CD8 (cluster of differentiation 8)

We established an 11-gene prognostic model that effectively stratifies liver cancer patients based on differentially expressed genes between tumor and adjacent non-tumor cells clustered by scRNA-seq data. The two risk groups had significantly different molecular characteristics. We identified 14 drugs that might be effective for high-risk HCC patients. Our study provides novel insights into tumor cell characteristics, aiding in research on tumor development and treatment.

Subsequently, gene ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses revealed that the hub genes were primarily involved in the progesterone-mediated oocyte maturation signaling pathway and oocyte meiosis...Finally, we explored potential drug candidates for the hub genes using Drug-Gene Interaction Database and discovered that there are no FDA-approved drugs for CCNB1 and CDCA8, highlighting a promising area for future research. Taken together, our results will be of immense importance in addressing the intricacies of TNBC.

P2, N=50, Active, not recruiting, National Cancer Institute (NCI) | Recruiting --> Active, not recruiting

P=N/A, N=50, Not yet recruiting, Institut Bergonié

We further demonstrated that the SA arginine pathway increased the abundance of ornithine, which may be a major contributor to reshaping of the TIME. Our findings demonstrated that SA, a novel risk factor, plays significant roles in the initiation and progression of GC, suggesting that SA might be a promising target for the diagnosis and treatment of GC.

Moreover, cDC_LAMP3 cells exhibited high CD274 expression, suggesting immune exhaustion and an increased susceptibility to carcinogenesis. This pioneering study provides valuable insights into CHC pathogenesis and immune responses, enhancing our understanding of potential therapeutic strategies.

Four key genes, including CYBB, MAPK14, PTGS2, and RELA, in the development of sepsis were identified through bioinformatics analysis, which play an important role in the immune process, and MAPK14 may be an important target for immune intervention.

ABAT functions to inhibit Treg differentiation in liver cancer through downregulation of GABA, thus promoting the antitumor activity of CD8+T cells.

Peptide CLP002 specifically bound residues of PD-L1 interaction with PD-1, blocked the mutual binding between PD-1 and PD-L1, and further improved the immune response ability of tumor infiltrating T cells. In this study, we developed a multi-pronged immunotherapy strategy of intelligent target finding, breaking through the physiological barrier through kinetic energy, accurately intervening the target and bioimaging, providing a new idea for breast cancer cells targeted therapy.

BIRC5 silencing attenuated HCC through blocking PPARγ pathway and regulating cuproptosis, which may offer therapeutic implications against HCC.

Notably, the co-administration of mIL12 and PD-1 blockade significantly enhanced the presence of central memory T cells (TCM) within tumors. This study is the first to provide evidence that the combination of mIL12 and PD-1 blockers promotes the generation of TCM, potentially contributing to a robust and durable antitumor effect.

Furthermore, BRY805 exhibited synergistic antitumor activity when combined with PD-L1 monoclonal antibodies. In a mouse xenograft model, BRY805 showed superior tumor control relative to monalizumab and demonstrated a favorable safety profile in non-human primate studies.

Engagement of innate and adaptive immune checkpoint molecules via CD47 × PD-L1 BisAb treatment resulted in robust CD8+ T cell responses, including the induction of tumor-resident CD8+ T cells that exhibited functionally superior anti-tumor immunity. These results demonstrate that innate immune activation potentiates anti-tumor adaptive responses, highlighting the use of dual checkpoint blockade as an optimal strategy for promoting CD8+ T cell-mediated protection.

Lastly, ovarian cancer and prostate cancer shared one immune trait: CD3 on resting Treg. Our MR study suggests a potential relationship between immune traits and cancers, particularly highlighting 14 immune traits that are simultaneously influenced by two or three of five cancer types, while also indicating that 6 immune traits may simultaneously contribute to the development of two of the cancers. This elucidation enables us to reveal a significant involvement of immune traits in cancer progression, providing critical insights into how immune traits affect cancer susceptibility.

The proliferation index Ki-67 was evaluated as high, being positive in more than 70% of the tumor cells. The patient died 39 days after the initial onset of symptoms.

Sensitivity analysis of common chemotherapeutic drugs showed that high expression of CALU could sensitize chemotherapeutic drugs such as 5Z-7-Oxozeaenol, AMG-706 and Cytarabine, but could lead to drug resistance to chemotherapeutic drugs such as Embelin, Salubrinal and Tipifarnib. Thus, our results indicate that CALU could be a biomarker and designing personalized treatment approaches for ccRCC patients. The online version contains supplementary material available at 10.1007/s43657-024-00169-7.

These findings indicate that TCR-transduced CD8 T cells can undergo antigen-dependent expansion when exposed to TriVax. Additionally, the expression of CA-STAT5 enhances T cell proliferation and persistence, partly by promoting resistance to PD-1/PD-L1-mediated inhibition in antitumor T cells.

P1/2, N=358, Recruiting, GI Innovation, Inc. | N=92 --> 358 | Trial completion date: Jun 2025 --> Apr 2027 | Trial primary completion date: Apr 2025 --> Nov 2025

This study provides a unique single-cell resource with clonal and longitudinal resolution during ICI therapy and reveals IFN signaling as a biomarker of immunotherapy response in HCC, suggesting a beneficial effect by combining IFN inducers with ICIs for patients with HCC.

We comprehensively interpreted the immune microenvironment pattern of OSCC based on the single-cell sequencing data and bulk sequencing data analysis. A robust immune feature-based prognostic model was developed for the precise treatment and prognosis evaluation of OSCC.

The marked increase in immune cells following ADT suggests an intensified immune response against prostate cancer.

Our findings offer a potential therapeutic strategy to maintain a dynamic balance within the TME and improve the immunotherapy efficacy by modulating the relative proportions and functional states of CXCL9 + TAMs and TREM2 + TAMs.

We found that iPD-L1 expression levels in diagnostic biopsy in ovarian cancer can predict the chemotherapy response score in interval debulking surgery.

Our research revealed the contribution of PTX3 to the peritoneal dissemination process in OC patients, identifying a novel potential biomarker and therapeutic target for this disease.

Overall, this research introduces a promising avenue for improving lung cancer treatment using PTM to stimulate an immune response and induce cell death in tumor cells. Further studies will be essential to validate these findings and explore clinical applications.

CD161 may inhibit ENKTL tumor development by regulating cell cycle and T-cell phenotype.

Thus, the therapeutic effectiveness appeared to largely depend on cancer-cell MHC-I expression, triggering CD8 T cell effector memory-driven responses against tumor cell antigens. Identifying the differential RT response to MHC-I induction may serve as a predictive marker for stratifying patients that are most likely to benefit from this combination therapy.

Depression is common in breast cancer patients and is associated with reduced antitumor immunity. There is limited knowledge regarding the specific mechanisms through which depression impairs antitumor immunity. Immunotherapy, which promotes the restoration of antitumor immunity, represents a promising treatment strategy for TNBC patients. However, the efficacy of immunotherapy can be compromised by depressive symptoms and the administration of glucocorticoids during treatment. It is still uncertain whether increasing glucocorticoid levels can reduce the efficacy of immunotherapy in patients with depression. The potential benefits of combining immunotherapy with glucocorticoid inhibitors compared with immunotherapy alone need to be evaluated for TNBC patients with concurrent depressive symptoms. Therefore, further clarification of the specific mechanisms by which depression impairs antitumor immunity is needed to inform future optimization of immunotherapy strategies.

These data support the hypothesis that in early-stage TNBC, high GR expression is significantly associated with infiltration of immunosuppressive regulatory T cells, suggesting a tumor-intrinsic role in shaping the immunosuppressive immune cell milieu. Furthermore, suppression of GR activity may regulate the tumor immune microenvironment and improve long-term outcomes in GR-high TNBC.

The RVd therapy, combining lenalidomide, bortezomib, and dexamethasone, is a mainstay treatment for multiple myeloma. Blocking MHC-I or depleting T cells alleviates the defective erythropoiesis of PRCA, suggesting that the interaction between erythroid cells with elevated MHC-I and T cells in the bone marrow might contribute to PRCA. Taken together, our study implicates a mechanism underlying lenalidomide-induced PRCA in treating cancer patients.

Mechanistically, early radiation-induced apoptosis promoted the proliferation of CD8 + T cells, while increased chemokine CCL2 levels from localized and distant tumor sites facilitated CAR-T and endogenous T cell infiltration, leading to systemic tumor suppression. This study proposes a promising approach for treating metastatic pancreatic cancer by combining radiotherapy and CAR-T therapy, elucidating the mechanism of CAR-T cell-enhanced radiotherapy effects ex vivo, and highlighting a novel strategy for combating metastatic pancreatic cancer.

In conclusion, our results indicate that histopathologic findings in patients treated with ICI therapy are not diagnostic and varied. Additionally, these results are in line with recent studies showing an expansion on CD8+ T cell subset in patients under ICI treatment and highlight the synergism of polytherapy.

Neutralizing IL-1α enhances the efficacy of single agent paclitaxel or combination therapy with PD-1 blockade in preclinical models. Low IL1A levels correlates with positive patient outcome in several solid malignancies, particularly in patients treated with chemotherapy.

Secondary outcomes include patient tolerability and potential antitumor effects. Collectively, our findings highlight the promising therapeutic potential of the -SG diet for treating solid tumors.

What's more, we also confirmed that the activation of CBLN2 could improve the efficiency of immune checkpoint blockade (ICB) treatment in the MC38 CRC model. In conclusion, the CBLN2-STAT3 axis may act as a novel potential target for CRC treatment.

Computational biomarkers, representing spatial properties of the tumor proliferation and immune cell infiltrates, provided independent prognostic information beyond conventional IHC markers in BC. Integrating Ki67-entropy and CD8-immunogradient indicators into prognostic models can improve patient stratification with regard to BCSS.

Combining CYT107 with atezolizumab was safe and resulted in lymphocyte expansion, a doubling of the CR rate, and durable responses exceeding 2 years, however, the ORR was similar to atezolizumab alone. Increased and sustained doses of CYT107 coupled with patient selection strategies should be further investigated.

Mutations in POLE might affect DNA polymerase epsilon function. These mutations also affect interactions with other proteins like proteins involved in different DNA repairing mechanisms. POLE mutations may lead to platinum resistance, but they can also trigger an immune response that improves prognosis.

Significantly, EMB-09 activated effector memory T cells in peripheral immune system, promoted the influx of stem-like CD8+ T cells into the tumor site, resulting in a more active phenotype of CD8+ tumor-infiltrating lymphocytes. In an ongoing first-in-human study in patients with advanced refractory solid tumors (NCT05263180), EMB-09 demonstrated a consistent pharmacodynamic response and early efficacy signals.

However, we also noted that the formation of NETs is a complex biological process involving the regulation of multiple cytokines and cellular interactions. Therefore, the exact roles of these genes and their specific mechanisms in the formation of NETs and the development of NB still need to be further investigated.

ICIs in combination with bevacizumab can not only improve the patient's prognosis but also yield safe and controllable adverse drug reactions in patients suffering from MSS/pMMR advanced CRC after failure to a 1st-line therapy.

We concluded that XELOX + DC-CIK immunotherapy for postsurgical CRC patients offers reduced rates of treatment-induced adverse events, extended 2-year DFS, enhanced immunity, and increased physiological antitumor responses.