RAC2 (Rac Family Small GTPase 2)

Therapeutically, HCT can be effective in progressive disease with organ damage, while others may require long-term medical management of chronic viral complications. Recognizing this rare, homozygous p.R68W variant and its functional consequences supports a precision-diagnosis approach to RAC2-related immunodeficiency and refines surveillance and treatment strategies for affected patients.

Our study uncovers layer-specific molecular landscapes in tongue OLP and identifies KRT17 as a candidate implicated in immune-epithelial crosstalk, providing novel insights into pathogenesis and a potential direction for future therapeutic exploration.

These results suggest that targeting efferocytosis pathways offers potential therapeutic strategies for ESCC, enhancing antitumor immunity and improving patient outcomes. The study underscores the complex interactions between tumor cells and the immune system, with efferocytosis representing a promising therapeutic target.

Our cross-disease analysis unveils a conserved GMP-TAM myeloid remodeling axis in glioma. The derived RS model may serve as a powerful marker for predicting prognosis, and also for predicting the benefits derived from immunotherapy, offering a novel tool for precision immunotherapy in glioma.

C3G plays a dual role in B-cell lymphoma: it acts as a tumor suppressor by inhibiting growth and promoting apoptosis, but may also facilitate metastasis via enhanced motility. This dual effect likely reflects a functional balance between Rap1 and Rac2 signaling. These findings underscore the complexity of C3G-regulated pathways in B cells and suggest that C3G may serve as a potential novel marker in hematologic malignancies.

The glycolytic pathway plays a critical role in the metabolic reprogramming of tumor cells during lung adenocarcinoma brain metastasis. Tumor glycolysis is closely associated with lung cancer progression, brain metastasis, and immune evasion. The Rac2 could be affected by lactylation, and then facilitate the formation of an immunosuppressive tumor microenvironment by induce the M2 polarization of macrophages.

We also observed the upregulation of matrix metalloproteinase (MMP) genes and components of the glycosaminoglycan degradation pathway in glioma cells on the collagen matrix compared with those on HA matrix. This study reveals the effect of collagen and HA on glioma cells at the transcriptional level and contributes to the understanding of potential targets for therapy.

Notably, the 50% inhibitory concentration (IC50) values of axitinib and sunitinib were significantly higher in Caki/AX cells than those in Caki-2 cells, indicating 2.83- and 1.2-fold resistance, respectively. By contrast, the IC50 values of sorafenib and erlotinib were decreased in Caki/AX cells. Moreover, Caki/AX cells showed resistance to everolimus, temsirolimus and rapamycin, and decreased sensitivity to vinblastine, vincristine, paclitaxel, doxorubicin and SN-38 compared with Caki-2 cells. Notably, etoposide, 5-fluorouracil, cisplatin and carboplatin sensitivities were comparable in both cell types...A PCR array related to vascular endothelial growth factor signalling showed that the mRNA levels of FIGF (also known as vascular endothelial growth factor D) and sphingosine kinase 1 were upregulated, whereas those of Rac family small GTPase 2 were downregulated in Caki/AX cells. Overall, these findings suggested that the upregulation of the ATP-binding cassette subfamily B member 1, FIGF and sphingosine kinase 1 mRNA levels, and downregulation of the Rac family small GTPase 2 mRNA levels may contribute to acquired resistance in Caki/AX cells.

Whole-exome sequencing revealed two candidate single-nucleotide polymorphisms: HAS3 rs2232228 and RAC2 rs13058338, which may be implicated in the genetic predisposition to anthracycline-related cardiomyopathy. This case highlights the importance of considering early-onset cardiotoxicity in pediatric patients and supports further research into genetic risk-based screening and prevention strategies.

Patients with defects in RAC2-associated regulators of actin usually present with late-onset symptoms due to normal immune profiles, but a higher rate of EBV and HPV infections, autoimmune cytopenia, asthma, and lymphoproliferation compared to defects in the CDC42 pathway. The severity of mutations in patients of the CDC42 group helps to estimate the prognosis of the disease and prioritization of HSCT.

The findings reveal that RAC2 drives hypoxia-associated radioresistance in NPC by amplifying ROS production, suggesting its potential as a therapeutic target for radiosensitization. This research provides new insights into overcoming hypoxia-mediated radioresistance in NPC treatment.

A decrease in the levels of mesenchymal markers, β-catenin, and its target gene, c-Myc, confirmed the suppression of the mesenchymal phenotype. In conclusion, mitochondrial oxidative stress inhibits the migratory capacity of breast cancer cells by targeting the β-catenin/c-Myc axis, indicating its potential as a novel druggable target to prevent cancer metastasis.