This subsequently activates the cyclic guanosine monophosphate-adenosine monophosphate synthase-stimulator of interferon genes (cGAS-STING) pathway, enhancing the innate immune response. In conclusion, it synthesizes a new type of bimetallic peroxides by one-step symbiosis for activating anti-tumor immunotherapy combined with immune checkpoint inhibitor.

These findings were validated in an independent cohort of 15 patients during 16-month follow-up. Overall, we identified a distinct immuno-suppressive TINK cell group, featuring IL10 + secreting and SELL expression with a strong relation to poor survival prognosis in TNBC patients post-NATI.

CAR-T and blinatumomab therapies demonstrate comparable safety and efficacy as bridging treatments to HSCT in patients with R/R B-ALL. Further studies are needed to optimize these treatment strategies.

Despite the patient's PD-1 negativity, the combination of anlotinib and tislelizumab may exert synergistic effects through distinct mechanisms, thereby potentially enhancing therapeutic efficacy. The integration of a multi-targeted tyrosine kinase inhibitor within this combination therapy regimen warrants further investigation.

Interestingly, the TRIM21-METTL3 axics mediated ferroptosis effectively increased the expression of immune checkpoint PD-L1 and strengthened antitumor immunity in pancreatic cancer. Together, our findings first elucidated the detailed molecular mechanism of METTL3 degradation and revealed the pivotal role of the TRIM21-METTL3 axis in regulating ferroptosis and antitumor immunity, which may serve as a potential target for pancreatic cancer treatment.

50% of mice bearing MC38 tumors were cured by αNKG2A-N215, and long-term immunological memory against the tumor was induced in these mice. These results indicate that NKG2A is another ideal target for delivery of an IL-2Rβγ agonist, and αNKG2A-N215, with specificities for both NKG2A and IL-2Rβγ, might be developed as a novel agent for immunotherapy.

Additionally, this review also evaluates combination therapies of immune checkpoint inhibitors and recently published clinical trials on lung cancer with CAR T cells. We offer insights into the way to optimize CAR T cell therapy for lung cancer by analyzing antigen selection, immune evasion, and the strategies to enhance T cell persistence and tumor infiltration.

CMMS detection has significant utility in the prognosis of patients at an early stage and identification of potential candidates for immunotherapy.

ADCC was maintained upon exposure to specific ABL or JAK-inhibitors, in contrast to the multi-target TKI dasatinib impeding SYK-dependent ADCC. In conclusion, optimized ML-NK cell and CD19 antibody-based immunotherapy combined with carefully selected TKI demonstrates significant in vitro treatment efficacy in kinase-driven leukemia.

Overall, the study developed a unique IRS for LUAD that may serve as a predictor of the clinical outcome and immunotherapy advantages for individuals with LAUD.

After combination with anti-PD-L1, the bacterial in situ vaccine further effectively enhance cancer immunotherapy and inhibit metastasis. We provide a promising strategy to amplify antitumor immune effects by an engineered bacterial vaccine, showing potential clinical applications.

These barriers are described to facilitate the understanding of ways to overcome them and increase the efficacy of immunotherapies through combination therapies. This means that by developing new knowledge of immunological targets and pathways, immunoprecision medicine for cancer could greatly enhance outcomes.

Indeed, its effectiveness lies in targeting immune checkpoints such as PD-1 and CTLA-4 inhibitors, as well as monoclonal antibodies like pembrolizumab and cetuximab, adoptive cell transfer methods (including CAR-T cell therapy), cytokine therapy such as IL-2, and tumor vaccines. This review will explore how the TME controls tumor proliferation and metastasis via autocrine-paracrine signaling pathways. It will then detail the effectiveness of immunotherapy in oral cancers, focusing on immune checkpoints, targeted monoclonal antibodies, adoptive cell transfer, cytokine therapy, and tumor vaccines.

Clinical data reveal that higher CXCL16 and CXCR6 levels in human tumors correlate with improved survival and T cell infiltration, underscoring the translational potential of this approach. This study positions VC as a safe, accessible, and cost-effective dietary enhancer for PTI, reshaping the role of dietary nutrients in cancer therapy and offering a strategy for overcoming treatment resistance.

The antitumor efficacy of ASP1570 was cancelled by CD8+ T-cell depletion, indicating that its antitumor effect depends on CD8+ cytotoxic T-cell activation. Collectively, ASP1570 potentially improves antitumor efficacy in both anti-PD-1-therapy-resistant and anti-PD-1-therapy-responsive tumors by overcoming multiple immunosuppressive signals.

MSS CRC tumours in patients with Lynch syndrome is an infrequent phenomenon and under-represented in the literature. The limited efficacy of immune checkpoint inhibitors is highlighted in this rare subset of patients.

Our in-silico study explains the low immunotherapy-response in high IC-expressing PAAD, wherein CSC plays a pivotal role. Further exploration portrayed correlation of CSCs with immunotherapy-resistance in other LR and HR cancers too, substantiating the need for personalized CSC evaluation and targeting for successful immunotherapy outcomes.

Neoadjuvant immunotherapy has high FDG-PET response rates in melanoma. FDG-PET response associates with pathological response and confers impressive RFS, suggesting this could be an important clinical tool.

We focus on the most recent studies dissecting functional states and spatial distribution of lung cDC1 across tumor stages and their impact on T cell responses to neoantigens. Finally, we highlight relevant gaps and emerging strategies to harness lung cDC1 immunostimulatory potential.

Current immunotherapeutic strategies, including immune checkpoint inhibitors, have shown promise for NSCLC patients with BM, demonstrating intracranial activity and manageable safety profiles. Future research is warranted to further explore the molecular and immune mechanisms underlying BM, aiming to develop more effective treatments.

Overall, this study unveils a feasible GRP78 nanobody-directed therapy strategy for single or combinatorial cancer intervention. This work finds that C5-PE38-induced cell death stimulates STING-dependent cytosolic DNA release to promote antitumor immunity, a mechanism not previously reported for PE38, providing valuable insights for its clinical use.

Specifically, the hydrophobic photosensitizer protoporphyrin IX (PpIX) is covalently linked to the hydrophobic peptide FFVLK and a PD-L1-targeting peptide sequence CLQKTPKQC, resulting in the formation of an amphiphilic photosensitizer-peptide conjugate (PpIX-FFVLK-CLQKTPKQC, called PFC), which is capable of encapsulating the autophagy inhibitor chloroquine (CQ)...This cascade immunomodulation promotes the dendritic cell maturation and CD8+ T cell activation, leading to a synergistic suppression of both primary and metastatic tumors. This work introduces an innovative autophagy modulation strategy with potent immunomodulatory capability, demonstrating a potential to trigger systemic antitumor immune responses through local treatment.

The expression of PDGFRB influences the regulation of the immune system and is closely associated with immune cell infiltration, immune checkpoints, immune-activating genes, immune suppressor genes, chemokines, and chemokine receptors. PDGFRB is a cancer gene closely associated with prognosis and immunity in cancer patients, and it may serve as an immune checkpoint.

Reversal of immunosuppression will restore immunosurveillance and eventually prevent progression into PDAC. We also review relevant published and ongoing non-surgical treatment approaches for high-risk IPMNs and PanINs.

This study introduces a novel prognostic model incorporating five ARGs, highlighting their potential as immune targets for cancer immunotherapy. The negative correlation between RHEB and LC3 suggests a therapeutic pathway for PCM intervention, laying the groundwork for more effective anti-cancer strategies. These findings advance the identification of novel immune targets and signaling pathways, aligning with precision medicine goals in cancer treatment.

The synergic effects of AMPK activators and/or PPAR agonists in cancer immunotherapy have been reported. In this review, we compare the roles of AMPK activators and PPAR agonists, and the efficacy of their combination in metabolic reprogramming of cytotoxic T cells in favoring cancer immunotherapy.

Moreover, pLCGM-OVA exhibited excellent T1 contrast (9.26 mM-1s-1), significantly enhancing T1-weighted magnetic resonance imaging signals of tumours, facilitating accurate melanoma diagnosis. Overall, this work presents a highly promising candidate for the development of potent immune agonists for melanoma treatment.

Our findings demonstrate that adenosine-A2AR signaling mediates resistance to immunotherapy and discover a novel potent and selective A2AR inhibitor with high efficacy in enhancing antitumor immune responses and reversing PD-L1 resistance. The combination of A2AR inhibitor and PD-L1 inhibitor represents a promising therapeutic strategy for antitumor therapy.

These findings increase our understanding of MACC1 as a potential prognostic biomarker and potential therapeutic target for cancer immunotherapy. The MRRS may play a critical role in predicting the response of LUAD patients to ICB therapy.

Addressing these challenges is crucial for guiding effective combination strategies and optimizing treatment outcomes. By examining both established facts and ongoing developments, this review provides a comprehensive overview of the status and potential of CD40 agonists in cancer immunotherapy.

In this work, a hafnium-based metal-organic framework (Hf-MOF), UiO-66-Hf(2OH)-CB-839/BSO@HA (UiO-66-Hf(2OH)-C/B@HA), was designed to codeliver telaglenastat (CB-839) and buthionine sulfoximine (BSO), which synergistically inhibited glutamine metabolism and alleviated tumor hypoxia...In the orthotopic HCC model, established with MYC-amplified tumor cells, intravenous administration of UiO66-Hf(2OH)-C/B@HA significantly potentiated the efficacy of radio-immunotherapy, resulting in superior tumor regression. In summary, our study provides insights into the design of Hf-MOF for radio-immunotherapy and proposes a promising therapeutic approach for MYC-amplified HCC.

PTC209/MnO2@BSA (bovine serum albumin) nanoparticles (PMB NPs) synthesized via a facile and green process are reported, wherein the released manganese (Mn) ions under acidic tumor microenvironment significantly enhance cGAS-STING signals and facilitate the dendritic cells maturation to unleash the T-cell-mediated immune response...Both in vitro and in vivo experiments elucidate that PMB NPs function as designed, exerting powerful immunotherapeutic and chemotherapeutic impacts to impede HNSCC growth and metastasis as well as bolster anti-PD-1-based ICB. Collectively, our findings provide a promising therapeutic strategy against HNSCC by combinational CSCs elimination and STING activation via metalloimmunotherapy.

Our retrospective analysis suggests that elevated IRF8 expression correlates with improved prognosis in LUAD, with higher IRF8 expression being predictive of a more robust immunotherapy response. Mechanistically, IRF8 expression is associated with a modulated tumor immune microenvironment and improved immunotherapeutic response.

In these external cohorts, SCORPIO maintained robust performance in predicting ICI outcomes, surpassing programmed death-ligand 1 immunostaining. These findings underscore SCORPIO's reliability and adaptability, highlighting its potential to predict patient outcomes with ICI therapy across diverse cancer types and healthcare settings.

This study uses single-cell sequencing and spatial transcriptomics on paired tumor specimens from 22 patients with oral squamous cell carcinoma (OSCC) enrolled in a randomized two-arm phase 2 trial, receiving neoadjuvant anti-PD-1 mono-immunotherapy or anti-PD-1 plus docetaxel-cisplatin-5-fluorouracil (TPF) immunochemotherapy. SELP+ HEVs and APOD+ myCAFs foster favorable immunomodulatory stromal niches for improved outcomes, while STMN1+ cECs and MYF5+ MSCs form immunosuppressive niches in tumor invasion regions, highlighting therapeutic targets. The trial was registered at ClinicalTrials.gov, and the registration number is NCT04649476.

Currently, 18 CD73 inhibitors are in clinical trials, showing promising results in combination therapy for various solid tumors. The development of CD73-specific companion positron emission tomography imaging ligands holds potential for facilitating diagnosis, patient selection, and treatment efficacy evaluation throughout the entire process of CD73-targeted therapeutic development.

This miR-1246-AGO2 complex disrupts IFN-γ-mediated signal transducer and activator of transcription 1 (STAT1) phosphorylation by stabilizing protein tyrosine phosphatase non-receptor 6 (PTPN6) mRNA, thereby suppressing the expression of downstream C-X-C motif chemokine ligands (CXCLs), IFN-stimulated genes (ISGs), and human leukocyte antigen (HLA) molecules, which collectively contribute to tumor immune evasion. In preclinical cancer models, inhibiting AGO2 with BCI-137 or targeting miR-1246 with its antagomir re-sensitizes tumor cells to IFN-γ, leading to the enhanced recruitment, activation, and cytotoxicity of CD8+ T cells and ultimately improving immunotherapy efficacy.

A recent phase I/II study tested the IDO1 inhibitor linrodostat with nivolumab +/- ipilimumab in patients with advanced solid tumors. While efficacy was not augmented, correlative analyses identified TDO2 as a resistance mechanism; dual targeting may be necessary to realize improved response to PD-1 inhibition.

GM-CSF priming was sufficient to enhance the ICB response in tumors with high S100A1 expression in preclinical models. These findings define S100A1 as a potential blood-based biomarker and a novel synergistic target for cancer immunotherapy.

The established EBV-positive ICC cell lines revealed enhanced immunogenicity driven by cGAS-STING pathway activation, providing valuable models for future research and insights into the mechanisms of improved immunotherapy sensitivity in EBVaICC.

This retrospective cohort study compared survival outcomes in pancreatic adenocarcinoma patients treated with two regimens: surgery+chemotherapy (nab-paclitaxel plus gemcitabine)+anti-PD1 (Tislelizumab) (S+AG+anti-PD1) (n = 37), and surgery+chemotherapy (S+AG) (n = 5). Combining surgery, chemotherapy, and immunotherapy may improve PFS in resectable pancreatic adenocarcinoma. While CTCs and HIF1A-positive CTCs may have prognostic value, AJCC staging remains the most reliable indicator.

In conclusion, NQO1 may play a critical role in M2 polarization and accelerates HCC progression. The NRSHC model and accompanying tools offer valuable insights for personalized HCC treatment.