Chittaranjan National Cancer Institute

ObjectiveTo investigate a panel of variables using four machine learning based classifiers, i.e., support vector machine (SVM), random forest (RF), artificial neural network (ANN) and logistic regression (LR) to make a diagnosis of ovarian cancer, differentiating it from benign ovarian masses.Materials and methodsA prospective observational pilot study was done between November 2021 and June 2023. Following data pre-processing to ensure compatibility with ML models, four ML algorithms, i.e., support vector machine (SVM), logistic regression (LR), random forest (RF) and artificial neural network (ANN) were tested by multimodal parameters from the datasets of 50 patients presenting with suspected epithelial ovarian cancer (Group A) or benign ovarian tumour (Group B). Statistical analysis was done using STATA version 14.0.ResultsWe found that the machine learning approach could predict malignant tumours with appreciably high accuracy similar to a few studies done so far in this field. All four ML algorithms showed high level of accuracy with a maximum AUROC of 0.92 in the RF model. Both RF and SVM had an accuracy of 85.87 and 83.05%.ConclusionThe ML algorithms can detect ovarian cancers with a high level of accuracy. Further, a large-volume prospective study on large volume data sets is required before inclusion of ML algorithms in clinical practice.

Molecular epidemiology targeting the impact of particulate matter ≤ 2.5μm in aerodynamic diameter (PM2.5) on pro-oncogenic signaling has been sparsely reported from the Indian industrial belt. This study investigated the effect of seasonal variation in PM2.5 on pro-oncogenic drivers in the pulmonary and systemic cellular environments of a thermal power plant participants in West Bengal, India during 2021-2022. PM2.5 levels were significantly higher during spring than monsoon, coinciding with reduced hemoglobin and lung function indices. Linear Mixed-Effects Regression (LMER) confirmed that elevated PM2.5 exposure was significantly associated with increased inflammatory response, enhanced matrix metalloproteinase-9 (MMP-9) activity, and upregulation of the epidermal growth factor receptor (EGFR)/phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) cascade, along with downregulation of phosphatase and tensin homolog (PTEN). These molecular alterations reflected enhanced proliferative and pro-angiogenic signaling and reduced apoptosis in the airway cells and the leukocytes. Collectively, the findings indicate that short-term seasonal surges in PM2.5, may induce subclinical molecular perturbations that predispose exposed individuals in industrial areas to activation of the EGFR/PI3K/AKT pro-oncogenic signaling.

BackgroundProtagonistic role of platelets promote capillary infiltration of tumors for distant metastasis along with immunosurveillance. Despite existing reports highlighting role of platelets in tumorigenesis, its impact on breast cancer stem cells (BCSCs) remain underexplored. Our first ever report on murine and human system, accentuate that, tumor educated platelets (TEPs) of luminal A and TNBC subtypes are distinct from healthy counterparts, collaborating with BCSCs to generate sub-variants that elevate tumor aggressiveness.MethodsImpact of TEPs on BCSCs was evaluated from primary breast tumor and blood samples of luminal A/TNBC patients along with EC/4T1 murine breast tumor models and MCF-7/MDA-MB-231 cell lines. For downstream assays, TEPs were co-cultured with breast tumor samples or cell lines, followed by magnetic sorting of lin−CD44+CD24− BCSCs. TEP induced alterations of BCSCs were evaluated from 3D tumorsphere, colony formation, transwell migration, scratch-wound healing, matrigel invasion, in-vitro tube formation assays. Fluorescence-confocal microscopy, RT-PCR, flow-cytometry, western-blotting was utilized to decipher the role of genes and protein involved in stemness, metastasis along with the transcription factors in the downstream signaling cascade, followed by verifications by RNAi.ResultsTEPs have elevated expression of P-selectin and interacts with BCSCs via P-selectin and PSGL1 on BCSCs surface. Treatment with aspirin had restorative impact on P-selectin level, converting TEPs from active to resting platelet (RP) state. Under TEPs influence, BCSCs were tumorigenic, clonogenic, multidrug resistant, invasive with numerous invadopodia and remained skewed towards mesenchymal phenotype. Administration of RP reduced TEP associated BCSC virulence both in-vivo and in-vitro. P-selectin-PSGL1 interaction results in binding of WNT to FRIZZLED followed by stabilization and nuclear translocation of β-catenin. Nuclear β-catenin promotes stemness-EMT (Epithelial to mesenchymal transition)-metastasis, along with stimulation of autocrine VEGF-VEGFR2 cascade. Inhibition of WNT and VEGFR2 by RNAi confirmed the critical role of this axis in regulating TEP’s influence on BCSCs.ConclusionThese insights into TEP-BCSC interplay, acknowledges TEPs, as-well-as unveils novel receptor-ligand signaling cascade between TEPs and BCSCs, that could be a beneficial therapeutic strategy to target cancer metastasis.Graphical abstractSupplementary InformationThe online version contains supplementary material available at 10.1186/s13058-025-02185-5.

Figure 1 Model proposing Atorvastatin mediated improvement of intratumoral DC function in hypercholesterolemia. Hypercholesterolemic tumour-microenvironment dampens DC functionality and maturation preventing anti-tumour cytotoxic activity of T-cells that remediates on statin pre-exposure

BackgroundNotch receptor–ligand interaction is ubiquitous and fundamental for coordinating cellular differentiation and determining cell fate for the development of various tissues and organs. Aberrant mutations in the Notch cascade result in various pathophysiological disorders, including cancer. Diverse aspects of carcinogenesis regulated by Notch include the shaping of anti-tumour T-cell immunity through antigen-presenting cell (APC)–T cell interaction and effector functions.Chief contentNotch depends on juxtacrine and paracrine signalling to influence intercellular communications in the tumour microenvironment. Several preclinical and clinical studies have revealed Notch as a bi-effector molecule, which has a differential effect depending on the immune contexture of the tumour microenvironment. The Notch cascade serves as an effective therapeutic target in preventing off-target cell death and promoting tumour-specific T-cell priming.ConclusionThis review revolves around Notch crosstalk with respect to the interaction between T-cell populations and other intratumoral cellular components, including professional antigen-presenting cells like dendritic cells, macrophages, B cells, immunosuppressive myeloid-derived suppressor cells, and cancer stem cells. It also summarizes the impact of targeting Notch signalling within intratumoral T cells in combination with traditional oncotherapies.

Motor impairments, common in children with Autism Spectrum Disorder (ASD), significantly affect their developmental trajectories, impacting balance, coordination, and gait. Traditional interventions often fail to address the interconnected motor, cognitive, and sensory challenges in ASD. This narrative review explores the efficacy of integrated dual-task gait and balance training combined with sensory-motor interventions, emphasizing their potential to enhance functional outcomes in children with ASD. Following the Scale for the Assessment of Narrative Review Articles (SANRA) and Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) frameworks, a comprehensive literature search was conducted on PubMed, ScienceDirect, and Google Scholar from 2010 to June 2025. The keywords with Boolean operators consisted of “autism spectrum disorder”, AND “dual-task training”, AND “sensory motor integration”, AND “gait training”, OR “balance training”, OR “motor coordination”. The studies reported that integrated dual-task and sensory-motor interventions significantly improve motor proficiency, postural control, and dynamic balance, with measurable gains in standardized assessments. Technology-enhanced modalities, including virtual reality and wearable sensors, enhance engagement and enable personalized progression, fostering neuroplasticity and functional transfer to daily activities. Benefits extend to attention regulation and executive function, supported by neuroimaging evidence of enhanced prefrontal cortical activation. However, challenges include therapist training, resource limitations, and insurance barriers, necessitating innovative solutions like scalable technology and telehealth. Future research should prioritize large-scale trials, standardized measures, and long-term follow-up to optimize protocols and support widespread clinical adoption.

Abstract Background: Colorectal cancer (CRC) continues to represent a major threat to cancer-related mortality, though advancements in diagnostic modalities and therapeutic strategies have been achieved. Oxaliplatin, a platinum-based chemotherapeutic agent with demonstrated efficacy against CRC, constitutes a cornerstone of standard treatment regimens. Nevertheless, its clinical utility is limited by drug resistance and significant adverse effects. Objective: This study aims to investigate the modulatory effects of caffeine on the therapeutic efficacy of oxaliplatin as an anticancer agent in CRC in vitro . Materials and Methods: 3-[4,5-Dimethylthiazole-2-yl]-2,5 diphenyl tetrazolium bromide (MTT) assay was performed to determine the cytotoxic effects of oxaliplatin and caffeine in monotherapy and combination on human CRC cell lines HCT-116 and HT-29 and healthy human peripheral blood mononuclear cells (PBMCs). Clonogenic assay was performed to evaluate the effect on cell proliferation. Flow cytometry-based Annexin V-FITC/PI dual staining was performed to detect apoptosis induction. The expression level of apoptosis-markers was examined by western blot. Results: The MTT assay demonstrated dose-dependent cytotoxicity of oxaliplatin and caffeine, both as monotherapies and in combination, against HCT-116 and HT-29 cells, while sparing normal PBMCs. Combination therapy lowered oxaliplatin’s IC 50 values through synergistic and additive interactions respectively in HCT-116 and HT-29. Co-treatment suppressed cell proliferation and induced apoptosis to a degree comparable to that of oxaliplatin monotherapy, with a more pronounced effect in HCT-116. Conclusion: These preliminary observations suggest that caffeine may enhance the anticancer efficacy of oxaliplatin and may potentially alleviate its adverse effects by enabling dose reduction in the CRC model in vitro .