Publications by authors named "Vipul Bhardwaj"

Endometrial Cancer (EC) is one of the most common gynecological malignancies. Despite its prevalence, molecular pathways, such as the Sonic Hedgehog (SHH) pathway, have not been extensively studied in the context of EC. This study aims to explore the clinical implications of SHH expression in EC, potentially uncovering new insights into the disease's pathogenesis and offering valuable insights for therapeutic strategies in EC.

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Article Synopsis
  • The study focuses on the role of Trefoil factor 3 (TFF3) in shaping the immunosuppressive tumor microenvironment (TME), which contributes to cancer progression and relapse.
  • It found a strong association between TFF3 and PVRL2, indicating that they work together in various cancers to create an environment that supports tumor growth.
  • The research also suggests that targeting both TFF3 and PVRL2 could lead to new therapeutic strategies, with potential drugs identified for inhibiting PVRL2.
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A hyperactive tumour microenvironment (TME) drives unrestricted cancer cell survival, drug resistance, and metastasis in ovarian carcinoma (OC). However, therapeutic targets within the TME for OC remain elusive, and efficient methods to quantify TME activity are still limited. Herein, we employed an integrated bioinformatics approach to determine which immune-related genes (IRGs) modulate the TME and further assess their potential theragnostic (therapeutic + diagnostic) significance in OC progression.

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It is now apparent that growth hormone (GH), an anterior pituitary hormone predominantly regulating postnatal somatic growth and metabolism, is also expressed in extrapituitary tissues. An extrapituitary synthetic site of GH that has garnered interest is the de novo or enhanced expression of GH in carcinoma or other cancers. In a number of cancers, including carcinoma of the mammary gland, endometrium, liver, prostate, and colon, the expression of GH is independently associated with more advanced clinicopathologic parameters of the cancer.

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The process of angiogenesis is well described for its potential role in the development of normal ovaries, and physiological functions as well as in the initiation, progression, and metastasis of ovarian cancer (OC). In advanced stages of OC, cancer cells spread outside the ovary to the pelvic, abdomen, lung, or multiple secondary sites. This seriously limits the efficacy of therapeutic options contributing to fatal clinical outcomes.

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Endometrial cancer (EC) is a prevalent uterine cancer that remains a major contributor to cancer-associated morbidity and mortality. EC diagnosed at advanced stages shows a poor therapeutic response. The clinically utilized EC diagnostic approaches are costly, time-consuming, and are not readily available to all patients.

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Nearly 70% of ovarian cancer (OC) patients experience recurrence within the first 2 years after initial treatment. Emerging evidence indicates that long non-coding RNAs (lncRNAs) play a pivotal role in the pathogenesis of OC progression, resistance to therapy and recurrent OC (ROC). Transcriptome profiling studies have reported differential expression patterns of lncRNAs in OC which are related to increased cell invasion, metastasis and drug resistance.

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Signal transducer and activator of transcription 3 (STAT3) is one of the crucial transcription factors, responsible for regulating cellular proliferation, cellular differentiation, migration, programmed cell death, inflammatory response, angiogenesis, and immune activation. In this review, we have discussed the classical regulation of STAT3 via diverse growth factors, cytokines, G-protein-coupled receptors, as well as toll-like receptors. We have also highlighted the potential role of noncoding RNAs in regulating STAT3 signaling.

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Cancer remains the second leading cause of mortality globally. In combating cancer, conventional chemotherapy and/or radiotherapy are administered as first-line therapy. However, these are usually accompanied with adverse side effects that decrease the quality of patient's lives.

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