RASGRP1 (RAS Guanyl Releasing Protein 1)

Based on the single-cell sequencing results of CD8+ T cells from TNBC patients, a prediction model was established, which facilitated prognosis prediction in TNBC patients and evaluated the patients' response to immunotherapy. In summation, this model could potentially assist in improving the efficacy of TNBC immunotherapy.

Further, epithelial cells, fibroblasts, and T cells were recognized as the primary cell types through which RASGRP1 exerts its effects. Finally, an analysis of the immune microenvironment and drug predictions provided fresh insights for the treatment of TNBC.

However, RasGRP1-overexpressing stem cells retain a metabolically quiescent cell-fraction, whereas this fraction is incompatible with KRASG12D. Our temporal proteomics and metabolomics datasets provide mechanistic insights into altered hematopoiesis at single cell resolution and support the idea that the exact identity and duration of signals from Ras lesions has profound impacts on stem cell maintenance and lineage-potential.

High-throughput screening and deep learning distilled a 45-gene panel to a small subset of genes critical to melanoma and warrant deeper in vivo functional analysis for their role and potential synergies in driving NC cell migration and invasion.

In vivo, leukopenia models induced by irradiation and cyclophosphamide were established in zebrafish and mice to determine MC's effect on neutrophil recovery...Notably, the upregulation of RASGRP1 by MC supports the generation of fully functional neutrophils, compared to those induced by G-CSF and GM-CSF alone. This study provides the first evidence that MC promotes neutrophil generation and antimicrobial activity through the IL-23R-mediated pathway, offering a promising therapeutic strategy for leukopenia.

Genetic testing identified a RASGRP1 homozygous loss-of-function variant with both parents being carriers. This is the first reported case of RASGRP1 deficiency in Malaysia, and we highlight the challenges clinicians face when the disease manifests in varied presentations.

Targeting ITGβ3, alone or in combination with cilengitide, offers a promising strategy to resensitize resistant HER2-positive breast cancer cells to Trastuzumab. These findings provide valuable insights into the mechanisms of Trastuzumab resistance and suggest potential therapeutic avenues for improving patient outcomes.

Therefore, the present review serves to underline the update on recent research pertaining to KMT2D gene, that could be a potential therapeutic target in downregulating glycolytic genes such as Pgk1, Ldha, Pgam1 and Gapdh; 2, epidermal growth factor receptor tyrosine kinase (EGFR-TK ) - ERBB2, RTK-RAS signaling, RAS activator genes Rgl1, Rasgrp1, Rasgrf1, Rasgrf 2 and Rapgef5 in suppressing the tumor progression that may represent novel targeted therapy for the management of cancer. This review will facilitate to understand the gene expression that inhibits cancer progression and which could serve as a potential molecular target in understanding cancer pathogenesis.

We have developed a risk prediction model for pediatric R/R ALL utilizing the genes BAG2, EPHA4, FBXO9, SNX10, and WNK1. This model provides a scientific foundation for early identification of R/R ALL in children.

We identified 67 approved drugs that showed a different effect between the high- and low-risk patients and the top 2 gene-drug pairs were IL12B-sunitinib and SCARF1-ruxolitinib. The 11-IRG risk signature model is a promising tool to predict the survival of breast cancer patients and the expressions of IL12B and SCARF1 may serve as potential targets for therapy of breast cancer.

The NK cell-related gene signatures were proved to be a reliable indicator of the success of immunotherapy in patients with DLBCL, thus providing a unique evaluation method.

This study provides novel insights into the role of RASGRP1 in insulin secretion and highlights its potential as a therapeutic target for diabetes. The limitations and challenges associated with studying RASGRP1 in disease are also discussed.