Nikita Balhara

Role of signaling pathways in endometrial cancer

Endometrial cancer (EC) is a prevalent gynecological malignancy with a complex molecular landscape, contributing to significant global morbidity and mortality. Dysregulated signaling pathways such as PI3K/AKT/mTOR and RAS/RAF/MEK drive EC progression by promoting uncontrolled cell proliferation, survival, angiogenesis, and metastasis. Mutations in genes like PTEN and PIK3CA further underpin tumor aggressiveness. Molecular alterations in these pathways not only serve as biomarkers for prognosis but also guide the formulation of targeted therapies, such as mTOR inhibitors and anti-angiogenic agents. While such therapies show promise, optimizing their efficacy and minimizing adverse effects requires further research. A comprehensive approach integrating early detection (e.g., addressing postmenopausal bleeding), preventive strategies (e.g., managing obesity), increasing diagnostic sensitivity (e.g., transvaginal ultrasound) and advanced molecularly tailored treatments (e.g., AI & ML) is critical to reducing the burden of this disease. By targeting key signaling pathways, leveraging AI-driven methodologies, and addressing treatment resistance, we can enhance patient outcomes, also mitigate the rising global impact of EC.

Understanding the HPV associated cancers: A comprehensive review

Human papillomavirus (HPV), a common cause of sexually transmitted diseases, may cause warts and lead to various types of cancers, which makes it important to understand the risk factors associated with it. HPV is the leading risk factor and plays a crucial role in the progression of cervical cancer. Viral oncoproteins E6 and E7 play a pivotal role in this process. Beyond cervical cancer, HPV-associated cancers of the mouth and throat are also increasing. HPV can also contribute to other malignancies like penile, vulvar, and vaginal cancers. Emerging evidence links HPV to these cancers. Research on the oncogenic effect of HPV is still ongoing and explorations of screening techniques, vaccination, immunotherapy and targeted therapeutics are all in progress. The present review offers valuable insight into the current understanding of the role of HPV in cancer and its potential implications for treatment and prevention in the future.

m6A modification and its clinical applications in gynaecological cancer

N6-methyladenosine (m6A) RNA modification plays a pivotal role in gynaecological cancers by regulating tumor initiation, progression, and therapeutic resistance. m6A RNA modification include writers (METTL3/14, RBM15, ZC3H13, WTAP), which catalyze methylation; erasers (ALKBH5, FTO), which remove methyl groups; and readers (YTHDC1, YTHDF1/2/3, IGF2BP1/2/3, HNRNPC/G, HNRNPA2BP1), which interpret m6A marks to regulate the RNA fate. These regulators alter basic RNA metabolism, such as splicing, mRNA stability, translation, and degradation. In gynaecological cancers, both oncogenic and tumor suppressive signaling pathways are also altered by these regulators. Due to their diagnostic, prognostic and predictive value, m6A regulators have emerged as promising biomarkers in gynaecological cancers in recent years. This review highlights the role of m6A regulators and critically evaluates their biomarker and clinical potential in gynaecological cancers.