This study provides the first comprehensive pan-cancer analysis of CTTN, revealing its significant overexpression in several cancers including breast, head and neck, and colorectal cancers. Elevated CTTN expression was associated with poor prognosis, reduced overall survival, and critical roles in actin cytoskeleton remodelling and signal transduction, suggesting its potential as a novel prognostic biomarker and therapeutic target.

This study identifies eight hub genes (CDH1, CDH2, MMP2, CD44, FN1, FGF2, SNAI1, and SNAI2) critically associated with EMT progression in cervical cancer, with CDH2 showing significant association with overall survival and FN1 linked to disease-free survival, underscoring their prognostic value.

This chapter explores molecular genetic alterations and their prognostic significance in gallbladder carcinogenesis, providing insights into the genetic landscape driving gallbladder cancer development and progression.

This chapter explores metabolomics as a powerful tool for identifying potential biomarkers in gallbladder carcinogenesis, covering metabolic profiling techniques, differential metabolite signatures, and their translational applications in early detection and diagnosis of gallbladder cancer.

Gallbladder cancer (GBC), a rare yet highly aggressive cancer with a high mortality rate due to late-stage diagnosis, could benefit from the identification of specific molecular markers like TRIP13, NEK2, and TPX2, which have shown promise in early detection and prognosis through in silico network analysis.

This chapter explores the critical role of Toll-like receptors (TLRs) in cancer progression, emphasizing their impact on the inflammatory microenvironment and chemoresistance. It also discusses the development of TLR agonists and antagonists as potential cancer therapies, highlighting how defects in TLR signaling pathways contribute to carcinogenesis and the emerging therapeutic strategies targeting these pathways.

We demonstrate that PARP1 is overexpressed and hyperactivated in cervical cancer, and its inhibition by olaparib enhances cisplatin-induced cell death, disrupts DNA repair pathways, induces apoptosis and anoikis, and shows strong therapeutic potential against cervical cancer.

We demonstrate that cyclin D1 and cyclin E2 are frequently overexpressed in early-stage gastric carcinoma and show significant correlation with various clinical parameters, with cyclin D1 emerging as a more sensitive and specific diagnostic biomarker, suggesting their potential utility in early detection of gastric cancer.

We show that CXCL12 is frequently downregulated and its promoter hypermethylated in cervical cancer, and exogenous CXCL12 treatment inhibits metastasis by reducing cell migration, invasion, and anchorage-independent growth, suggesting CXCL12 acts as a tumor suppressor in cervical cancer and its silencing may promote metastasis.

We developed redox-responsive, folic acid and trastuzumab-functionalized PEG-PLA polymersomes with multiple disulfide linkages to enhance intracellular delivery and therapeutic efficacy of doxorubicin in breast cancer, achieving ~90% tumor regression with minimal cardiotoxicity.

We investigated the expression and localization of the tumor suppressor p27Kip1 in cervical cancer cells, revealing its down-regulation and mislocalization, which contribute to increased proliferation, altered cell cycle progression, and reduced apoptosis during cervical cancer development.

We explored the anti-tumor effects of staurosporine in the tumor microenvironment of cervical cancer, demonstrating its ability to inhibit key cancer progression events such as cell proliferation, migration, invasion, and anoikis resistance by targeting pathways critical to tumor growth and metastasis.

We show that cervical cancer cells overexpress MCM4 to cope with replicative stress, and while MCM4 depletion alone does not affect short-term growth, prolonged cisplatin treatment reveals HPV-dependent sensitivity—highlighting a potential therapeutic vulnerability in HPV16-positive cells linked to MCM4 regulation.

This study investigates the expression of specific cytokines (TNF-α, IL-1β, IL-6, IL-8, and VEGF) in gallbladder cancer (GBC) patients, revealing upregulation of IL-1β, TNF-α, IL-8, and VEGF as potential biomarkers associated with tumor size, staging, differentiation, serosal invasion, and metastasis, while IL-6 showed no expression.

We show that FOXO1, a key regulator of cell proliferation and apoptosis, is frequently downregulated in cervical cancer due to PI3K/AKT-mediated post-translational inactivation, and that PI3K inhibition restores FOXO1 activity, leading to reduced cell viability and increased apoptosis—highlighting PI3K/AKT as a potential therapeutic target.

We provide the first evidence that epigenetic silencing of CXCR4 in cervical cancer impairs cellular response to paracrine SDF-1α, leading to loss of cell adhesion—an essential step in metastasis—highlighting the role of SDF-1α/CXCR4 signaling in cervical tumor microenvironment and disease progression.

This study reveals that MCM4, MCM5, MCM6, MCM10, and RECQL4 are significantly overexpressed in cervical cancer and are associated with tumor progression and clinicopathological features, highlighting their potential roles in disease advancement.

We transformed the salt-sensitive cyanobacterium Anabaena doliolum with N-methyltransferase genes from Aphanothece halophytica, enabling it to synthesize glycine betaine (GB) and significantly enhance salt tolerance, potentially offering a biotechnological approach for developing stress-resistant, nitrogen-fixing cyanobacteria as biofertilizers in sustainable agriculture.

This study replicates the association of common variants in CDKN2A/2B (rs10811661) and WFS1 (rs6446482) with type 2 diabetes in the population of Eastern Uttar Pradesh, India, showing that these SNPs significantly increase the risk of T2DM, with larger effect sizes compared to European populations. Both SNPs were found to be linked to higher fasting and postprandial glucose levels in carriers.