bims-tuinly Biomed News
on Tumor-infiltrating lymphocytes therapy
Issue of 2026–04–12
fourteen papers selected by
Pierpaolo Ginefra, Ludwig Institute for Cancer Research



  1. Front Immunol. 2026 ;17 1801722
      The recent U.S. FDA approval of lifileucel, a non-engineered, autologous tumor-infiltrating lymphocyte (TIL) therapy, for unresectable or metastatic melanoma represents a major milestone for cellular therapies in solid tumors. This review examines the clinical foundation, regulatory development, limitations, and evolution of TIL therapy in metastatic melanoma. Randomized academic data from the phase III M14TIL trial established the efficacy of TIL therapy. The C-144-01 study leading to lifileucel approval demonstrated median duration of response of 36.5 months, median overall survival (OS) of 13.9 months, and estimated 5-year OS rate of 19.7%, a major advance in this anti-PD-1/PD-L1 resistant cohort without effective treatment options. Despite durable responses, classical TIL therapy requires intensive nonmyeloablative lymphodepletion and high-dose interleukin-2 (IL-2), contributing to substantial toxicity and treatment-related mortality that remain barriers to broader implementation. We discuss safety-driven trial terminations related to cytokine augmentation and feasibility or strategic factors underlying discontinuation of programs, underscoring translational challenges beyond biologic efficacy. Engineered TIL platforms aim to improve persistence and reduce systemic cytokine dependence. OBX-115, designed with regulatable membrane-bound IL-15 expression, eliminates the need for IL-2 infusion and has shown early clinical activity. KSQ-001EX uses CRISPR/Cas9 to inactivate SOCS1, while KSQ-004EX additionally targets Regnase-1 to enhance TIL function. Emerging strategies including IL-2-independent expansion platforms, PD-1-edited TILs, and neoantigen-enriched products illustrate ongoing innovation. TIL therapy remains among the most promising strategies in melanoma and solid tumors after immunotherapy failure. Ongoing research aims to optimize cell dose, phenotype, tumor procurement, treatment sequencing, and rational combinations to improve durable benefit.
    Keywords:  efficacy; metastatic melanoma; safety; tumor microenvironment; tumor-infiltrating lymphocytes
    DOI:  https://doi.org/10.3389/fimmu.2026.1801722
  2. Int J Biol Sci. 2026 ;22(6): 2869-2884
      Tumor-reactive T cells are central to cancer immunotherapy, and immune checkpoint inhibitors (ICIs) have revolutionized treatment by relieving immune suppression on tumor-reactive T cells, yet response rates remain suboptimal. Adoptive T cell therapy can supplement tumor-reactive T cells, but accurately identifying tumor-reactive CD8⁺ T cells within tumor-infiltrating lymphocytes (TILs) remains challenging. CD39 (ENTPD1) is a rate-limiting enzyme in adenosine metabolism, leading to the view that CD39 is associated with immune suppression because of the inhibitory function of adenosine in tumor immunity. However, its role in tumor-reactive CD8⁺ TIL endures as controversial. In this study, we reassess the tumor-reactive potential of CD39⁺CD8⁺ TILs using clonotype-resolved single-cell multi-omics. Compared to CD39⁻CD8⁺ TILs, CD39⁺CD8⁺ TILs exhibited features of proliferation, activation, and T cell-mediated cytotoxicity, alongside reduced TCR clonal diversity and increased TCR clonal expansion, indicating tumor reactivity. TCR-T cells engineered with TCRs from CD39⁺CD8⁺ TILs mediated robust antigen-specific killing in vitro. Importantly, reinfusion of CD39⁺CD8⁺ TILs significantly inhibited tumor growth and demonstrated favorable safety in vivo. At the patient level, we further demonstrated that CD39⁺CD8⁺ TILs are enriched for effector programs and pathways linked to T-cell activation and cytotoxicity, and exhibit reduced TCR clonal diversity with pronounced clonal expansion. The intratumoral abundance of CD39⁺CD8⁺ TILs also correlated with earlier tumor stage and improved overall survival, and a CD39⁺CD8⁺ TIL-derived gene signature predicted ICI response and prognosis, supporting CD39 as a practical biomarker to enrich tumor-reactive CD8⁺ TILs and to improve adoptive cell transfer strategies in future clinical practice.
    Keywords:  CD39 (ENTPD1); TIL therapy; adoptive cell therapy; bladder cancer; single-cell sequencing analysis; tumor-infiltrating lymphocyte
    DOI:  https://doi.org/10.7150/ijbs.130389
  3. bioRxiv. 2026 Mar 13. pii: 2025.10.15.682695. [Epub ahead of print]
      Adoptive cell therapy (ACT) with tumor-infiltrating lymphocytes (TIL) is a form of personalized immunotherapy that requires ex vivo expansion of autologous TILs and their reinfusion back into the patient. Predicting TIL expansion at the time of diagnosis may improve selection of patients that can benefit from ACT-TIL. It can also prevent high treatment-related costs and delays in treatment of patients whose cancer specimens would not yield successful TIL growth. We developed PETIL, a machine-learning model optimized for data of a medium size to determine a minimal combination of features (demographic, clinical, and biological specimen-based) that is predictive of expansion of TILs from a resected bladder cancer. We used a retrospectively identified set of data from bladder cancer patients at Moffitt Cancer Center for the training and testing cohorts. Additionally, we used data from a recent feasibility clinical trial at Moffitt Cancer Center as a blinded validation cohort. PETIL uses random forest method to identify a combination of robust predictive features, support vector machine model to determine the optimal classification hyperparameters, and Matthews correlation coefficient method to adjust the decision-boundary threshold for imbalanced data. Our model yielded AUC=0.740 for the testing cohort and AUC=0.857 for blinded validation cohort. Thus, our PETIL model optimized for data of medium size has favorable performance metrics for predicting TIL expansion from a given tumor.
    Authors Summary: Treatment with autologous tumor-infiltrating lymphocytes (TIL) that are expanded ex vivo from a given tumor and then reinfused into the patient is a promising personalized immunotherapy. However, the TIL expansion takes about 4-6 weeks, thus developing tools that predict whether TIL growth will be successful can help to avoid delays in treatment of patients whose cancer specimens would not yield successful TIL expansion. Our Predictor of Expansion of TIL (PETIL) is a machine-learning model that uses patients' demographic information, clinical tumor classification, and biological tumor specimen-based measurements to determine a minimal set of these data features that are predictive of TIL expansion outcome. We applied this model to data from bladder cancer patients collected at Moffitt Cancer Center and showed that PETIL has favorable performance metrics for the dataset of a moderate size. This computational predictor can support clinicians in determining which patients are candidates for TIL immunotherapy. The developed PETIL pipeline can also be adjusted to data from other solid tumors.
    DOI:  https://doi.org/10.1101/2025.10.15.682695
  4. Clin Transl Oncol. 2026 Apr 09.
       PURPOSE: To investigate the predictive performance of PD-L1 expression and tumor-infiltrating lymphocytes (TILs) in pre-treatment biopsies for the response to neoadjuvant chemoimmunotherapy in non-small cell lung cancer (NSCLC).
    METHODS: This retrospective study included 82 NSCLC patients who received neoadjuvant chemoimmunotherapy. PD-L1 expression (tumor cell [TC%], immune cell [IC%], and combined positive score [CPS]), TILs density, and the lymphocyte-to-tumor ratio (LTR) were quantitatively assessed using digital image analysis (IA). Diagnostic performance was evaluated for major pathological response (MPR), pathological complete response (pCR), and event-free survival (EFS).
    RESULTS: Of the 82 patients, 48 (58.5%) achieved MPR and 25 (30.5%) achieved pCR. TC%-IA and TILs density were significantly associated with pathological response. For predicting MPR, TC%-IA (AUC = 0.67) showed better performance than IC%-IA (AUC = 0.61) and CPS-IA (AUC = 0.66). Similarly, for pCR, TC%-IA (AUC = 0.59) outperformed IC%-IA (AUC = 0.55) and CPS-IA (AUC = 0.47). TILs density yielded AUCs of 0.70 for MPR and 0.69 for pCR, while LTR-IA achieved AUCs of 0.71 and 0.61, respectively. The combination of TC%-IA ≥ 1% and LTR-IA ≥ 1 further improved predictive performance, with AUCs of 0.76 for MPR and 0.67 for pCR. Prognostic analysis showed that TC%-IA ≥ 1%, CPS-IA ≥ 10, and LTR-IA ≥ 1 were significantly associated with prolonged EFS.
    CONCLUSIONS: Image-based PD-L1 scoring on TC% combined with LTR ≥ 1 serves as a predictive biomarker for both pathological response and EFS in NSCLC patients receiving neoadjuvant chemoimmunotherapy. LTR can serve as a surrogate for TILs scoring and predicts long-term EFS.
    Keywords:  Computer pathology; Neoadjuvant chemoimmunotherapy; Non-small cell lung cancer; PD-L1 expression; Tumor-infiltrating lymphocytes
    DOI:  https://doi.org/10.1007/s12094-026-04268-x
  5. J Adv Res. 2026 Apr 05. pii: S2090-1232(26)00285-7. [Epub ahead of print]
       INTRODUCTION: The tumor microenvironment (TME) promotes immune evasion by fostering regulatory immune programs. Although CD8+ regulatory T cells have been described, their identity, upstream drivers and impact in tumors remain incompletely defined.
    OBJECTIVES: To define the phenotype, regulation determinants, and functional of CD86high CD8+ T cells in tumor immunity.
    METHODS: Murine tumor models were used to isolate tumor-infiltrating lymphocytes (TILs) for flow cytometry (FCM), functional co-cultures, and RNA-seq. Upstream cues were probed through cytokine stimulation and transcription factor analyses. Dendritic cells (DCs) conditioning was tested with bone marrow derived DCs and OT-I/OT-II antigen-specific systems. The in vivo function of CD86 on CD8+ T cells was evaluated using conditional Cd86 knockout in CD8+ T cells mouse model.
    RESULTS: CD86 was markedly upregulated on tumor-infiltrating CD8+ T cells, defining a CD86high subset that accumulated in tumors. Transcriptomic profiling revealed enrichment of immunoregulatory and terminal-exhaustion programs while preserving effector modules. CD86high cells upregulated Il12rb1 and IRF5; exogenous IL-12 increased the frequency and intensity of CD86 expression showing dose and time dependent effects, whereas IRF5 inhibition curtailed this induction, establishing an IL-12-IRF5 axis controlling CD86. Functionally, CD86high CD8+ T cells selectively suppressed antigen-specific OT-I/OT-II responses, reducing IFN-γ, IL-2, and Ki-67, and reprogrammed DCs toward a regulatory phenotype characterized by increased IDO, IL-10, CTLA-4, and CD39. Genetic ablation of Cd86 in CD8+ T cells reduced tumor growth, diminished CD39 and PD-1 on TILs, enhanced IFN-γ and granzyme B, and remodeled the myeloid compartment toward immunostimulatory DCs with elevated CD40/CD80/CD86 and reduced IDO/IL-10/CTLA-4/CD39.
    CONCLUSIONS: CD86high CD8+ T cells constitute a distinct immunoregulatory subset in cancer. Their differentiation is driven by an IL-12-IRF5 program, and their crosstalk with DCs via CD86/CTLA-4 engagement promotes tolerogenic remodeling of the TME. Targeting CD86 on CD8+ T cells may disrupt this suppressive circuit and potentiate antitumor immunity.
    Keywords:  CD8(+) T cells; CD86; Immunoregulation; Tumor microenvironment
    DOI:  https://doi.org/10.1016/j.jare.2026.04.006
  6. J Immunother Cancer. 2026 Apr 09. pii: e014378. [Epub ahead of print]14(4):
      Autologous tumor-infiltrating lymphocyte (TIL) therapy has recently been approved by the US Food and Drug Administration and Health Canada for the management of patients with advanced melanoma refractory to first-line immune checkpoint inhibitors, with regulatory assessments underway in other jurisdictions. TIL therapy typically involves a multistep process including surgical tumor resection, non-myeloablative lymphodepletion, infusion of autologous polyclonal T cells, and administration of high-dose interleukin-2 (HD-IL-2). Toxicities are predominantly associated with the induction chemotherapy regimen and post-TIL infusion HD-IL-2, rather than the TIL product itself. Over half of treated patients experience cytopenias, pyrexia, rigors, and gastrointestinal symptoms, with additional toxicities including acute kidney injury, rash, peripheral neuropathy, diarrhea, alopecia, and hypotension. Severe but less frequent adverse events include neutropenic sepsis, cytokine release syndrome, capillary leak syndrome, neurotoxicity, autoimmune sequelae, and cardiac dysfunction. These toxicities typically occur in a predictable temporal window and resolve within 10-12 days post-TIL infusion. Despite this, management often requires rigorous supportive care, and thus, toxicity remains a barrier to broader patient eligibility and wider implementation. Currently, no validated biomarkers exist to predict toxicity risk, underscoring the need for further research. This is particularly critical in the context of emerging combinatorial approaches integrating TIL therapy with other immunomodulatory agents, which may compound toxicity and complicate clinical management.
    Keywords:  Adoptive cell therapy - ACT; Immune related adverse event - irAE; Treatment related adverse event - trAE; Tumor infiltrating lymphocyte - TIL
    DOI:  https://doi.org/10.1136/jitc-2025-014378
  7. Cancer Immunol Immunother. 2026 Apr 06. pii: 135. [Epub ahead of print]75(5):
       BACKGROUND: Colorectal liver metastases (CRLM) are a major cause of cancer-related deaths. Glucose transporter 1 (GLUT1) is a key mediator of glycolytic metabolism in malignant and immune cells; however, the prognostic relevance of compartment-specific GLUT1 patterns in CRLM remains undefined. We hypothesized that spatial GLUT1 expression at the tumor-liver interface may reflect clinically relevant microenvironmental biology.
    METHODS: We retrospectively analyzed data of 192 patients who underwent curative-intent resection for CRLM (75 solitary; 117 multiple). GLUT1 expression was assessed by immunohistochemistry in the tumor tissue (Tu) and infiltration margin (Im) and was correlated with overall survival using Cox regression. Double immunofluorescence for CD8 and GLUT1 was performed for qualitative visualization at the infiltration margin. In an exploratory subset (n = 5), flow cytometry and in vitro killing assays were conducted on GLUT1⁺ versus GLUT1⁻ CD8⁺ tumor-infiltrating lymphocytes (TILs).
    RESULTS: Tumoral GLUT1 correlated with Ki67 (Spearman's ρ = 0.31, p = 0.003) but was not independently associated with overall survival in the main cohort (multivariable HR 1.183, 95% CI 0.74-1.90; p = 0.485). In the main cohort, capsule presence remained strongly associated with improved survival (HR 0.35, 95% CI 0.21-0.58; p < 0.001). In contrast, high invasive-margin GLUT1 was independently associated with improved survival in the predefined solitary cohort (HR 0.379, 95% CI 0.18-0.81; p = 0.012). Double immunofluorescence demonstrated the qualitative co-localization of the GLUT1 signal with CD8⁺ cells at the infiltration margin. In exploratory assays (n = 5), flow cytometry suggested GLUT1 enrichment in CD8⁺ terminally differentiated effector memory T cells re-expressing CD45RA (TEMRA), and GLUT1⁺ TIL fractions showed higher in vitro tumor cell killing compared with GLUT1⁻ cells.
    CONCLUSION: GLUT1 shows compartment- and context-dependent associations in the CRLM. While tumor-core GLUT1 is linked to proliferative activity, invasive-margin GLUT1 is associated with favorable outcomes in solitary metastases. Immunofluorescence and functional data provide hypothesis-generating context and warrant validation with quantitative spatial immune profiling and independent cohorts.
    Keywords:  CD8+ T cells; Colorectal liver metastases; GLUT1; Immunometabolism; Tumor microenvironment
    DOI:  https://doi.org/10.1007/s00262-026-04378-z
  8. Asian Pac J Cancer Prev. 2026 Apr 01. pii: 92165. [Epub ahead of print]27(4): 1497-1503
       OBJECTIVE: The purpose of this study was to investigate the association of CD8⁺ tumor-infiltrating lymphocytes (CD8⁺ TILs), microvascular density (MVD), and vascular endothelial growth factor (VEGF) with the TNM (Tumor-Node-Metastasis) stage, as well as to analyze their interrelationships in colorectal adenocarcinoma.
    METHODS: This cross-sectional study involved 50 FFPE samples of colorectal adenocarcinoma from the Laboratory of Anatomical Pathology at Dr. Soedarso Hospital. Microvascular density (MVD) was assessed on hematoxylin-eosin (H&E) slides, while CD8⁺ tumor-infiltrating lymphocytes (CD8⁺ TILs) and vascular endothelial growth factor (VEGF) expression were evaluated using immunohistochemistry (IHC). Correlation analysis was conducted between the biomarkers and the TNM stage, including its components depth of tumor invasion, lymph node status, and distant metastasis using the Chi-square test. Spearman's correlation was used to assess the relationships among CD8⁺ TILs, MVD, and VEGF.
    RESULTS: High CD8⁺ TILs expression was significantly associated with negative lymph node status (p = 0.047; OR = 0.31, 95% CI = 0.098-1.001), absence of distant metastasis (p = 0.008; OR = 0.130, 95% CI = 0.025-0.680), and low TNM stage (p = 0.011; OR = 0.221, 95% CI = 0.067-0.727). The distribution of high MVD was correlated with deeper tumor invasion (p = 0.004; OR = 9.036, 95% CI = 1.741-46.890), positive lymph node status (p < 0.001; OR = 10.286, 95% CI = 2.768-38.215), and high TNM stage (p = 0.002; OR = 6.612, 95% CI = 1.924-22.728). High expression of VEGF showed a significant correlation with deeper tumor invasion (p = 0.036; OR = 0.675, 95% CI = 0.544-0.837). Spearman's test revealed a negative correlation between CD8⁺ TILs and MVD (r = -0.280, p = 0.049), and a positive correlation between MVD and VEGF (r = 0.303, p = 0.032).
    CONCLUSION: High CD8⁺ TILs and low MVD are favorable prognostic factors in colorectal adenocarcinoma, whereas increased MVD and VEGF expression indicate tumor aggressiveness and enhanced angiogenesis. The combination of immune and angiogenic biomarkers with TNM staging could improve prognostic evaluation in colorectal adenocarcinoma.
    Keywords:  CD8+ TILS; MVD; TNM stage; VEGF; colorectal adenocarcinoma
    DOI:  https://doi.org/10.31557/APJCP.2026.27.4.1497
  9. Front Immunol. 2026 ;17 1770222
      Potency assays for cellular immunotherapies have advanced considerably yet remain only partially aligned with the complex requirements of solid tumors, where trafficking, persistence, metabolic fitness and spatially constrained effector function are key determinants of in vivo performance. Critical quality attributes and mechanism of action can be used to anchor more informative potency strategies for tumor-infiltrating lymphocytes and CAR-engineered platforms, including CAR T, CAR-NK, CAR-M and CAR-γδ T cells. Emerging three-dimensional models, spatial biology, label-free real-time technologies and AI-enabled analytics are examined as routes to integrate microenvironmental stressors and dynamic single-cell behavior into assay design. A "plying" framework is proposed to organize potency assessment into layered, iteratively refined panels that span lean, regulatory compliant release testing through to comprehensive exploratory profiling, providing a practical path toward clinically relevant and regulatorily acceptable potency assurance for solid tumor immunotherapy products.
    Keywords:  3D tumor culture models; CAR T-cell therapy; CAR-engineered immune cell platforms; artificial intelligence; axicabtagene ciloleucel; potency assays; regulatory frameworks for advanced therapies; spatial biology
    DOI:  https://doi.org/10.3389/fimmu.2026.1770222
  10. JCO Glob Oncol. 2026 Apr;12(4): e2500474
       PURPOSE: This study investigated whether the benefit of patients with recurrent and/or metastatic nasopharyngeal carcinoma (R/M NPC) from immune checkpoint inhibitor (ICI)-containing regimens was correlated with the presence of tumor microenvironment (TME) cell subpopulations that correlate with clinical outcomes.
    PATIENTS AND METHODS: A total of 73 patients with R/M NPC from four prospective trials in three centers using nivolumab monotherapy, nivolumab + gemcitabine, nivolumab + ipilimumab, or avelumab + axitinib were included. Lunit SCOPE IO, an artificial intelligence-powered spatial TME analyzer, analyzed tumor-infiltrating lymphocytes (TILs), macrophages (MPs), fibroblasts (FBs), and endothelial cells in the intratumoral area and adjacent stroma.
    RESULTS: The median progression-free survival (PFS) was 7.3 months, and the median overall survival (OS) was 30.0 months for the entire cohort. Higher intratumoral immune infiltrates showed association with improved treatment response, with both intratumoral TILs (hazard ratio [HR], 0.44 [95% CI, 0.24 to 0.83]; P = .0081) and intratumoral MPs (HR, 0.5 [95% CI, 0.27 to 0.91]; P = .0209) showing associations with improved PFS in the combined cohort. In contrast, stromal immune populations did not show clear correlations (stromal TILs: HR 1.14, P = .6681; stromal MPs: HR 0.9, P = .7278). Higher stromal FB density was also associated with poor outcomes, showing a trend toward shorter PFS and a significant reduction in OS (HR, 2.44 [95% CI, 1.16 to 5.11]; P < .05).
    CONCLUSION: The results from this multinational cohort suggest that high intratumoral infiltrations of TILs and MPs, along with low stromal FB densities, may be associated with better response to ICI-containing treatment in NPC. Further studies in larger, expanded cohorts are warranted, and prospective validation is needed.
    DOI:  https://doi.org/10.1200/GO-25-00474
  11. Cancer Rep (Hoboken). 2026 Apr;9(4): e70535
       BACKGROUND: The objective of this study was to establish a new model for predicting the prognosis of endometrial carcinoma (EC) using tumor-infiltrating lymphocytes (TILs) based on artificial intelligence (AI).
    METHODS: Patients with EC who were treated between 1989 and 2022 were included in this study. For each patient, one hematoxylin and eosin-stained slide containing the most invasive frontline of the tumor was selected and digitized. The area within a 500 μm width span, extending 250 μm toward the stroma and tumor from the manually annotated invasive frontline, was automatically annotated. The average number of lymphocytes per area (μm2) in the annotated area was calculated using AI. Patients were classified into the High-TIL and Low-TIL groups, and survival analysis was conducted. Four mismatch repair (MMR)-related proteins were evaluated using immunohistochemical staining.
    RESULTS: A total of 659 patients were included: 346 (52.5%) in the High-TIL group and 313 (47.5%) in the Low-TIL group. MMR deficiency was observed more frequently in the High-TIL group than in the Low-TIL group (p < 0.01). Progression-free survival (PFS) and overall survival (OS) were better in the High-TIL group than in the Low-TIL group (both p < 0.01). Multivariate analysis revealed that TIL status was a prognostic factor for PFS (hazard ratio [HR] (95% confidence interval [CI]) 0.61 (0.43-0.87); p < 0.01) and OS (HR (95% CI) 0.54 (0.33-0.86); p = 0.01).
    CONCLUSION: TILs evaluated using AI could accurately and significantly predict the prognosis of EC. Further studies are needed to establish new methods for evaluating TILs in ECs.
    Keywords:  artificial intelligence; endometrial carcinoma; mismatch protein repair; prognosis; tumor‐infiltrating lymphocytes
    DOI:  https://doi.org/10.1002/cnr2.70535
  12. Front Immunol. 2026 ;17 1800533
       Background: T cell-based immunotherapies have improved outcomes in lung adenocarcinoma (LUAD), yet many patients develop primary or acquired resistance. Tumor-intrinsic mechanisms that suppress CD8+ T cell function remain incompletely understood.
    Methods: Public LUAD transcriptomic datasets were analyzed to assess the association of ATPase family AAA domain-containing protein 2 (ATAD2) with prognosis and immune infiltration. Atad2-deficient LUAD cell lines were generated using CRISPR/Cas9 and co-cultured with activated CD8+ T cells to evaluate cytotoxicity, cytokine production, PD-1 expression and survival. The mediating role of lactic acid (LA) was confirmed using conditioned medium exposure, exogenous LA supplementation, and LDHA overexpression rescue experiments. ATAD2-mediated transcriptional regulation of LDHA was investigated by ChIP-qPCR and c-Myc overexpression. Subcutaneous tumor models were used to determine the effects of Atad2 deletion on LA accumulation, CD8+ T cell infiltration, tumor growth, and response to anti-PD-1 therapy.
    Results: ATAD2 was significantly upregulated in LUAD and correlated with poor survival and decreased CD8+ T cell infiltration. Atad2 deletion enhanced CD8+ T cell function and survival, effects reversed by exogenous LA. Mechanistically, ATAD2 enhanced c-Myc-dependent LDHA transcription, leading to increased lactic acid production and an immunosuppressive microenvironment. LDHA overexpression restored LA levels and reversed the immune-activating effects of Atad2 loss. In vivo, Atad2 deficiency reduced intratumoral LA, remodeled the immunosuppressive microenvironment, increased CD8+ T cell infiltration, inhibited tumor growth, and improved sensitivity to anti-PD-1 therapy.
    Conclusions: ATAD2 drives immunotherapy resistance in LUAD by activating an ATAD2-LDHA-LA axis that impairs CD8+ T cell function. Targeting ATAD2 may broadly restore antitumor immunity and enhance the efficacy of T cell-based immunotherapies.
    Keywords:  ATAD2; LDHA; T cell therapy resistance; lactic acid; lung adenocarcinoma
    DOI:  https://doi.org/10.3389/fimmu.2026.1800533
  13. Zhonghua Bing Li Xue Za Zhi. 2026 Apr 08. 55(4): 346-352
      Objective: To assess the utility of histopathological and immunohistochemical characteristics in identifying POLE-mutated (POLEmut) endometrial carcinoma (EC). Methods: A total of 1 541 EC cases that underwent molecular classification at Peking University Third Hospital from January 2018 to December 2024 were included. Cases were categorized into POLEmut and non-POLEmut groups (including p53-abnormal, mismatch repair-deficient, and no specific molecular profile subtypes). A comparative analysis of histopathological features, mismatch repair (MMR) protein expression, and p53 immunostaining patterns was performed. A multivariable logistic regression-derived prediction model for POLEmut status was developed and internally validated. Results: POLEmut tumors showed significantly higher frequencies of prominent peritumoral lymphocytes (PTLs) and tumor-infiltrating lymphocytes (TILs), high-grade nuclei, bizarre nuclei, clear cytoplasm, and ambiguous morphology compared with non-POLEmut tumors (all P<0.05). Multivariable analysis identified severe PTLs/TILs infiltration, high-grade nuclei, ambiguous morphology, and clear cytoplasm as independent positive correlates for POLE mutation status, while aberrant p53 expression and MMR protein loss were negative correlates. The scoring system showed robust discrimination, with an area under the curve (AUC) of 0.867 in the training set (n=1 319) and 0.873 in the test set (n=222). At the ≥3- point cutoff, it provided a sensitivity of 80.8%, specificity of 66.3%, and negative predictive value (NPV) of 96.3% in the test set. Calibration analysis indicated good overall performance (Brier score=0.045), though local miscalibration was observed in intermediate-and low-risk subgroups. Conclusions: This POLEmut scoring system achieves high sensitivity and high NPV for initial screening of POLEmut EC. Despite a relatively low positive predictive value requiring confirmatory sequencing, it effectively enriches candidates needing POLE gene sequencing in resource-limited settings. Future multicenter validation is warranted to assess its clinical utility.
    DOI:  https://doi.org/10.3760/cma.j.cn112151-20250820-00564
  14. Cancer Epidemiol Biomarkers Prev. 2026 Apr 08.
       BACKGROUND: While males exhibit higher colorectal cancer (CRC) incidence and mortality rates than females, the underlying mechanisms remain unclear. We hypothesized that females mount stronger anti-tumor T cell responses, contributing to their improved survival.
    METHODS: Tumor samples from a discovery cohort (MECC, N=2,750) and an independent replication cohort (Spanish study, N=444) underwent immunosequencing to quantify T cell receptor (TCR) abundance and clonality. Tumor-infiltrating lymphocytes per high powered field (TILs/hpf) were also scored in the discovery cohort. Multivariable logistic regression estimated odds ratios (ORs) for the associations between sex and T cell metrics. The data were then stratified by sex, and multivariable Cox proportional hazards regression estimated hazard ratios (HRs) for the associations between T cell metrics and 5-year overall and CRC-specific survival, adjusting for known prognostic indicators.
    RESULTS: Multivariable analysis demonstrated no association between sex and TCR abundance, clonality, or TILs/hpf (p>0.05 for all) in both discovery and replication cohorts. In multivariable survival analysis, higher TCR abundance and TILs/hpf were consistently associated with improved survival across sexes in both cohorts. TCR clonality showed inconsistent associations across cohorts and sexes. Importantly, formal interaction testing showed no significant interaction between sex and T cell metrics in relation to survival outcomes for both cohorts.
    CONCLUSIONS: We observed no significant sex differences in CRC-associated T cell responses and no significant interaction between sex and T cell responses in relation to survival.
    IMPACT: Sex differences in CRC are unlikely to be explained by differences in the robustness and diversity of tumor-associated T cell responses.
    DOI:  https://doi.org/10.1158/1055-9965.EPI-25-1579