Introduction: Rosette-forming glioneuronal tumors (RGNT) and papillary glioneuronal tumors (PGNT) account for < 1% of brain tumors. Genetic data regarding RGNT and PGNT is still evolving. We aimed to perform a detailed clinicopathological analysis on rosette-forming and papillary glioneuronal tumors and to evaluate these for common, known genetic mutations. Materials and methods: Our cohort consisted of 6 cases of these rare glioneuronal tumors diagnosed over a period of 5 years. IDH1, ATRX, p53, and BRAF V600E mutations were evaluated on immunohistochemistry, and cases of RGNT were screened for the mutations in PIK3CA gene at hotspots exon 4, 9, and 20. Results and conclusions: Our findings confirm the presence of PIK3CA gene mutations in RGNT along with two novel mutations in PIK3CA gene, of which one is proposed to be of prognostic significance.

Novel coronavirus-2019 (nCoV-2019) emerged as a potentially infectious respiratory disease caused by newly discovered β-coronavirus. nCoV-19 has emerged as a global pandemic due to the rapid transmission and high infection rate commonly involved in acute respiratory illness. Literature search includes various databases like Google Scholar, PubMed, ScienceDirect, and Scopus for studies published using a different combination of keywords “coronavius”, “COVID-19”, “SARS”, “MERS”, “antiviral drugs”, “vaccines”, and “immunity”. We collected epidemiology data from the Worldometer portal (data available till 9 October, 2020). Fever, dry cough, dyspnea, sore throat, or fatigue are common clinical symptoms of the infection. Cytotoxic T-cells and T-helper cells plus Cytotoxic T cells (CD8+) account for maximum (approximately 80%) of total infiltrate in the pulmonary region of the affected nCoV individuals and act as a significant contributor to the clearance of the infection. This review intends to outline the literature concerning the mode of actual transmission, immune response, and possible therapeutic approach against the virus.

The paper, titled “Proposal to Explain the Cause of Long COVID Based on the Concept of Host Factor Variants,” explores the potential causes of long COVID through the lens of host factor variants, particularly cellular variants and MHC polymorphisms....

This study explores an important topic in breast cancer treatment and the potential role of NLR as a biomarker. It provides valuable insights into the limitations and complexities of using NLR as a predictor of pCR in TNBC and HER2-positive breast ca...

Background: Phosphatase and tensin homolog (PTEN) is a key tumor suppressor gene that negatively regulates the PI3K/AKT pathway. PTEN deficiency is the most frequent molecular alteration in triple‐negative breast cancer (TNBC); however, the relationship between PTEN protein loss and underlying genomic alterations remains incompletely understood. Methods: Fifty TNBC cases were evaluated for PTEN protein expression by immunohistochemistry on tissue microarrays. PTEN hotspot mutations (Exons 1, 5, 7, and 9) were analyzed using Sanger sequencing, whereas copy number alterations were assessed by multiplex ligation‐dependent probe amplification (MLPA) assay. PTEN alterations were correlated with clinicopathological characteristics. External validation of PTEN mRNA and protein expression and prognostic significance was performed using publicly available TCGA/CPTAC datasets and Kaplan–Meier plotter. Results: PTEN protein loss was observed in 41/50 TNBC cases (82%), indicating that PTEN deficiency is a frequent event in this subtype. PTEN mutations were detected in six cases (12%) and were confined exclusively to Exon 5, comprising one missense mutation (c.277C>A) and two truncating mutations (c.430del and c.433del). MLPA identified PTEN copy number alterations in four cases (8%), including heterozygous deletions and duplications. No significant association was observed between PTEN protein expression and genomic alterations, highlighting a substantial genotype–phenotype discordance. Analysis of independent public datasets confirmed significantly reduced PTEN mRNA and protein expression in TNBC compared with luminal and HER2‐positive breast cancers. Patients with low PTEN expression showed a trend toward shorter overall survival (23.5 vs. 38.9 months), though the difference did not reach statistical significance. Conclusions: PTEN protein loss is highly prevalent in TNBC but is only partially explained by mutations and copy number alterations, suggesting that additional regulatory mechanisms, such as epigenetic or posttranscriptional events, contribute to PTEN inactivation. These findings underscore the biological importance of PTEN deficiency in TNBC and support further investigation of PTEN as a potential prognostic biomarker and therapeutic target.