7-gene signature

Low-risk patients may benefit from more tailored monitoring and personalized immunotherapy regimens. However, more investigations are required to validate its accuracy and effectiveness in a prospective cohort with larger sample sizes.

In particular, a survival-predicting model was made specifically for patients with glioma to predict its survival and immune response to ICIs. C-MET was screened and validated for its tumor driver gene and immune regulation function (inducing t-cell exhaustion) in glioma.

This study evaluated the differences between the MLL, RUNX1, and inv(16) AML subtypes at the single-cell level, discovered gene signatures that effectively discriminate between the three subtypes as well as other AML and healthy samples, and revealed that the poorer prognosis of the MLL subtype may be attributable to dysregulation of CD8+ T-cell proliferation caused by abnormalities in the SPI-B TF and the LCK signaling pathway.

Collectively, our data provide a 7-gene signature that serves as a potential biomarker for BLCA, especially MIBC. Moreover, this 7-gene signature highlights the role of the tumor immune microenvironment in prognosis and thus might be related to the response to anti-programmed cell death protein 1-based immunotherapy.

Also, a post-therapy T-cell cluster associated with relapse samples exhibits downregulation of MHC Class I and T-cell regulatory genes. Altogether, this study deeply characterizes pediatric AML relapse- and CCR-associated samples to provide insights into the BM microenvironment landscape.

We identified and validated a 15-gene expression signature for robust prognostication and stratification of patients with stage II colorectal cancer, with superior performance when compared with currently used biomarkers. Therefore, the 15-gene expression signature has the potential to improve the prognostication and treatment decisions for patients with stage II colorectal cancer.

The findings demonstrate the prognostic and therapeutic relevance of a novel 7-gene signature in CRC. Its association with immunosuppressive activity can help identify novel actionable therapeutic targets.

Functional RNAi screen of our TYMP dependent EC genes, we found that a group of 5 genes - Flot1, Ccl5, Vars2, Samd9l and Ube2l6 are critical for endothelial cell death mediated by RIG-I activation. Our observations identify mechanisms by which RIG-I drives EC dysfunction and define pathways that can be pharmacologically targeted to ameliorate RIG-I induced vascular inflammation.

Our findings suggested that the seven genes identified in this study are valuable prognostic predictors for patients with PAAD. These findings provided us with a novel insight that it is useful for understanding cell cycle mechanisms and for identifying patients with PAAD with poor prognosis.

Our study highlights that unmanipulated leukapheresis share peculiar immunophenotypic and transcriptional features that correlate with CAR T-cell expansion and survival of pts treated with Tisa-cel and Axi-cel. Despite these results warrant functional validation and confirmation in larger cohort (ongoing), the gene signature identified may represent a pre-manufacturing predictive biomarker of CAR T-cell efficacy that might preferentially drive their employment versus other newly approved therapies, such as bispecific T-cell engagers, at the single patient level.

Critically, the results from the GEPIA and TISIDB web portals indicated that the expression of the 7-gene signature was associated with survival, clinical stage, and immune subtypes of LUAD patients. We identified a CXCR-related gene signature that could assess prognosis and provide a reference for the diagnosis and treatment of LUAD.

Cisplatin, gemcitabine, methotrexate, mitomycin C, paclitaxel, and vinblastine are sensitive to different groups based on the expression of CDK6 and risk. Functional experiments suggested that CDK6 promotes the proliferation of UM-UC-3 cells. We constructed a seven-gene prognostic signature as an effective marker to predict the outcomes of BLCA patients and guide individual treatment.

Cross-validations confirmed prognostic value for the 7-gene signature from the GEO cohort by the TCGA cohort but not for the 3-gene signature from the TCGA cohort by the GEO cohort. We develop and validate a 7-gene prognostic signature (SCAF11, NOD1, NLRP2, NLRP1, GPX4, CASP8, and AIM2) with independent prognostic value for patients with LUAD.

And we listed ten candidate small-molecules drugs that exhibited a high correlation with the prognosis of cervical cancer. Thus, the prognostic model can accurately predict the prognosis of patients with CC and may be helpful for the development of new hypoxia-immune prognostic markers and therapeutic strategies for CC.

Furthermore, we found that the low-risk group may be associated with the immune-related pathway and the high-risk group was with the cell cycle-related pathway, which also showed an impact on the prognosis. These seven immune-related gene risk signatures provided an effective method for prognostic stratification in ER (+) and/or PR (+) and HER2 (-) BC.

GSEA analysis suggested that the high-risk group was correlated with multiple oncogenic signatures and invasive-related pathways. These results indicated that this risk model can accurately predict recurrence after hepatectomy and offer novel research directions for personalized treatment in HCC patients.

We constructed an autophagy-based 7-gene signature, which could serve as an independent prognostic indicator for cases of GBM and sheds light on the role of autophagy as a potential therapeutic target in GBM.

We performed a comprehensive comparison of the performance evaluation of five well-known feature selection methods for mining features from various high-dimensional datasets. We identified signature genes using supervised learning for the specific omic data for the disease. The study will help incorporate higher order dependencies among features.

We constructed a new ARG-related prognostic model, which can be a prognostic biomarker and offers insights into identifying potential therapeutic targets for PDAC.

The protein expression of seven model genes was consistent with the mRNA expression. Our IRRG prognostic model can effectively forecast LUAD prognosis and is tightly related to immune infiltration.

The combined 7-gene signature could serve as a biomarker for predicting BC prognosis. The nomogram built by risk score and other clinical factors could be an effective tool for predicting the prognosis of patients with BC.

Finally, in vitro experiments demonstrated that the combination of gemcitabine and cisplatin could induce ferroptosis in AsPC1 cells, probably through elevated SAT1 expression. Taken together, Our 7-gene signature has significant values in predicting the PAAD patients' OS, and it may help inform the clinical treatment of PAAD.

The study builds a novel 7-gene signature as a prognostic marker for the survival prediction of patients with LUAD. The current findings provided a set of new prognostic and diagnostic biomarkers and therapeutic targets.

We conclude that the expression of 7-gene signature may lead to improved patient prognosis. Further studies are required for consideration in clinical practice.

Univariate and multivariate regression analyses showed that a 7-gene signature constructed from the robust DEGs was useful for predicting ESCC prognosis. Our results might facilitate the exploration of potential targeted TME therapies and prognostic evaluation in ESCC.

The HRisk group was strongly associated with upregulation of both cancer-related pathways and stromal scores, while higher proportions of anti-tumor immune cells and immune signatures were enriched in the LRisk group. In conclusion, the signature based on 7 ferroptosis-related genes could be applicable for predicting the prognosis of HNSCC, indicating that ferroptosis may be a potential therapeutic target for HNSCC.

Our results demonstrate that CAIX can be a reliable surrogate hypoxia marker and prognostic indicator for TNBC. The identification of CAIX-linked 7 gene-signatures and their relationship with 6 enriched cellular functions further support the implication and influence of hypoxia-mediated CAIX expression in tumour microenvironment and breast cancer development.

Background: Lapatinib (L), a HER2 signaling, tyrosine kinase inhibitor, demonstrated numerically higher pCR in NSABP B-41 when added to paclitaxel (AC→P) and trastuzumab (T) following doxorubicin + cyclophosphamide (62% v 52.5%). The significant association of the modified 8-gene benefit groups with pCR in the AC→P+T arm suggests this signature could identify pts who may benefit from dual HER2-targeted neoadjuvant therapy. This could be tested in a meta-analysis including other neoadjuvant trials.Support: Lombardi CCC; BCRF; GSK; P30CA051008; Genentech; NSABP

Collectively, this ECM-related 7-gene signature provides a novel insight for survival prediction among GC patients. The zinc finger protein CTCF regulates ECM-related genes, thereby promoting GC cell growth and migration.

A seven-gene signature correlated with cellular glycolysis was developed to predict the survival of BC patients. The results include insight into cellular glycolysis mechanisms and the detection of patients with poor BC prognosis.