Notes

HIGD‑1B suppresses hypoxia‑induced mitochondrial fragmentation by regulatory OPA1 bosom inside cardiomyocytes.
p16 is overexpressed in oral squamous cell carcinoma patients who are positive for human papilloma virus. The p53 tumor suppressor gene is commonly mutated in human cancer. The aim is to correlate clinical and pathological features with p16 and p53 expression. This is a prospective, observational study of 50 consecutive cases (43 males and 7 females) who underwent surgery for oral cancer. p16 and p53 were determined by immunohistological staining. The results were obtained and analyzed using chi-square test (Statistical Software SPSS 21.0 version); p value ≤ 0.05 was considered significant. Of the 50 cases, p16 and p53 were overexpressed in 30% and 54% of patients, respectively. Overexpression of p16 was not significantly associated with age, subsites of oral cavity, or degree of differentiation. However, smokeless tobacco was significantly associated with p16 expression (p = 0.012). Similarly, overexpression of p53 was not correlated with age, subsites of oral cavity, or degree of differentiation. Seventy-five percent of poorly differentiated cancers had overexpression of p53 though this did not reach statistical significance (p = 0.279). p53 was overexpressed in smokers (80.95%) and those consuming alcohol (60%).In the last two decades, India has witnessed a substantial increase in the incidence of breast cancer and associated mortality. Studies on the prevalence of molecular subtypes of breast cancer in India have reported inconsistent results. Therefore, we conducted a systematic review of observational studies to document the prevalence of molecular subtypes of breast cancer. A complete literature search for observational studies was conducted in MEDLINE and EMBASE databases using key MeSH terms ((molecular classification) OR (molecular subtypes)) AND (breast cancer)) OR (breast carcinoma)) AND (prevalence)) AND (India). Two reviewers independently reviewed the retrieved studies. The screened studies satisfying the eligibility were included. The quality of included studies was assessed using the selected STROBE criteria. The overall pooled prevalence of luminal A, luminal B, HER2-enriched, and triple-negative breast cancer (TNBC) subtypes of breast cancer were 0.33 (95% CI 0.23-0.44), 0.17 (95% CI 0.12-0.23), 0.15 (95% CI 0.12-0.19), and 0.30 (95% CI 0.27-0.33), respectively. Subgroup analyses were performed by mean age of patients, time period, region, and sample size of the study. Among molecular subtypes of breast cancer, luminal A was the most prevalent subtype followed by TNBC, luminal B, and HER2-enriched subtypes. The overall prevalence of TNBC in India is high compared to other regions of the world. Additional research is warranted to identify the determinants of high TNBC in India. Differentiating TNBC from other molecular subtypes is important to guide therapeutic management of breast cancer.The process of tumorigenesis in gastric carcinoma involves multiple genetic alterations including overexpression of PD-L1, amplification of Her2neu, and mutation of p53. In the present study, the expressions of PD-L1 and Her2neu were analyzed in relation to clinicopathological parameters including p53 in gastric and gastroesophageal junction adenocarcinoma. We examined 100 biopsy and resection samples of gastric and gastroesophageal junction carcinomas for PD-L1, Her2neu, and p53 protein expressions using immunohistochemistry. Scorings were done based on intensity and percentage of tumor cells expressing the markers. Follow-up and survival analyses were done wherever data was available. PD-L1 and Her2neu were seen in 37% and 38% respectively. The analysis showed PD-L1 expression was significantly associated with depth of invasion (p = 0.0007), nodal metastasis (p = 0.0003), and AJCC staging (p = 0.0085). Her2neu negative including equivocal expression was significantly associated with histological grading (p on-confirmation of equivocal cases by fluorescent in situ hybridization.Telomerase reverse transcriptase gene promoter (TERTp) mutation is a potential candidate for pathogenesis and therapeutic target of tonsillar squamous cell carcinomas (TSCCs) in association with human papillomavirus (HPV). Their clinical relevance has not been validated under the new 8th American Joint Committee on Cancer (AJCC) staging system. We analyzed real-time peptide nucleic acid-mediated PCR and sequencing methods (TERTp mutation) and real-time PCR-based assay (HPV) in 80 surgically resected TSCCs. The 8th edition staging system improved the stratification of the early and advanced stages and between T or N categories for overall survival over the 7th edition. TERTp mutation was found in 7.5%, and HPV in 80.0% of the patients. The majority (83.3%) of TERTp mutation cases were HPV-positive TSCCs. Applying the 8th edition staging system, TERTp mutation was an independent factor of poor prognosis for disease-free survival (DFS) in TSCC patients, supporting the clinical significance of TERTp mutation in tonsil cancer. TERTp mutations were also negatively correlated with overall survival and DFS in HPV-negative TSCCs. Conclusively, TERTp mutation provides negative prognostic impact on survival of surgically managed tonsil cancers staged with the AJCC 8th edition.The locoregional recurrence in oral cancer is not predicted by the histopathological parameters solely as the normal morphological looking cells harbor the genomic instability which acts as the potential tumor cells for recurrence in future. Therefore, there is an urgent need of the biomarker for prognostic stratification of patients with high risk of disease recurrence and appropriate management. Eighty oral squamous cell carcinoma (OSCC) patients were included in the study during the period 2012 to 2014 at Apollo Hospitals and Kalinga Institute of Medical sciences, Bhubaneswar. OSCC tissue samples were collected at the time of surgical excision, and immunohistochemistry (IHC) was performed to check the expression of β-catenin in cut margin (CM) and tumor. Statistical analysis was carried out using SPSS based on clinical and pathological records. It was observed that among 80 patients, 33.75% (27 patients) developed recurrence. The recurrence rate was low for 6 out of 27 patients (22.2%) where β-catenin is positive in tumor and negative in cut margin, while it was quite high in 21 out of 27 (77.8%) when marker is negative in tumor but positive in cut margin (CM). The odds of recurrence among patients having high levels of Pancreatic malignancies carry a dismal prognosis globally, with pancreatic adenocarcinomas (PDAC) being particularly aggressive and stubborn. Unfortunately, several therapeutic strategies that show promise in other cancers have failed to make sizeable impact on pancreatic tumor outcomes. Responses to immunotherapies are especially rare in pancreatic cancer, and patients are in need of innovative approaches that can result in more durable responses. Current research in preclinical models and humans has suggested this resistance is due to a uniquely inflammatory and dysfunctional tumor microenvironment; these findings lay the groundwork for targeting these barriers and improving outcomes. Clinical analyses have also revealed unprecedented heterogeneity in tumor and stromal biology of PDAC, underscoring the need for more personalized approaches and combinatorial therapies. This review will highlight the current state of translational research focusing on PDAC immunity, summarize ongoing clinical efforts to tackle PDAC vulnerabilities, and underscore some unresolved challenges in implementing therapies more broadly. A better understanding of immune contexture and tumor heterogeneity in this disease will greatly accelerate drug discovery and implementation of precision medicine for PDAC.The Suvar, Enhancer of zeste, and Trithorax (SET) and myeloid-Nervy-DEAF-1 (MYND) domain-containing protein 3 (SMYD3) is a histone lysine methyltransferase and has been recently unveiled to play significant roles in the progression of human cancer via regulating various key cancer-associated genes and pathways. The role of SMYD3 in gallbladder cancer (GBC) still needs to be studied. In the present study, we examined the SMYD3 gene expression at mRNA and protein level to look its impact on risk for developing gallbladder carcinogenesis. SMYD3 expression was evaluated by immunohistochemistry and reverse transcriptase PCR (RT-PCR) from 30 cases each of GBC and cholelithiasis patients. The expression was compared with different clinicopathological parameters. The SMYD3 expression was found to be significantly upregulated in GBC than cholelithiasis group (p less then  0.05). https://www.selleckchem.com/products/ag-270.html The SMYD3 with increased expression level was observed in 73.3% of the GBC cases (p less then  0.05). Moreover, mRNA SMYD3 expression was observed in 73.3% of GBC and 10% of control (p less then  0.05). Our results indicated that the overexpression of SMYD3 plays an important role in the GBC progression, and SMYD3 may represent useful biomarker for gallbladder cancer patients.Large-scale molecular profiling and DNA sequencing has revolutionized cancer research. Precision medicine is a rapidly developing area in cancer care but it is not uniformly applied across different tumor types. Biomarker-based therapy is associated with improved outcomes, both in terms of progression-free survival and overall survival. Comprehensive genomic profiling (CGP) uses next-generation sequencing to analyze the complete coding sequence of hundreds of genes from a small amount of tissue. Genes included in these assays are those associated with cancer development or have diagnostic, prognostic, familial, or therapeutic implications Genomic profiling is emerging as a clinically viable tool to personalize patient's treatment. This article discusses how the insights gained through CGP can impact treatment plan in common gynecological cancers.Head and neck cancers (HNC) are extremely aggressive, highly recurrent, and the sixth most common cancer worldwide. Neuropeptide substance P, along with its primary receptor, neurokinin-1 (NK-1R), is overexpressed in HNC and is a central player in inflammation and growth and metastasis of several cancers. However, the precise SP-mediated signaling that promotes HNC progression remains ill defined. Using a panel of HNC lines, in this study, we investigated the effects of SP on proliferation and migration of HNC. Tumor cells were also treated with SP and alterations in inflammatory cytokines and chemokines, and their cognate receptors were analyzed by real-time PCR. Furthermore, we investigated the role of SP in inducing epithelial-mesenchymal transition (EMT), and matrix metalloproteases that promote tumor invasion. Our results showed that SP significantly increased tumor cell proliferation and migration and induced the expression of several genes that promote tumor growth, invasion, and metastasis which was suppressed by a specific NK1R antagonist L-703606. SP also activated NFκB that was suppressed on inhibiting NK1R. Collectively, our data shows that SP-NK1R-mediated inflammatory signaling comprises an important signaling axis in promoting HNC and may prove to be effective clinical target against HNC cells that are resistant to traditional therapy.
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