Chondrosarcoma (CS) is a rare and heterogeneous group of malignant cartilaginous tumors characterizedby variation in histological subtype, molecular profile, clinical behavior, prognosis, and treatment response.Conventional CS constitutes the majority of cases, whereas dedifferentiated, mesenchymal, periosteal,and clear cell subtypes comprise smaller cohorts with distinct biological characteristics and clinicaloutcomes. Histological grade, anatomical location, tumor size, and surgical margin status remain majorprognostic determinants. Molecular studies have identified recurrent alterations involving IDH1/IDH2, TP53,RB1, CDKN2A/B, CDK4, MDM2, and the HEY1-NCOA2 fusion. Surgical resection remains the major treatment option for localized disease. Conventional chemotherapyand radiotherapy have limited activity in most conventional CS. Mesenchymal and dedifferentiated CS demonstratecomparatively greater chemotherapy sensitivity. Current research is exploring three mechanisticallydistinct therapeutic approaches: death receptor 5 (DR5) agonism, IDH1/2 inhibition, and antiangiogenic/immunotherapy combinations. Ivosidenib, a mutant IDH1 inhibitor, achieved a median progression-free survival(mPFS) of 7.4 months and an objective response rate (ORR) of 23.1% in patients with conventional CS,leading to the phase III randomized, double-blind, placebo-controlled confirmatory CHONQUER trial. Ozekibart(INBRX-109), a tetravalent DR5 agonist, demonstrated a mPFS of 7.6 months. The phase II ChonDRAgonstudy evaluating ozekibart versus placebo demonstrated a mPFS of 5.52 months. Immunotherapy remains challenging because of the immunosuppressive tumor microenvironment. However,antiangiogenic agents combined with PD-1 blockade have shown promising activity. Overall, CS treatmentis evolving toward molecularly and immunologically informed strategies. Future trials should prioritize histology-specific, biomarker-enriched approaches integrating genomic, immune, and clinicopathological factorsto enable personalized treatment.
INTRODUCTION: Dysgeusia is a common but often underrecognized complication of chemotherapy that canreduce nutritional intake and body weight, impair quality of life (QoL), and compromise treatment adherence.The aim of this study was to describe the prevalence of dysgeusia and its association with nutritional riskand QoL during chemotherapy for gastrointestinal cancer. MATERIAL AND METHODS: A cross-sectional pilot survey was conducted among 30 patients receiving chemotherapyfor gastrointestinal cancer, recruited from a hospital chemotherapy department (n = 12, interviewedin person) and through online support groups (n = 18, self-administered). Measures included a structuredquestionnaire on taste preferences, food intake, and appetite, the Nutritional Risk Screening 2002 (NRS 2002),and the European Organisation for Research and Treatment of Cancer Quality of Life QuestionnaireCore 30 (EORTC QLQ-C30). All anthropometric data were self-reported. Analyses were exploratory, withoutcorrection for multiple comparisons. RESULTS: Seventeen of 30 participants (56.7%) reported dysgeusia, most often a metallic or bitter tasteand aversion to protein-rich foods, particularly red meat. Fifteen (50.0%) had NRS 2002 scores of 3 or more,and the median score was higher among those reporting taste changes (3 vs. 2). Self-reported weight lossover three months was greater in this group (median 5 kg vs. 1 kg; p = 0.019), as were gastrointestinalsymptoms. Dysgeusia severity correlated with the self-reported number of chemotherapy cycles (rho = 0.44;p = 0.015). Quality of life was lower in patients reporting dysgeusia. CONCLUSIONS: In this pilot sample, dysgeusia co-occurred with higher nutritional risk, more gastrointestinalsymptoms, and lower QoL. The findings are hypothesis-generating and require confirmation in larger prospectivecohorts with objectively measured anthropometry.
Triple-negative breast cancer (TNBC) is a therapeutically defined but molecularly heterogeneous breastcancer phenotype representing 10–15% of invasive breast cancers and carrying a disproportionate burdenof early relapse, visceral dissemination, central nervous system progression, and chemotherapy dependencebecause it lacks the therapeutic targets provided by ER, PR, and HER2 expression. Recent gainsfrom pembrolizumab-based chemoimmunotherapy, PARP inhibition in germline BRCA-associated disease,TROP2-directed antibody-drug conjugates (ADCs), and HER2-low ADC strategies have improved selectedoutcomes, yet median progression-free survival in advanced TNBC frequently remains measured in monthsrather than years, and durable benefit is restricted to biomarker-enriched subgroups. This review evaluatesemerging and underutilized targets including B7-H4, HER3, LIV-1, Nectin-4, tissue factor, ROR1, CD47-SIRPalpha,LAG-3, TIM-3, TIGIT, ATR, CHK1, WEE1, PI3K-AKT-mTOR, Wnt-beta-catenin, Notch, TGF-beta, androgenreceptor, glucocorticoid receptor, EZH2, BET proteins, glutamine metabolism, AXL, MET, integrins, and cancerstem-cell programs through the linked lenses of target prevalence, mechanistic indispensability, druggability,internalization potential, resistance biology, and biomarker feasibility. The central argument is that the nexttherapeutic leap in aggressive TNBC will depend less on nonspecific escalation of cytotoxic exposure and moreon quantitative patient selection, multi-omic target validation, rational ADC payload design, microenvironmentreprogramming, and resistance-informed combinatorial sequencing.
A 25-year-old male patient was admitted to the Department of Pneumonology, Oncology and Allergologybecause of non-small cell carcinoma of the left lung with squamous cell and NOS components. His medicalhistory included an episode of removing asbestos from a roof without protective equipment for several daysapproximately 7 years earlier and a cough lasting for about 6 months. The patient was also a light smokerand had a family history of cancer. Multiple metastases to the lungs, bones, and central nervous system werediagnosed. The patient underwent radiotherapy to the scapula, spine, iliac bone, and occipital lobe. He wasqualified for chemoimmunotherapy with carboplatin, paclitaxel, and cemiplimab. After 2 weeks, the patientwas admitted to the Emergency Department because of breathlessness, dizziness, tinnitus, and nausea.CT and MRI of the cerebrum and cerebellum showed more metastatic lesions (approximately 50) than in the previousexamination; therefore, brain radiotherapy was continued. The patient's condition deteriorated during hospitalization,with severe headache, nausea, and periodic loss of coherent contact. The patient died due to respiratoryfailure and cardiac arrest. This case shows that squamous cell lung cancer can occur in very young people,and physicians must be aware of this possibility even in such a young group of patients. Exposure to carcinogenssuch as asbestos or tobacco smoke may increase the risk of developing lung cancer in this young population.
