Analyzing the influence of IL18 in regulation of YAP1 in breast oncogenesis using cBioportal.

BACKGROUND: Yes-associated protein 1 (YAP1) is responsible for tumor growth, progression and metastasis. The mechanisms controlling the generation and relative ratio of the functional YAP1 and other co-factors are not well-understood. Various literature reported that co-factors like cytokines significantly influence signaling pathways to introduce epithelial immunity and regeneration, which later helps increase cancer-related phenotypes. Among various cytokines, IL-18 has emerged as a major player in inflammation and progression of different types of cancers. Till now, much information has not been known about the role of YAP1 in tumor aggressiveness and immune evasion in breast cancer with respect to IL-18. AIM: We aimed to explore the effect of YAP1 in tumor aggressiveness and immune evasion in breast invasive carcinoma and metastatic breast cancer in the context of Interleukin-18 (IL-18) in silico. METHODS AND RESULTS: We used publicly available data generated by The Cancer Genome Atlas (TCGA) Research Network through cBioportal web platform. Kaplan-Meier method was used to determine the overall survival and comparison between curves were made using Log-Rank test. The p values were determined by Fisher's exact test with the null hypothesis. Correlation plots were analyzed by comparison with gene copy numbers from the GISTIC2.0, available through cBioportal. Our analyses suggest that IL-18 influences YAP1 expression in breast oncogenesis via Interferon-gamma (IFN-γ) production. Patients having a higher expression of IL-18 possess a better prognosis and higher YAP1 expression with lower IL18 drives to poor clinical results in breast cancer. CONCLUSION: This can provide new approaches to better understand the relation between YAP1 and IL-18 in breast cancer progression by performing in vitro and in vivo studies. Also, IL-18 can be considered as a potential target for tumor treatment in YAP1 overexpressed breast carcinoma.

Meta-Analysis of Prevalence of Triple-Negative Breast Cancer and Its Clinical Features at Incidence in Indian Patients With Breast Cancer.

PURPOSE: Breast cancer is the most common cancer in women in India, with higher incidence rates of aggressive subtypes, such as triple-negative breast cancer (TNBC). METHODS: A systematic review was performed to compute pooled prevalence rates of TNBC among patients with breast cancer, and clinical features at presentation were systematically compared with non-TNBC in an Indian cohort of 20,000 patients. RESULTS: Combined prevalence of TNBC among patients with breast cancer was found to be on the higher side (27%; 95% CI, 24% to 31%). We found that the estrogen receptor (ER) expression cutoff used to determine ER positivity had an influence on the pooled prevalence and ranged from 30% (ER/progesterone receptor [PR] cut ff at 1%) to 24% (ER/PR cutoff at 10%). Odds for TNBC to present in the younger age-group were significantly higher (pooled odds ratio [OR], 1.35; 95% CI, 1.08 to 1.69), with a significantly younger mean age of incidence (weighted mean difference, -2.75; 95% CI, -3.59 to -1.92). TNBC showed a significantly higher odds of presenting with high grade (pooled OR, 2.57; 95% CI, 2.12 to 3.12) and lymph node positivity (pooled OR, 1.39; 95% CI, 1.21 to 1.60) than non-TNBC. CONCLUSION: Systematic review and meta-analysis of 34 studies revealed a high degree of heterogeneity in prevalence of TNBC within Indian patients with breast cancer, yet pooled prevalence of TNBC is high in India. High proportions of patients with TNBC present with aggressive features, such as high grade and lymph node positivity, compared with patients without TNBC. We emphasize the need for standardized methods for accurate diagnosis in countries like India.

Gliolectin positively regulates Notch signalling during wing-vein specification in Drosophila.

Notch signalling is essential for animal development. It integrates multiple pathways controlling cell fate and specification. Here we report the genetic characterization of Gliolectin, presumably a lectin, a cytoplasmic protein, significantly enriched in Golgi bodies. Its expression overlaps with regions where Notch is activated. Loss of gliolectin function results in ectopic veins, while gain of its function causes loss of wing veins. It positively regulates Enhancer of split mß, a target of Notch signalling. These observations suggest that it is a positive regulator of Notch signalling during wing development in Drosophila.