CLEC5A (C-Type Lectin Domain Containing 5A)

In summary, our study uncovers a suppressive role for CLEC5A in OS tumorigenesis and metastasis through the modulation of the calcineurin/NFATc1 signaling pathway. The deregulation of this pathway significantly impacts OS progression, highlighting its potential as a predicted and therapeutic target for metastatic OS.

In conclusion, we created a new prognostic model including 9 inflammation-related genes. This model has produced meaningful results in evaluating patient prognosis, which may help with future therapeutic strategies for patients with uMGMT GBM.

In conclusion, SPP1 overexpression may be a biomarker of chemoresistance and poor prognosis in angiosarcoma. Further investigation is needed to uncover the precise roles and underlying mechanisms of SPP1.

In summary, the discovery of PANoptosis genes, ANXA3, S100A9, TXN, CLEC5A, and TMEM263 proved to be quite helpful in the early detection of pediatric septic shock patients. These early results, which need to be further confirmed in basic and clinical research, are extremely important for understanding immune cell infiltration in the pathophysiology of pediatric septic shock.

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.

Expression of some of the identified genes correlated with favorable outcome and response to checkpoint inhibitors: MSR1, CD80, OLR1, ABCA1, TMEM245, and ATP13A3 predicted outcome to anti PD(L)1 therapies, and MSR1, CD80, OLR1, ANO6, ABCA1, TMEM245, and ATP13A3 to anti CTLA4 therapies, including a subgroup of melanoma treated patients. In this article we provide evidence of genes strongly associated with the presence of Tregs that modulates the response to check point inhibitors.

Interestingly, phellopterin might inactivate the positive feedback circuit to suppress ovarian cancer progression. Collectively, our investigation revealed that phellopterin mitigated ovarian cancer proliferation and chemoresistance through suppressing the PU.1/CLEC5A/PI3K-AKT feedback loop, and predicted phellopterin as a new and effective cytotoxic drug and CLEC5A as a potential target for the treatment of ovarian cancer.

Correspondingly, IL-6-producing ptMΦs and SOCS3-expressing CD8+ T cells are spatially associated within tumors. Overall, we demonstrate a novel axis associated with ICB resistance in BC whereby distinct pro-inflammatory MΦs suppress CD8+ T cells.

Our results highlight transcriptomic similarities and differences in ET patients according to the degree of maturation of the malignant clone and the type of mutation. The genes and processes altered in both CD34 + cells and mature neutrophils may reveal altered sustained processes that could be studied as future therapeutic targets for ET patients.

Conclusions In summary, we identify genes expressed in a subset of immune cells that predict efficacy to checkpoint inhibitors. Further prospective studies are ongoing to confirm these findings in patients.

CLEC5A may promote the development and migration of colon cancer by triggering the AKT/mTOR signaling pathway. Furthermore, COL1A1 could serve as the target gene of CLEC5A.