Protein-calorie malnutrition is very frequent in cancer patients and is associated with an increase in morbidity and mortality. Recently, the Global Leadership Initiative on Malnutrition (GLIM) criteria were proposed to standardize the diagnosis of malnutrition. Nevertheless, these criteria were not validated in prospective studies. Our objective is to determine the prevalence of malnutrition in cancer inpatients using different diagnostic classifications, including GLIM criteria, and to establish their association with length of stay and mortality. Hence, we designed a prospective study. Within the first 24 hours of admission to the Inpatient Oncology Unit, subjective global assessment (SGA) was carried out, and anthropometric data (body mass index (BMI), mid-arm circumference (MAC), arm muscle circumference (AMC), fat-free mass index (FFMI)) and hand grip strength (HGS) were obtained to assess the reduction of muscle mass according to GLIM criteria. Length of stay, biomarkers (albumin, prealbumin, C-reactive protein (CRP)), and in-hospital and six-month mortality were evaluated. Regarding the 282 patients evaluated, their mean age was 60.4 ± 12.6 years, 55.7% of them were male, and 92.9% had an advanced-stage tumor (17.7% stage III, 75.2% stage IV). According to SGA, 81.6% of the patients suffered from malnutrition (25.5% moderate malnutrition, and 56.1% severe malnutrition), and, based on GLIM criteria, malnutrition rate was between 72.2 and 80.0% depending on the used tool. Malnourished patients (regardless of the tool used) showed significantly worse values concerning BMI, length of stay, and levels of CRP/albumin, albumin, and prealbumin than normally nourished patients. In logistic regression, adjusted for confounding variables, the odds ratio of death at six months was significantly associated with malnutrition by SGA (odds ratio 2.73, confidence interval (CI) 1.35–5.52, p = 0.002), and by GLIM criteria calculating muscle mass with HGS (odds ratio 2.72, CI 1.37–5.40, p = 0.004) and FFMI (odds ratio 1.87, CI 1.01–3.48, p = 0.047), but not by MAC or AMC. The prevalence of malnutrition in advanced-stage cancer inpatients is very high. SGA and GLIM criteria, especially with HGS, are useful tools to diagnose malnutrition and have a similar predictive value regarding six-month mortality in cancer inpatients.

Our objective was to evaluate the clinical application of third lumbar vertebra (L3)-computer tomography (CT)-determined sarcopenia as a marker of muscle mass in cancer inpatients diagnosed with malnutrition according to the Global Leadership Initiative on Malnutrition (GLIM) criteria and to establish its association with 6-month mortality. Methods: This was an observational, prospective study in patients from an inpatient oncology unit. We performed a nutritional assessment according to GLIM criteria, including muscle cross-sectional area at L3 by CT and skeletal muscle index (SMI). Six-month mortality was evaluated. Results: A total of 208 patients were included. The skeletal muscle cross-sectional area at L3 was 136.2 ± 32.5 cm² in men and 98.1 ± 21.2 cm² in women. The SMI was 47.4 ± 12.3 cm²/m² in men and 38.7 ± 8.3 cm²/m² in women. Sarcopenia (low SMI) was detected in 59.6% of the subjects. Using SMI as a marker of low muscle mass in application of GLIM criteria, we found 183 (87.9%) malnourished patients. There were 104 deaths (50%) at 6 months. The deceased patients had a lower skeletal muscle cross-sectional area (112.9 ± 27.9 vs. 126.1 ± 37.8 cm²; p = 0.003) and a lower SMI (41.3 ± 9.5 vs. 45.7 ± 12.9 cm²/m²; p = 0.006). An increased risk of 6-month mortality was found in malnourished patients according to GLIM criteria using SMI (HR 2.47; 95% confidence interval 1.07–5.68; p = 0.033). Conclusions: Low muscle mass, assessed by L3-CT, was observed to affect more than half of cancer inpatients. The deceased patients at 6 months had a lower skeletal muscle cross-sectional area and SMI. Malnutrition according to GLIM criteria using CT-determined sarcopenia was shown to adequately predict 6-month mortality.

Alterations in BRCA1/2 (BRCA) and other homologous recombination repair (HRR) genes have a negative impact on outcomes in patients with metastatic castration-resistant prostate cancer (mCRPC). Poly(adenosine diphosphate-ribose) polymerase inhibitors, the only treatment demonstrated to improve the prognosis of patients with mCRPC, are also being developed for the treatment of patients with metastatic hormone-sensitive prostate cancer (mHSPC). To fully assess their potential benefit in this setting, it is essential to understand how BRCA and HRR defects may influence the prognosis of conventionally treated patients with low and high disease volume. Eligible mHSPC patients diagnosed between January 2018 and December 2023 underwent paired somatic/germline DNA sequencing. Cases with alterations in one or more HRR genes were classified as BRCA, HRR non-BRCA, non-BRCA or non-HRR. Radiographic progression-free survival, time to castration resistance and overall survival were reported for all subgroups; associations between mutations and outcomes were assessed after controlling for treatment modality and baseline characteristics using inverse probability of treatment weighting models. Of 556 patients, 159 (28.6%) had HRR gene alterations: 69 (12.4%) with BRCA and 90 (16.2%) with HRR non-BRCA mutations. mHSPC was synchronous in 451 patients (81.1%) and was classified as high-volume (CHAARTED criteria) in 306 (55%) patients. Within the HRR subgroup, patients with BRCA mutations had significantly worse outcomes across all endpoints (P < 0.005 for all comparisons). Differences in prognosis by BRCA and HRR status were observed in both low- and high-volume subgroups and were independent of treatment with androgen receptor pathway inhibitors or taxanes. Presence of HRR mutations, particularly BRCA alterations, significantly worsened prognosis, regardless of disease volume or treatment regimen. These findings underscore the importance of integrating tumour biology for accurate risk stratification in mHSPC and the design of new treatment strategies and follow-up.

Prostate-specific antigen (PSA) has been the primary biomarker used for the detection and monitoring of prostate cancer for decades. However, its limited specificity and prognostic accuracy have led to the development of novel molecular and imaging biomarkers aimed at improving the clinical characterization of localized disease. This review critically examines recent advances in urinary biomarkers (e.g., PCA3, SelectMDx), tissue-based genomic assays (Oncotype DX Prostate, Prolaris, Decipher), and imaging techniques such as multiparametric magnetic resonance imaging (mpMRI) and prostate-specific membrane antigen positron emission tomography (PET-PSMA). We evaluate their diagnostic performance, prognostic value, and clinical utility in risk stratification and individualized treatment decision-making. Methodological and clinical barriers to their routine implementation are also discussed. Current evidence supports the multidisciplinary integration of these biomarkers to overcome the limitations of PSA, improve biopsy decision-making, better distinguish indolent from aggressive tumors, and optimize therapeutic strategies. Finally, future research directions aimed at validating and incorporating emerging biomarkers into clinical practice are outlined, with the goal of improving outcomes in patients with localized prostate cancer.

The vascular endothelial growth factor (VEGF) and receptor is a therapeutic target because of the importance of this pathway in carcinogenesis. This pathway regulates and promotes angiogenesis as well as increases endothelial cell proliferation, permeability, and cancer survival. Ramucirumab is a new fully human monoclonal antibody that targets the VEGF receptor-2, an important key receptor implicated in angiogenesis. Ramucirumab has been approved for the treatment of second-line advanced or metastatic non-small cell lung cancer (NSCLC) in combination with the chemotherapy agent docetaxel. This was based on the result of the randomized trial REVEL of 1,253 patients with metastatic NSCLC previously treated with a platinum-based combination therapy. The authors observed a significant improvement in overall survival (OS) with an acceptable toxicities profile. In this study, patients were randomized to receive ramucirumab plus docetaxel or placebo with docetaxel. The combination of docetaxel and ramucirumab showed an improved OS (hazard ratio [HR]: 0.86; 95% CI: 0.75, 0.98). Median OS was 10.5 months in the ramucirumab arm versus 9.1 months in the placebo arm. Regarding side effects, the toxicity described on the ramucirumab arm were principally diarrhea, fatigue, and neutropenia. The most common (5%) adverse reactions of grade 3 and 4 in the ramucirumab arm were fatigue, neutropenia, febrile neutropenia, leukopenia, and hypertension. Adding ramucirumab to docetaxel improves QoL of patients, and does not impair symptoms or functioning. There are currently several trials in progress evaluating the effects of ramucirumab in combination with other drugs in patients with advanced NSCLC.