bims-tuinly Biomed News
on Tumor-infiltrating lymphocytes therapy
Issue of 2026–08–30
seventeen papers selected by
Pierpaolo Ginefra, Ludwig Institute for Cancer Research



  1. Oncol Res. 2026 ;34(9): 9
      Cervical cancer, particularly its advanced stages, requires novel therapeutic paradigms. Cellular immunotherapy exploits the constitutive expression of HPV E6/E7 oncoproteins as near-ideal tumor-specific antigens. This review systematically evaluates four principal platforms under investigation: tumor-infiltrating lymphocytes (TILs), TCR-engineered T cells, CAR-T cells, and CAR-NK cells. We critically analyze the preclinical rationale, clinical trial landscape, safety considerations, and manufacturing challenges for each modality. TIL therapy has achieved durable complete responses and an FDA Breakthrough Therapy designation. TCR-T cells enable precise targeting of intracellular viral epitopes but are HLA-restricted. CAR-T cells offer potent, MHC-independent recognition, yet face on-target/off-tumor toxicity and a suppressive tumor microenvironment. CAR-NK cells present a favorable safety profile and off-the-shelf potential. We conclude that the future of this field lies in rational combination strategies (e.g., with immune checkpoint blockade) and next-generation engineering (e.g., armored CARs, logic gates, allogeneic platforms) to overcome manufacturing complexity, toxicity, and high costs. Overcoming these barriers is essential to extend these therapies to resource-limited settings where the burden of cervical cancer is highest.
    Keywords:  Cell therapy; T-cell receptor (TCR)-engineered T cells; cervical cancer; chimeric antigen receptor (CAR)-T cells; clinical trials; immunotherapy; tumor-infiltrating lymphocytes
    DOI:  https://doi.org/10.32604/or.2026.084736
  2. Appl Immunohistochem Mol Morphol. 2026 Aug 25.
      Preferentially expressed antigen in melanoma (PRAME) expression has been described in Merkel cell carcinoma (MCC), but its clinicopathologic and biological significance remains incompletely characterized. We investigated PRAME expression in MCC and its relationship with Merkel cell polyomavirus (MCPyV) status, PD-L1 expression, tumor-infiltrating lymphocytes (TILs), clinicopathologic features, and clinical outcome. Thirty-five MCC cases from 3 centers were retrospectively reviewed. Histopathologic features and immunohistochemical expression of PRAME, PD-L1, MCPyV, and p53 were reassessed. PRAME positivity was defined as staining extent scores of 3+ or 4+ combined with at least moderate staining intensity. TILs were evaluated on hematoxylin and eosin sections. Clinicopathologic correlations were assessed statistically, and overall survival and distant metastasis-free survival were analyzed using Kaplan-Meier and Cox regression methods. PRAME expression was identified in 10 of 33 evaluable tumors (30.3%). Most positive cases showed diffuse nuclear staining, although one tumor demonstrated heterogeneous PRAME expression. MCPyV positivity was seen in 51.4% of cases, and PRAME expression was more frequent in MCPyV-positive tumors (P=0.057). Combined PRAME/PD-L1 positivity was associated with higher TIL density (P=0.018). PRAME expression was not associated with clinicopathologic parameters or survival. Lower PD-L1 expression (CPS <1) was independently associated with shorter overall survival. PRAME was expressed in approximately one-third of MCCs. PRAME expression was not independently associated with survival outcomes. Higher expression rates in MCPyV-positive tumors and associations with selected immune-related parameters warrant further investigation.
    Keywords:  Merkel cell carcinoma; Merkel cell polyomavirus; PD-L1; PRAME; immunohistochemistry; tumor-infiltrating lymphocytes
    DOI:  https://doi.org/10.1097/PAI.0000000000001352
  3. Endocr Relat Cancer. 2026 Aug 24. pii: ERC-26-0116. [Epub ahead of print]
      MammaPrint® refines risk stratification in early oestrogen receptor-positive, HER2-negative breast cancer, evolving from a binary to a four-tier classification (UltraLow, Low, High-Risk1, High-Risk2). The relationship between routine histopathological features, immune infiltration and genomic risk within this framework remains incompletely characterised in luminal disease. We retrospectively analysed 492 luminal breast carcinomas with available MammaPrint® results. Clinicopathological variables (including histological subtype, grade, Ki-67, hormone receptor expression, lymphovascular invasion (LVI) and HER2-low status) were recorded. Stromal tumor-infiltrating lymphocytes (TILs) were quantified according to Salgado et al. criteria and spatially categorised as immune-deserted, stromal-restricted, immune-excluded or inflamed patterns. CD4 and CD8 infiltration was assessed by immunohistochemistry on tissue microarrays. Associations with binary and four-tier MammaPrint® categories were examined using multivariable models. High-Risk tumours (41%) were enriched for increased grade, Ki-67 and LVI; and lower PR expression. In High-Risk inflamed spatial patterns were more frequent and median TILs levels were significantly higher compared with Low-Risk (15% vs. 5%, p<0.001). CD4 and CD8 infiltration increased with genomic risk; and CD4 retained a modest but statistically significant association after adjustment for conventional pathological variables. In the four-tier model, UltraLow/Low tumours showed minimal TILs and were enriched for invasive lobular carcinoma, whereas High-Risk1/High-Risk2 displayed progressively higher proliferative and immune features. No association was observed between HER2-low status and genomic risk. Immune infiltration parallels proliferative and genomic risk gradients in luminal breast cancer. These findings indicate that immune descriptors align with the genomic risk continuum, although their independent prognostic contribution beyond established genomic assays requires further evaluation.
    Keywords:  Breast Cancer; HER2-Low; MammaPrint; TILs
    DOI:  https://doi.org/10.1530/ERC-26-0116
  4. Gels. 2026 Aug 01. pii: 678. [Epub ahead of print]12(8):
      Hydrogel-enabled adoptive cell therapy (ACT) offers a localized and controllable strategy for improving cellular immunotherapy in solid tumors. Hydrogels can enhance cell retention and persistence, support immune cell function within the tumor microenvironment, and reduce systemic toxicity associated with broadly delivered immune stimulants. However, delivery of living immune cells imposes practical constraints on hydrogel selection, including cytocompatible encapsulation, minimal handling and injection stress, adequate transport of oxygen and soluble cues, and an appropriate balance between local retention and timely cell egress. This review summarizes natural, synthetic, and hybrid hydrogel platforms and compares physical/supramolecular assembly, covalent and enzymatic crosslinking, and photo-crosslinking. Injectable in situ-forming depots and shear-thinning/self-healing gels are highlighted for locoregional administration. Key design and reporting dimensions of hydrogels are linked to immune cell outcomes relevant to ACT. These properties include mechanics and viscoelasticity, porosity and mass transport, degradability and remodeling, bioadhesion and extracellular matrix (ECM) mimicry, and immunogenicity versus immune shielding. Finally, a cell-type-tailored framework is presented for chimeric antigen receptor T (CAR-T), T cell receptor-engineered T (TCR-T), and tumor-infiltrating lymphocyte (TIL) products, natural killer (NK) cells, and dendritic cells (DCs) or macrophage/monocyte-derived effectors. Distinct biological requirements are used to motivate corresponding material architectures and cue presentation strategies. The review also provides quantitative reporting guidance, identifies evidence gaps for γδ T cells, and discusses in vivo validation, combination ACT strategies, and translational handling constraints.
    Keywords:  CAR-NK cells; CAR-T; adoptive cell therapy; cancer immunotherapy; dendritic cells; gamma-delta T cells; granular hydrogels; immune cell delivery; injectable hydrogels; macrophage engineering
    DOI:  https://doi.org/10.3390/gels12080678
  5. Front Oncol. 2026 ;16 1904492
      Targeted therapy and immune checkpoint inhibition have improved the treatment of non-small cell lung cancer (NSCLC); however, it remains one of the leading causes of cancer-related mortality worldwide. While all these therapeutic strategies have yielded clinical benefit in specific patient groups, resistance and tumor heterogeneity, short-term responses, and immune evasion remain current challenges in long-term therapeutic success. These constraints have led to the exploration of new precision immuno-oncology approaches for more specific targeting more efficient stimulation of antitumor immune responses and overcoming resistance mechanisms. Among these new modalities, antibody-drug conjugates (ADCs), therapeutic cancer vaccines, and adoptive cellular therapies are significantly changing the systemic treatment paradigm in NSCLC. Simultaneously, advances in neoantigen discovery, mRNA vaccine technology, and personalized vaccine design have renewed interest in therapeutic cancer vaccines for generating durable antitumor immune responses. In parallel, adoptive cellular immunotherapies, such as chimeric antigen receptor (CAR)-T cells, natural killer (NK)-cells, and tumor-infiltrating lymphocytes (TILs) are growing as effective approaches to improve immune-mediated tumor eradication in NSCLC. This manuscript summarizes the recent developments of these next-generation precision immuno-oncology platforms, highlighting their working mechanisms, progress in translation, and clinical use. It also explores strategies for combinational therapy, predictive biomarkers, inhibitors of tumor microenvironment modulation, and mechanisms of resistance in the context of therapeutic efficacy and patient selection. Collectively, these developing immunotherapeutic platforms as a whole constitute a brighter paradigm for more personalized and effective systemic treatment approaches in NSCLC.
    Keywords:  adoptive cell therapy; antibody-drug conjugates (ADCs); engineered immune cells; non-small cell lung cancer (NSCLC); precision immuno-oncology; therapeutic cancer vaccines
    DOI:  https://doi.org/10.3389/fonc.2026.1904492
  6. Front Med (Lausanne). 2026 ;13 1896491
       Background: Programmed death-ligand 1 (PD-L1) expression and CD8+ tumor-infiltrating lymphocyte (TIL) density are established biomarkers of tumor-immune interaction in breast cancer; however, the biological and prognostic significance of their combined assessment across molecular subtypes remains incompletely defined. This study aimed to characterize combined PD-L1/CD8 immune phenotypes, evaluate their clinicopathological associations, and explore their relationship with survival outcomes in a molecularly heterogeneous breast cancer cohort.
    Methods: This multicenter retrospective study included 137 patients with invasive breast carcinoma from two institutions. PD-L1 expression was evaluated separately in tumor cells (TCs) and tumor-infiltrating lymphocytes (TILs) by immunohistochemistry. CD8+ TIL density was also assessed immunohistochemically, and tumors were classified as CD8-high or CD8-low using a predefined threshold of ≥50%. Based on combined PD-L1 and CD8 status, cases were categorized into four immune phenotypes: Type I (PD-L1+/CD8-high), Type II (PD-L1+/CD8-low), Type III (PD-L1-/CD8-high), and Type IV (PD-L1-/CD8-low). Associations between immune phenotypes, clinicopathological characteristics, and survival outcomes were analyzed using appropriate statistical methods.
    Results: PD-L1 positivity was observed in 62 of 137 tumors (45.3%) and was significantly associated with higher histological grade (p = 0.020), but not with pathological tumor stage, clinical stage group, or lymph node status. A significant positive correlation was identified between PD-L1 expression in the immune-cell compartment and CD8+ TIL density (Spearman ρ = 0.453, p < 0.001), whereas no correlation was observed between tumor cell PD-L1 expression and CD8+ TIL density (ρ = -0.021, p = 0.812). In a hypothesis-generating subgroup comparison limited by small cell counts, CD8-high status was more frequent in Luminal B than in triple-negative breast cancer (36.0 vs. 13.7%; p = 0.036). The most common immune phenotype was Type IV (43.1%), whereas Type I accounted for 9.5% of cases. In exploratory analysis, patients with the Type I phenotype had the highest mortality rate (23.1%) and the shortest median follow-up-based survival estimate (37 months) among the four groups (log-rank p = 0.014); given the small number of events (11 deaths overall, 3 within the Type I subgroup) and the use of follow-up duration with cross-sectional mortality rather than fully annotated time-to-event data, these findings should be interpreted as exploratory associations rather than definitive prognostic evidence.
    Conclusions: Combined PD-L1/CD8 immune phenotyping identifies biologically distinct immune microenvironmental states in breast cancer beyond conventional molecular subtype classification. While PD-L1 positivity was associated with high histological grade and immune-cell infiltration, the PD-L1+/CD8-high phenotype demonstrated the least favorable survival profile in this predominantly hormone receptor-positive cohort on unadjusted analysis, an association that was attenuated to borderline significance after adjustment for baseline metastatic burden. These findings support the concept that concurrent PD-L1 expression and abundant CD8+ T-cell infiltration may not invariably reflect effective antitumor immunity and may instead be consistent with an exhausted or functionally impaired immune state. If validated in larger cohorts with direct assessment of T-cell exhaustion markers, combined PD-L1/CD8 phenotyping may provide clinically relevant insights for immune stratification and patient selection in immunotherapy-oriented approaches.
    Keywords:  CD8; PD-L1; adaptive immune resistance; breast cancer; immune phenotype; t cell exhaustion; tumor microenvironment; tumor-infiltrating lymphocytes
    DOI:  https://doi.org/10.3389/fmed.2026.1896491
  7. Urol Oncol. 2026 Aug 22. pii: S1078-1439(26)00659-9. [Epub ahead of print]44(10): 643-651
      CD103+ tissue-resident memory T cells are emerging mediators of antitumor immunity whose prognostic significance in bladder cancer, across muscle-invasive and metastatic urothelial carcinoma, remains undefined at a meta-analytic level. We performed a systematic review and meta-analysis of cohorts with histologically confirmed muscle-invasive bladder cancer or metastatic urothelial carcinoma, comparing high vs. low CD103+ tumor-infiltrating lymphocyte density assessed by immunohistochemistry or ITGAE mRNA expression, with overall survival endpoint. PubMed, Embase, Scopus, and Cochrane CENTRAL were searched from inception through March 2026. Pooled hazard ratios (HR) with 95% confidence intervals (CIs) were estimated using a restricted maximum likelihood random-effects model. Subgroup analyses were performed by treatment context, disease stage, and assessment method. The protocol was registered at OSF (u36xv). Three studies comprising 6 cohorts were included. High CD103⁺ infiltration was significantly associated with prolonged overall survival (HR: 0.50, 95% CI: 0.30-0.83). A significant treatment-context interaction (P = 0.005) favored patients undergoing surgery with adjuvant chemotherapy (HR: 0.20) over those receiving immunotherapy (HR: 0.69). Stage-stratified analysis showed a significant interaction (P = 0.003), with pronounced benefit in muscle-invasive bladder cancer (HR: 0.27) but a non-significant trend in metastatic urothelial carcinoma (HR: 0.79). Immunohistochemistry-based cohorts showed a numerically larger effect than ITGAE mRNA cohorts. High CD103⁺ tumor-infiltrating lymphocyte infiltration may be associated with improved overall survival in bladder cancer, particularly in muscle-invasive bladder cancer patients undergoing surgery with adjuvant chemotherapy. Prospective validation in larger, stage-homogeneous cohorts is warranted to establish CD103 as a prognostic biomarker. These findings are hypothesis-generating and CD103 assessment is not currently ready for clinical use.
    Keywords:  CD103; Muscle-invasive bladder cancer; Tumor infiltration lymphocytes; Urothelial cancer
    DOI:  https://doi.org/10.1016/j.urolonc.2026.07.031
  8. Lancet Oncol. 2026 Sep;pii: S1470-2045(26)00339-6. [Epub ahead of print]27(9): 1181-1192
    International Immuno-Oncology Biomarker Working Group
       BACKGROUND: Tumour-infiltrating lymphocytes (TILs) are a robust prognostic marker in patients with triple-negative breast cancer. Artificial intelligence (AI)-derived computational tools assessing TILs could improve efficiency, but require independent validation against clinical outcomes. We aimed to compare the prognostic performance of AI-derived TIL scores with pathologist-scored TILs in a large, prospectively collected dataset pooled from randomised controlled trials.
    METHODS: CATALINA was an independent, external validation study using prospectively collected long-term clinical outcome data pooled from seven randomised clinical trials conducted at multiple sites. We independently evaluated two previously validated AI pipelines that generate five computationally assessed tumour-infiltrating lymphocyte (cTIL) scores by masked, independent deployment of locked models. cTIL scores were correlated with the mean of the pathologist-scored stromal TILs (sTILs) in 220 digitised haematoxylin and eosin whole slide images in a cohort of patients with early-stage triple-negative or HER-2 positive breast cancer, previously scored by trained pathologists in a TIL-reproducibility study. Prognostic performance was assessed in a separate cohort of patients with early triple-negative breast cancer pooled from seven prospective, randomised adjuvant trials. Multivariable Cox regression models adjusted for clinicopathological factors and study heterogeneity assessed associations of cTIL score and sTIL score with invasive disease-free survival, distant disease-free survival, and overall survival. 5-year discrimination was estimated using time-dependent area under the receiver operating characteristic curve (AUC).
    FINDINGS: Individual data were collated from 1759 patients, of whom 1356 had complete clinicopathological data, pathologist sTIL scores, and cTIL scores available. Modest correlation (r 0·375-0·473) was observed between cTIL scores and the mean pathologist sTIL score. Both sTIL and cTIL were independently associated with 5-year invasive disease-free survival, distant disease-free survival, and overall survival after adjustment for clinicopathological factors (hazard ratio for invasive disease-free survival was 0·73 [95% CI 0·66-0·82]; q<0·0001, distant disease-free survival was 0·70 [0·61-0·79]; q<0·0001, and overall survival was 0·72 [0·63-0·82]; q<0·0001 for sTIL scores and 0·80 [0·73-0·89]; q<0·0001, 0·77 [0·69-0·86]; q<0·0001, and 0·79 [0·70-0·88]; q=0·0002, respectively, for percentage_lymphocyte scores). In models adjusted for clinicopathological variables and sTIL score, cTIL score did not maintain a statistically significant prognostic association. Both sTIL and cTIL scores improved the 5-year AUC over clinicopathological variables alone, while cTIL score did not significantly further improve AUC when combined with clinicopathological variables and sTIL score.
    INTERPRETATION: Two cTIL models deployed entirely without retraining or modification provided statistically significant prognostic information and improved risk discrimination compared with clinicopathological variables alone in this large, platform-based, independent validation study. Although cTIL score did not incrementally improve prognostication compared with models combining clinicopathological variables with sTIL score, these findings support the application of cTILs as a reproducible prognostic biomarker, particularly in settings where routine or widespread pathologist assessment is unavailable.
    FUNDING: Breast Cancer Research Foundation (USA).
    DOI:  https://doi.org/10.1016/S1470-2045(26)00339-6
  9. Lancet Oncol. 2026 Sep;pii: S1470-2045(26)00255-X. [Epub ahead of print]27(9): e420-e433
    International Immuno-Oncology Biomarker Working Group
      Tumour-infiltrating lymphocytes (TILs) are prognostic and predictive biomarkers in breast cancer. High pre-treatment TILs are associated with a favourable prognosis and improved response to systemic therapies. However, the role of TILs in mediating response to radiotherapy in breast cancer remains underexplored, with scarce clinical evidence to date. In this Review, we present an overview of current evidence and potential mechanisms, highlight opportunities for integrating TILs into radiation oncology trials and clinical practice, and call for standardised TIL reporting to accelerate biomarker-driven individualisation of radiotherapy in breast cancer.
    DOI:  https://doi.org/10.1016/S1470-2045(26)00255-X
  10. Cancers (Basel). 2026 Aug 18. pii: 2669. [Epub ahead of print]18(16):
      Background/Objectives: Glioblastoma (GBM) remains a lethal primary CNS malignancy with limited response to immunotherapy. Adoptive cellular therapy (ACT) improves survival in preclinical models, yet tumors ultimately recur. While T cell exhaustion is a common mechanism of resistance, the contribution of dendritic cell (DC) dysfunction remains unclear. We aimed to define mechanisms of immune escape following ACT, focusing on DC function and the role of hypoxia. Methods: Using a murine glioma model (KR158B-luc), mice were treated with ACT consisting of tumor RNA-pulsed DC vaccines and adoptively transferred T cells. Tumor-infiltrating immune populations were analyzed by flow cytometry. DC function was assessed using T cell activation assays. Bulk RNA sequencing and gene set enrichment analysis were performed on sorted DCs. Hypoxia was modeled in vitro, and HIF1α was perturbed using CRISPR-mediated knock-out. Results: ACT significantly increased survival but did not prevent tumor recurrence. Escaped tumors contained abundant cytotoxic, non-exhausted T cells, indicating that T cell dysfunction was not the primary driver of recurrence under ACT. Instead, tumor-associated DCs exhibited impaired T cell activation despite preserved antigen uptake. Transcriptomic analyses revealed reduced antigen presentation and co-stimulatory signaling, alongside increased expression of tolerogenic factors. ACT-treated tumors demonstrated heightened hypoxia pathway activation, with elevated HIF1α expression in DCs. Hypoxia induced DC tolerogenic programs and reduced their ability to activate T cells, an effect partially reversed by HIF1α disruption. Increased immune infiltration and inflammation following ACT further amplified hypoxia signaling and enhanced DC tolerance. Conclusions: DC dysfunction is one of the key mechanisms of immune escape following ACT in glioma. Hypoxia-driven tolerization of DCs impairs sustained anti-tumor immunity, highlighting the hypoxia-DC axis as a promising therapeutic target to enhance immunotherapy efficacy.
    Keywords:  adoptive cellular therapy; dendritic cell dysfunction; hypoxia pathway; immune evasion
    DOI:  https://doi.org/10.3390/cancers18162669
  11. Lancet Oncol. 2026 Sep;pii: S1470-2045(26)00247-0. [Epub ahead of print]27(9): 1168-1180
    APHINITY Steering Committee and Investigators and The International Immuno-Oncology Biomarker Working Group
       BACKGROUND: Stromal tumour-infiltrating lymphocytes (sTILs) are prognostic in early-stage HER2-positive breast cancer, but their role in the context of dual HER2 blockade remains undefined. We evaluated manual, digital, and artificial intelligence (AI)-based sTIL quantification, together with AI-derived spatial metrics, for prognostic and treatment-benefit stratification using tumour samples from the phase 3 APHINITY trial.
    METHODS: In the APHINITY trial, 4805 patients were randomly assigned to receive chemotherapy plus trastuzumab with pertuzumab or chemotherapy plus trastuzumab with placebo. Median follow-up was 74·1 months (IQR 68·3-75·4). We analysed 4262 haematoxylin and eosin-stained images using manual assessment, an automated digital approach, AI-based lymphocyte quantification (AI percentage lymphocytes), and two AI-derived spatial features (AI-TIL and immune hotspot). Interobserver reproducibility was assessed in 262 randomly chosen tumour samples scored independently by five pathologists. Multivariable Cox models were used to assess associations between TIL levels and invasive disease-free survival (primary outcome in APHINITY), distant recurrence-free interval, and overall survival. The heterogeneity of pertuzumab benefit was evaluated using subgroup analyses, subpopulation treatment effect pattern plot analyses, and nested Cox models with treatment-by-biomarker interaction terms.
    FINDINGS: Manual scoring showed high interobserver reproducibility (intraclass correlation coefficient 0·84 [95% CI 0·79-0·88]). Concordance between manual and automated methods was modest. AI-based scoring (AI percentage lymphocytes) reclassified 120 (11·6%) of 1035 node-positive tumours from immune-low (by manual scoring) to immune-high; this subgroup of patients showed greater separation of 5-year invasive disease-free survival curves between pertuzumab and placebo groups compared with patients whose tumours were concordantly classified as immune-low by both manual and AI-based approaches. Higher levels of TILs were associated with improved invasive disease-free survival for all sTIL measurement approaches and spatial measurements (hazard ratios [HRs] 0·41-0·93). Pertuzumab was associated with improved invasive disease-free survival at higher sTIL levels across all measurement approaches (HRs 0·36-0·48), but was not associated with higher values of spatial measures. The largest 6-year absolute improvements with pertuzumab were observed in patients with node-positive disease whose tumours scored in the highest level of immune infiltration of manual sTIL scoring (≥70·0%; mean absolute improvement 12·1 percentage points [SD 2·8]). In nested prognostic and predictive models, AI-based immune hotspot scores provided the most consistent additional information when combined with any sTIL measurement (all p<0·010).
    INTERPRETATION: Standardised manual sTIL scoring was reproducible, and digital and AI-based methods showed consistent prognostic stratification and potential for treatment-benefit stratification despite only modest correlation between platforms. AI spatial metrics provided complementary information beyond sTIL density and could support more scalable immune assessment. Future studies are needed to validate these approaches in independent cohorts and to clarify their clinical utility for stratifying contemporary HER2-directed therapies.
    FUNDING: None.
    DOI:  https://doi.org/10.1016/S1470-2045(26)00247-0
  12. Med Mol Morphol. 2026 Aug 24.
      Immune checkpoint inhibitors (ICIs) have become an important therapeutic option for oral cancers; however, reliable biomarkers predicting treatment efficacy remain limited. In this study, we investigated the association between intratumoral immune cell subsets, regional lymph node (RLN) immune status, and clinical responses to ICIs in patients with recurrent oral cancer. Pretreatment tumor tissues and RLNs were analyzed by immunohistochemistry to evaluate tumor-infiltrating lymphocytes, including CD8+, CD103+, CD3+, ICOS+, and CD163+ cells, as well as programmed death-ligand 1 (PD-L1) expression and CD169+ sinus macrophages. Treatment responses were assessed according to RECIST version 1.1. Responders to ICIs exhibited higher densities of CD8+ and CD103+ T cells compared with non-responders, whereas no significant associations were observed for CD3+, ICOS+, CD163+ cells, or PD-L1 expression. Elevated pretreatment serum C-reactive protein (CRP) levels were associated with poorer responses. CD169+ sinus macrophages in RLNs did not correlate significantly with treatment efficacy or T-cell infiltration. These findings suggest that intratumoral effector and tissue-resident memory-like T-cell infiltration, together with systemic inflammatory status, may influence ICI efficacy in recurrent oral cancer, and could improve patient stratification for immunotherapy.
    Keywords:  CD103; CD8; Immune checkpoint inhibitors (ICIs); Predictive biomarkers; Recurrent oral cancer; Tissue-resident memory T cells
    DOI:  https://doi.org/10.1007/s00795-026-00473-3
  13. Front Immunol. 2026 ;17 1913598
      CD8+ T cells are core effector cells of adaptive immunity. However, in chronic infection and tumor microenvironments, they often lose their effector functions. Under persistent antigenic and metabolic stress, CD8+ T cells may progressively acquire a stable dysfunctional state termed T cell exhaustion. Post-translational modifications (PTMs) constitute a rapid and dynamic regulatory system that targets four core functional modules: membrane receptor signaling, transcription factors, metabolic enzymes, and epigenetic regulators. These modules are interconnected through a multi-layered PTM network. Within this network, PTMs orchestrate a stepwise cascade that proceeds from signal initiation through metabolic reprogramming to transcriptional and epigenetic remodeling. Ultimately, this cascade consolidates the exhaustion program via stable epigenetic memory. Accordingly, we propose a "PTM-driven signal-metabolism-epigenetic locking model" as the central framework of this review. Focusing on five key PTMs, namely phosphorylation, ubiquitination, glycosylation, acetylation, and lactylation, we elucidate how these modifications cooperatively regulate CD8+ T cell exhaustion. Critically, the PTM network drives progressive locking of the exhausted state through three epigenetic layers: DNA methylation, chromatin remodeling, and histone modifications. These layers collectively contribute to the progressive stabilization of the exhausted state over time. This framework integrates transient environmental signals, metabolic fluctuations, and transcriptional changes into permanent cell fate decisions. Building upon this mechanistic understanding, the review further explores novel strategies targeting the PTM network to reverse exhaustion and enhance immunotherapeutic efficacy. This review provides a clear and comprehensive framework for understanding how PTMs govern CD8+ T cell exhaustion and lays a solid foundation for the development of next-generation immunotherapies.
    Keywords:  CD8+ T cells; cancer immunotherapy; epigenetic locking; post-translational modifications; t cell exhaustion
    DOI:  https://doi.org/10.3389/fimmu.2026.1913598
  14. JCO Oncol Pract. 2026 Aug 25. OP2600407
       PURPOSE: Although inpatient toxicity associated with tumor-infiltrating lymphocyte (TIL) therapy and interleukin-2 administration is well characterized, risks facing patients after hospital discharge are less understood. Better characterization of outpatient adverse events (AEs) could guide the optimal frequency and duration of follow-up in delivering care for this growing patient population.
    METHODS: We conducted a retrospective analysis of all patients with advanced melanoma discharged from Memorial Sloan Kettering Cancer Center after receiving investigational or commercial lifileucel from October 2020 to October 2024. We reviewed the incidence and timing of new treatment-related AEs (TRAEs), blood product administration, and readmission among all patients from the time of hospital discharge to the time of the start of a subsequent systemic therapy or death.
    RESULTS: Over a median follow-up of 5 months from discharge (IQR, 3-18), two patients (3.9%) developed new grade 3 TRAEs, including grade 3 neutropenia and hypoxia occurring 73 and 104 days after discharge, respectively. Four patients (7.8%) were readmitted for TRAEs including cytopenias, dyspnea, and syncope, at a median of 49 days (IQR, 22-81) after discharge. Twelve patients (24%) received outpatient transfusions, including a median of two units of packed RBCs (IQR, 1-4) and four units of platelets (IQR, 2-4).
    CONCLUSION: Overall, rates of new severe toxicity and treatment-related readmissions were low among patients discharged after lifileucel. These findings support individualized follow-up in this population compared with other cellular therapies and highlight the need for specific postdischarge guidelines for patients receiving TIL therapy.
    DOI:  https://doi.org/10.1200/OP-26-00407
  15. ACS Cent Sci. 2026 Aug 26. 12(8): 1223-1236
      Interleukin-2 (IL-2) is a potent mediator of T-cell activation with significant potential for cancer immunotherapy, yet its clinical utility is severely constrained by its narrow therapeutic window. Here we report a chemically masked IL-2 prodrug (Cm-proIL2) that enables tumor-microenvironment-responsive cytokine activation through tumor-associated protease cleavage. Site-specific conjugation of a poly-(ethylene glycol) (PEG) moiety selectively masks peripheral receptor engagement, while PEG removal within the tumor microenvironment restores IL-2 receptor binding and reduces molecular size, thereby enhancing intratumoral lymphocyte penetration and effector T cell functionality. Building on this modular platform, we further engineered a PD-1-targeted nanobody fusion, PD1-Cm-proIL2, to enable the cis delivery of IL-2 activity to PD-1+ tumor-infiltrating T cells. PD1-Cm-proIL2 induces robust antitumor immunity, resulting in complete tumor regression and durable protection upon tumor rechallenge in a murine colorectal cancer model. Together, these findings demonstrate the feasibility of chemically masked, tumor-responsive cytokine activation as a strategy for improving the therapeutic index of IL-2-based immunotherapies.
    DOI:  https://doi.org/10.1021/acscentsci.6c00344
  16. J Clin Med. 2026 Aug 13. pii: 6266. [Epub ahead of print]15(16):
      Background: Neoadjuvant chemotherapy followed by interval debulking surgery is an established treatment strategy for selected patients with advanced epithelial ovarian cancer. However, simple postoperative prognostic tools integrating pre-treatment disease extent and post-treatment pathological stage remain limited. The neoadjuvant rectal (NAR) score was originally developed as a composite stage-migration endpoint in rectal cancer and has subsequently been explored in other solid tumors. We evaluated the feasibility and prognostic value of an ovarian NAR-like score (oNAR) in patients with advanced ovarian cancer treated with neoadjuvant chemotherapy and interval debulking surgery. Methods: This single-center retrospective cohort included patients with advanced ovarian cancer treated with platinum-taxane-based neoadjuvant chemotherapy followed by interval debulking surgery. The oNAR score was calculated using clinical T category before neoadjuvant chemotherapy and pathological T and N categories after interval surgery: oNAR = [5 × ypN - 3 × (cT - ypT) + 12]2/9.61. The primary analysis evaluated oNAR as a continuous score. Low, intermediate, and high oNAR categories based on the original rectal NAR thresholds were used only for exploratory visualization. The primary endpoint was progression-free survival (PFS). Cox regression, Kaplan-Meier analysis, log-rank testing, Harrell concordance index, and exploratory ROC analysis were used. Results: Among 74 reviewed records, 73 patients had sufficient cT, ypT, and ypN data for oNAR calculation and were included in the primary analysis. Thirty-one PFS events and 10 deaths occurred. The median oNAR was 14.98 (IQR, 14.98-30.07). As a continuous variable, higher oNAR was associated with shorter PFS (HR per 1-point increase, 1.036; 95% CI, 1.010-1.061; p = 0.0055), corresponding to an HR of 1.42 per 10-point increase. The Harrell C-index for PFS was 0.669. In a parsimonious comparison, oNAR showed higher discrimination than ypN alone and discrimination comparable to a combined ypT/ypN model. PFS differed significantly across low-, intermediate-, and high-oNAR groups (log-rank p = 0.0053). Median PFS was not reached in the low-oNAR group, compared with 13.47 months in the intermediate group and 12.09 months in the high group. The association persisted in sensitivity analyses restricted to patients with complete/optimal cytoreduction, maximal cytoreduction, and high-grade serous histology. Conclusions: The oNAR score was feasible to calculate using routinely available clinical and pathological staging variables and was significantly associated with PFS after neoadjuvant chemotherapy and interval debulking surgery. These findings support oNAR as a feasible stage-migration-based prognostic summary that may help capture post-NACT pathological T/N information and warrants external validation in larger ovarian cancer cohorts.
    Keywords:  interval debulking surgery; neoadjuvant chemotherapy; neoadjuvant rectal score; oNAR; ovarian cancer; prognostic score; progression-free survival
    DOI:  https://doi.org/10.3390/jcm15166266