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Biology subjects

Razmpour, T.

Publications and source records attributed to Razmpour, T..

3 recordsLinked to original sources

Diffusion Models vs. DCGANs for Class-Imbalanced Lung Cancer CT Classification: A Comparative Study

Effective lung cancer detection from CT scans remains critically challenged by class imbalance where benign and normal cases are underrepresented, leading to biased machine learning models with reduced sensitivity for minority classes and potentially missed diagnoses in cancer screening applications. We present a comprehensive comparative analysis of Diffusion Models and Deep Convolutional Generative Adversarial Networks (DCGANs), both incorporating modern architectural enhancements including spectral normalization, self-attention mechanisms, and conditional generation, for addressing class imbalance in lung cancer CT classification. Using the IQ-OTH/NCCD dataset comprising 1,097 CT images across normal, benign, and malignant categories with statistical validation across 10 independent runs, we evaluated both approaches through quantitative image quality metrics (Frechet Inception Distance, Kullback-Leibler divergence, Kernel Inception Distance, and Inception Score) and downstream classification performance. While Diffusion models consistently outperformed DCGANs across most image quality measures, the clinical significance was confirmed through task-based validation. Both generative approaches successfully addressed class imbalance: DCGAN-augmented datasets achieved overall accuracy of 0.9760 {+/-} 0.0116 with benign recall improvement from 0.833 to 0.933, while Diffusion-augmented datasets reached superior performance of 0.9959 {+/-} 0.0068 with perfect benign recall (1.000 {+/-} 0.000). Critically for cancer screening where false negatives carry severe consequences, Diffusion maintained the highest malignant detection sensitivity (0.997 {+/-} 0.008) with substantially lower performance variance, demonstrating more consistent synthetic data quality. These findings establish that while both modern architectures can mitigate class imbalance, Diffusion models superior recall performance and lower variability position them as the preferred approach for high-stakes clinical applications, demonstrating that ultimate validation must prioritize downstream clinical task performance over image quality metrics alone.

cancer biology↗

GAN-Enhanced Machine Learning and Metabolic Modeling Identify Reprogramming in Pancreatic Cancer

Pancreatic Ductal Adenocarcinoma (PDAC) is one of the deadliest forms of cancer and presents a significant clinical challenge due to poor prognosis and limited treatment options. In this study, we developed a novel framework integrating genome-scale metabolic modeling (GSM) with machine learning to identify metabolic biomarkers and vulnerabilities in PDAC. We addressed the inherent class imbalance in cancer datasets by generating synthetic healthy samples using a Wasserstein Generative Adversarial Network with Gradient Penalty (WGAN-GP), implementing a three-step biological filtration process to ensure their validity. Our approach achieved 94.83% accuracy in distinguishing between healthy and cancerous metabolic states. Systems-level analysis revealed three key dysregulated pathways: heparan sulfate degradation, O-glycan metabolism, and heme degradation. We identified impaired lysosomal degradation of heparan sulfate proteoglycans as a potential contributor to PDAC pathogenesis, providing a mechanistic explanation for the previously observed association between lysosomal storage disorders and pancreatic cancer. Additionally, we found that nervonic acid transport (MAR00336) was the most discriminative reaction between healthy and cancerous states, with gene-level analysis highlighting FABPs, SLC27As, ACSLs, and ACSBGs as key molecular drivers of metabolic reprogramming in PDAC. Overall, our multi-level approach connected genetic drivers to functional metabolic consequences, revealing coordinated upregulation of fatty acid transport and activation processes. These findings enhance our understanding of PDAC metabolism and present potential therapeutic targets, demonstrating the value of integrated computational approaches in cancer research.

cancer biology↗

Genome-scale metabolic modeling and machine learning unravel metabolic reprogramming and mast cell role in lung cancer through a multi-level analysis

Lung cancer remains a leading cause of cancer-related deaths worldwide, with immune interactions, particularly involving mast cells, playing a crucial role. Mast cells contribute to both pro- and anti-tumorigenic activities, influencing immune modulation, angiogenesis, and tissue remodeling. This study provides a comprehensive multi-level analysis of metabolic alterations in lung cancer through genome-scale metabolic modeling (GSM) and machine learning. Using 43 paired lung tissue samples, we developed metabolic models of lung cancer and mast cells, revealing a significant reduction in resting mast cells in cancerous tissues. Our Random Forest classifier accurately distinguished between healthy and cancerous states, identifying key metabolic signatures. We found that lung cancer cells selectively upregulate valine, isoleucine, histidine, and lysine metabolism in the aminoacyl-tRNA pathway to support their elevated energy demands. Mast cell metabolism exhibited enhanced histamine transport and increased glutamine consumption in the tumor microenvironment, suggesting a shift towards immunosuppressive activity. Additionally, our novel Metabolic Thermodynamic Sensitivity Analysis (MTSA) showed impaired biomass production in cancerous mast cells across physiological temperatures (36 to 40C), indicating metabolic vulnerabilities. By elucidating the metabolic adaptations of mast cells and lung cancer cells, our study highlights their interplay in tumor progression and identifies potential therapeutic targets and diagnostic markers for future investigation. Author SummaryOur research examines the intricate relationship between lung cancer and mast cells, a type of immune cell, using advanced computational methods. We developed detailed metabolic models of lung tissue and mast cells through a multi-level approach to understand how their metabolism changes in cancer. Our findings reveal that lung cancer cells modify their metabolic pathways to meet increased energy demands, including enhanced utilization of four specific amino acids within the aminoacyl-tRNA pathway. In addition, mast cells in lung cancer environments show increased histamine release and glutamine consumption, suggesting they become more active in ways that might promote tumor growth. Additionally, we found that cancerous mast cells are less able to adapt to temperature changes compared to healthy ones, which could impact how they respond during fever or inflammation. These insights provide new perspectives on how lung cancer affects the immune system and could lead to novel approaches for diagnosis and treatment. By understanding these complex interactions, we aim to contribute to the development of more effective strategies for combating lung cancer.

cancer biology↗