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Animesh Acharjee

Publications and source records attributed to Animesh Acharjee.

3 recordsLinked to original sources

T-SMmOTE: tweaked synthetic majority minority oversampling technique for data scarcity issue in multi omics studies.

MOTIVATION: Multiomics data offer a rich data mine for modeling complex as well as day-to-day diseases, but their practical deployment is constrained by the limited sample availability. To this end, generating synthetic samples is a viable remedy. Extant schemes operating along this line, however, are mostly limited to augmenting the minority class in imbalanced datasets and often produce synthetic samples that lack sufficient diversity and fail to faithfully capture the underlying data distribution. As a result, the full potential of synthetic augmentation in multi-omics learning remains underexplored. The aim is to address the data scarcity problem in multi-omics domain. We propose a synthetic oversampling framework, which is dedicated to addressing overall data scarcity in multi-omics datasets and the lack of diversity in synthetic samples. Contrary to conventional methods that restrict augmentation to minority classes and rely on interpolation of two neighbors, our method generates diverse yet distribution-aligned synthetic samples by interpolating three neighbors and extends this augmentation paradigm to the majority class. The framework first balances the dataset by generating synthetic minority samples, and subsequently augments the balanced dataset by oversampling both majority and minority classes. RESULTS: Empirical evaluation on multi-omics data obtained from three heterogeneous health scenarios-inflammatory bowel disease, multi-organ dysfunction syndrome, and colorectal cancer-substantiates the utility of the proposed scheme in improving the predictive performance. The models trained on T-SMmOTE-augmented data achieve higher Matthews correlation coefficient values, along with improvedscores for both majority and minority classes. Notably, oversampling of the majority class improves the cognition of the minority class as well. We also explore the consistency of the class distributions between the original and augmented class-specific datasets. These findings confirm the capability of our scheme to learn from small, high-dimensional multi-omics datasets and highlight its potential for non-invasive disease detection. AVAILABILITY AND IMPLEMENTATION: https://github.com/payelu/TSMm.

Journal Article

RNF43 Mutations Are Associated With the Classical Molecular Subtype, Vigorous Antitumor Immune Responses, and Prolonged Survival in Pancreatic Adenocarcinoma.

RNF43 mutations were correlated with microsatellite status in colorectal cancer and with fewer and later recurrences in pancreatic ductal adenocarcinoma (PDAC). Here, we undertake a detailed assessment of RNF43 mutations in PDAC. A total of 313 PDACs (308 microsatellite stable [MSS] and 5 microsatellite-instable [MSI] cases) underwent next-generation sequencing (Oncomine Tumor Mutation Load assay; Thermo Fisher). Spatial analyses (NanoString) classified PDACs according to their transcriptomic and proteomic immune signaling. Fluorescent imaging was used to define spatial compartments (tumor: pancytokeratin+/CD45- and leukocytes: pancytokeratin-/CD45+). Each of 20 PDACs with RNF43 mutations (RNF43mut) and without RNF43 mutations (RNF43wt) underwent multiplex immunofluorescence analysis to determine immune status. A total of 153 PDACs (22 RNF43mut and 131 RNF43wt cases) underwent bulk RNA sequencing to assign into molecular subtypes. Overall, 24 RNF43 mutations were identified (22 MSS PDACs and 2 MSI PDACs). The incidence of RNF43 mutations in MSS PDACs (7.1%) was consistent with The Cancer Genome Atlas (6.7%). However, RNF43 mutations were more frequent among MSI PDACs (40%). Additionally, RNF43mut had differential frequencies of other mutations (including Wnt pathway genes), higher tumor mutational burden values (5.5 mut/mb vs 1.67 mut/mb; P < .01), and significantly longer overall survival (47 vs 18 months; P < .0001) than RNF43wt. Moreover, RNF43mut exhibited significantly higher densities of CD8+ T lymphocytes, dendritic cells, and B lymphocytes (P < .001) and an upregulation of ITGAX, CD11c, CD8, and HLA-DR compared with RNF43wt. Patients with RNF43mut PDACs were more often of the classical molecular subtype (20/22, 90.9%). RNF43mut PDACs showed high tumor mutational burden values, suggesting increased neoantigen load coupled with an abundance of antigen-presenting immune cells and an upregulation of immune determinants promoting antigen presentation. All this contributes to stronger antitumor immune responses and improved clinical outcomes.

Humans

Deciphering microbial and metabolic influences in gastrointestinal diseases-unveiling their roles in&#xa0;gastric cancer, colorectal cancer, and inflammatory bowel disease.

INTRODUCTION: Gastrointestinal disorders (GIDs) affect nearly 40% of the global population, with gut microbiome-metabolome interactions playing a crucial role in gastric cancer (GC), colorectal cancer (CRC), and inflammatory bowel disease (IBD). This study aims to investigate how microbial and metabolic alterations contribute to disease development and assess whether biomarkers identified in one disease could potentially be used to predict another, highlighting cross-disease applicability. METHODS: Microbiome and metabolome datasets from Erawijantari et al. (GC: n&#x2009;=&#x2009;42, Healthy: n&#x2009;=&#x2009;54), Franzosa et al. (IBD: n&#x2009;=&#x2009;164, Healthy: n&#x2009;=&#x2009;56), and Yachida et al. (CRC: n&#x2009;=&#x2009;150, Healthy: n = 127) were subjected to three machine learning algorithms, eXtreme gradient boosting (XGBoost), Random Forest, and Least Absolute Shrinkage and Selection Operator (LASSO). Feature selection identified microbial and metabolite biomarkers unique to each disease and shared across conditions. A microbial community (MICOM) model simulated gut microbial growth and metabolite fluxes, revealing metabolic differences between healthy and diseased states. Finally, network analysis uncovered metabolite clusters associated with disease traits. RESULTS: Combined machine learning models demonstrated strong predictive performance, with Random Forest achieving the highest Area Under the Curve(AUC) scores for GC(0.94[0.83-1.00]), CRC (0.75[0.62-0.86]), and IBD (0.93[0.86-0.98]). These models were then employed for cross-disease analysis, revealing that models trained on GC data successfully predicted IBD biomarkers, while CRC models predicted GC biomarkers with optimal performance scores. CONCLUSION: These findings emphasize the potential of microbial and metabolic profiling in cross-disease characterization particularly for GIDs, advancing biomarker discovery for improved diagnostics and targeted therapies.

Humans