Solid Tumors (RECIST) v1.1 and categorized as responders (complete or partial response) and non-responders (stable or progressive disease). Progression-free survival (PFS) and overall survival (OS) were recorded. Median serum levels of endocan (405.5 vs. 269.0 pg/mL), PDGF-DD (499.9 vs. 315.1 pg/mL), and PDGF-CC (2330 vs. 1118 pg/mL) were significantly higher in the mCRC group compared to controls (p < 0.001). In multivariable logistic regression, all three biomarkers were independently associated with non-response to chemotherapy [Odds ratio (ORs): 1.10 for endocan, 1.05 for PDGF-DD, 1.05 for PDGF-CC; all p < 0.05]. For disease progression, Cox regression showed that higher levels of endocan [Hazard ratio (HR) = 1.04], PDGF-DD (HR = 1.03), and PDGF-CC (HR = 1.04) were significant predictors (all p < 0.01). Similar associations were observed for overall mortality (HR = 1.04, 1.02, and 1.02, respectively; all p < 0.05). Endocan, PDGF-DD, and PDGF-CC are elevated in mCRC and independently predict poor treatment response and adverse survival outcomes, highlighting their potential as prognostic biomarkers.