---
title: "Spatial transcriptomics links lipid and mitochondrial metabolism to T cell exclusion in esophageal"
id: "british-journal-of-cancer-1-spatial-transcriptomic-sequencing-identifies-lipid-metabolism-and-mitochondrial"
canonical_url: "https://medichelpline.com/clinical-feed/british-journal-of-cancer-1-spatial-transcriptomic-sequencing-identifies-lipid-metabolism-and-mitochondrial"
content_type: "clinical_feed_article"
specialty: "Oncology"
source_name: "British Journal of Cancer"
source_url: "https://www.nature.com/articles/s41416-026-03635-3"
published_at: "2026-10-21T12:00:00.000Z"
evidence_level: "Journal Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Spatial transcriptomics links lipid and mitochondrial metabolism to T cell exclusion in esophageal
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/british-journal-of-cancer-1-spatial-transcriptomic-sequencing-identifies-lipid-metabolism-and-mitochondrial
- **Specialty:** [Oncology](https://medichelpline.com/clinical-feed/oncology.md)
- **Primary Source:** British Journal of Cancer
- **Source URL:** [Original Journal Publication](https://www.nature.com/articles/s41416-026-03635-3)
- **Published At:** 2026-10-21T12:00:00.000Z
- **Evidence Rating:** Journal Feed
## Executive GIST (TL;DR)
- Investigators used spatial whole-transcriptome sequencing to compare treatment‑naive esophageal adenocarcinomas (EACs) with low versus high intratumoral **CD8+** T cell density. - The cohort comprised 12 tumours selected by a pathologist for region-of-interest (ROI) analysis; ROIs contained co-localised cancer (CK+) and immune (CD45+) compartments. - Authors validated spatial findings using bulk transcriptome data from **TCGA** and metabolic profiling by **SCENITH** performed on fresh tumour specimens (n = 5). - Cancer cell transcriptomes clustered by T cell infiltration status; **CD8-low** tumours showed reduced antigen-presentation gene expression and upregulation of **lipid metabolism** and **mitochondrial** respiration pathways. - In contrast, cancer cells from **CD8-high** tumours exhibited higher cytokine signalling and apoptotic pathway activity, according to the spatial data. - Analysis of the CD45+ (immune) compartments revealed enrichment of the **PGC-1α** pathway in CD8-low tumours, a signature linked to mitochondrial biogenesis and immunosuppressive myeloid phenotypes. - TCGA bulk data supported the spatial transcriptomic observations; the authors reported concordant pathway-level signals. - Functional metabolic testing with SCENITH indicated macrophages from CD8-low tumours were more dependent on mitochondrial metabolism. - The study team concluded that impaired antigen presentation and altered mitochondrial/lipid metabolism in cancer cells may drive **T cell exclusion** in EAC and proposed metabolic targeting as a hypothesis to improve anti-tumour immunity and response to neoadjuvant chemoradiotherapy. - The source did not report specific therapeutic dosing, interventional trials, or regulatory milestones; it framed metabolic targeting as a hypothesis requiring further mechanistic and translational study.
## Clinical Analysis & Structured Key Points
## Your privacy, your choice We use essential cookies to make sure the site can function. We also use optional cookies for advertising, personalisation of content, usage analysis, and social media, as well as to allow video information to be shared for both marketing, analytics and editorial purposes. By accepting optional cookies, you consent to the processing of your personal data - including transfers to third parties. Some third parties are outside of the European Economic Area, with varying standards of data protection. See our [privacy policy](https://www.nature.com/info/privacy) for more information on the use of your personal data. Manage preferences for further information and to change your choices. Accept all cookies Reject optional cookies [Skip to main content](https://www.nature.com/articles/s41416-026-03635-3#content) Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. Advertisement [ ![British Journal of Cancer](https://media.springernature.com/full/nature-cms/uploads/product/bjc/header-76ac17391903a21e28f15ff5df31f5fa.svg) ](https://www.nature.com/bjc) * [ View all journals ](https://www.nature.com/siteindex) * [ Saved research ](https://www.nature.com/saved-research) * [ Search ](javascript:;) ## Search Search articles by subject, keyword or author Show results from All journals This journal Search [ Advanced search ](https://www.nature.com/search/advanced) ### Quick links * [Explore articles by subject](https://www.nature.com/subjects) * [Find a job](https://www.nature.com/naturecareers) * [Guide to authors](https://www.nature.com/authors/index.html) * [Editorial policies](https://www.nature.com/authors/editorial_policies/) * [Log in](https://idp.nature.com/auth/personal/springernature?redirect_uri=https://www.nature.com/articles/s41416-026-03635-3) * [ Content Explore content ](javascript:;) ## Explore content * [ Research articles ](https://www.nature.com/bjc/research-articles) * [ Reviews & Analysis ](https://www.nature.com/bjc/reviews-and-analysis) * [ News & Comment ](https://www.nature.com/bjc/news-and-comment) * [ Current issue ](https://www.nature.com/bjc/current-issue) * [ Collections ](https://www.nature.com/bjc/collections) * [Follow us on X ](https://twitter.com/BrJCancer) * [Sign up for alerts ](https://journal-alerts.springernature.com/subscribe?journal_id=41416) * [ RSS feed ](https://www.nature.com/bjc.rss) * [ About the journal ](javascript:;) ## About the journal * [ Journal Information ](https://www.nature.com/bjc/journal-information) * [ Open access publishing ](https://www.nature.com/bjc/open-access) * [ Editors ](https://www.nature.com/bjc/editors) * [ Contact ](https://www.nature.com/bjc/contact) * [ Special Issues ](https://www.nature.com/bjc/special-issues) * [ For Advertisers ](https://www.nature.com/bjc/advertising) * [ Subscribe ](https://www.nature.com/bjc/subscribe) * [ Publish with us ](javascript:;) ## Publish with us * [ For Authors & Referees ](https://www.nature.com/bjc/authors-and-referees) * [ Language editing services ](https://authorservices.springernature.com/go/sn/?utm_source=For+Authors&utm_medium=Website_Nature&utm_campaign=Platform+Experimentation+2022&utm_id=PE2022) * [Open access funding](https://www.nature.com/bjc/open-access-funding) * [Submit manuscript ](https://mts-bjcancer.nature.com/) * [ Sign up for alerts ](https://journal-alerts.springernature.com/subscribe?journal_id=41416) * [ RSS feed ](https://www.nature.com/bjc.rss) 1. [nature](https://www.nature.com/) 2. [british journal of cancer](https://www.nature.com/bjc) 3. [articles](https://www.nature.com/bjc/articles?type=article) 4. article Spatial transcriptomic sequencing identifies lipid metabolism and mitochondrial respiration as central features of T cell excluded esophageal adenocarcinomas [ Download PDF ](https://www.nature.com/articles/s41416-026-03635-3.pdf) [ Download PDF ](https://www.nature.com/articles/s41416-026-03635-3.pdf) * Article * [Open access](https://www.springernature.com/gp/open-science/about/the-fundamentals-of-open-access-and-open-research) * Published: 21 October 2026 Cellular and Molecular Biology # Spatial transcriptomic sequencing identifies lipid metabolism and mitochondrial respiration as central features of T cell excluded esophageal adenocarcinomas * [Jasper Sanders](https://www.nature.com/articles/s41416-026-03635-3#auth-Jasper-Sanders-Aff1-Aff2-Aff3) [ORCID: orcid.org/0009-0005-9521-0557](https://orcid.org/0009-0005-9521-0557)[1](https://www.nature.com/articles/s41416-026-03635-3#Aff1),[2](https://www.nature.com/articles/s41416-026-03635-3#Aff2),[3](https://www.nature.com/articles/s41416-026-03635-3#Aff3), * [Nico Hahn](https://www.nature.com/articles/s41416-026-03635-3#auth-Nico-Hahn-Aff4)[4](https://www.nature.com/articles/s41416-026-03635-3#Aff4), * [Emma N. Bos](https://www.nature.com/articles/s41416-026-03635-3#auth-Emma_N_-Bos-Aff1-Aff2-Aff3)[1](https://www.nature.com/articles/s41416-026-03635-3#Aff1),[2](https://www.nature.com/articles/s41416-026-03635-3#Aff2),[3](https://www.nature.com/articles/s41416-026-03635-3#Aff3), * [Deni M. van Schie](https://www.nature.com/articles/s41416-026-03635-3#auth-Deni_M_-Schie-Aff5) [ORCID: orcid.org/0009-0002-3460-3320](https://orcid.org/0009-0002-3460-3320)[5](https://www.nature.com/articles/s41416-026-03635-3#Aff5), * [Isaac J. Nijman](https://www.nature.com/articles/s41416-026-03635-3#auth-Isaac_J_-Nijman-Aff6)[6](https://www.nature.com/articles/s41416-026-03635-3#Aff6), * [Nicole C. T. van Grieken](https://www.nature.com/articles/s41416-026-03635-3#auth-Nicole_C__T_-Grieken-Aff2-Aff7) [ORCID: orcid.org/0000-0001-9992-0760](https://orcid.org/0000-0001-9992-0760)[2](https://www.nature.com/articles/s41416-026-03635-3#Aff2),[7](https://www.nature.com/articles/s41416-026-03635-3#Aff7), * [Donald L. van der Peet](https://www.nature.com/articles/s41416-026-03635-3#auth-Donald_L_-Peet-Aff8)[8](https://www.nature.com/articles/s41416-026-03635-3#Aff8), * [Hanneke W. M. van Laarhoven](https://www.nature.com/articles/s41416-026-03635-3#auth-Hanneke_W__M_-Laarhoven-Aff2-Aff9)[2](https://www.nature.com/articles/s41416-026-03635-3#Aff2),[9](https://www.nature.com/articles/s41416-026-03635-3#Aff9), * [Joep Grootjans](https://www.nature.com/articles/s41416-026-03635-3#auth-Joep-Grootjans-Aff2-Aff3-Aff10)[2](https://www.nature.com/articles/s41416-026-03635-3#Aff2),[3](https://www.nature.com/articles/s41416-026-03635-3#Aff3),[10](https://www.nature.com/articles/s41416-026-03635-3#Aff10), * [Maarten F. Bijlsma](https://www.nature.com/articles/s41416-026-03635-3#auth-Maarten_F_-Bijlsma-Aff5)[5](https://www.nature.com/articles/s41416-026-03635-3#Aff5), * [Jan Van den Bossche](https://www.nature.com/articles/s41416-026-03635-3#auth-Jan-Bossche-Aff4) [ORCID: orcid.org/0000-0002-7852-2891](https://orcid.org/0000-0002-7852-2891)[4](https://www.nature.com/articles/s41416-026-03635-3#Aff4), * [Tanja D. de Gruijl](https://www.nature.com/articles/s41416-026-03635-3#auth-Tanja_D_-Gruijl-Aff1-Aff2)[1](https://www.nature.com/articles/s41416-026-03635-3#Aff1),[2](https://www.nature.com/articles/s41416-026-03635-3#Aff2) & * … * [Sarah Derks](https://www.nature.com/articles/s41416-026-03635-3#auth-Sarah-Derks-Aff1-Aff2-Aff3) [ORCID: orcid.org/0000-0002-4547-7457](https://orcid.org/0000-0002-4547-7457)[1](https://www.nature.com/articles/s41416-026-03635-3#Aff1),[2](https://www.nature.com/articles/s41416-026-03635-3#Aff2),[3](https://www.nature.com/articles/s41416-026-03635-3#Aff3) Show authors [_British Journal of Cancer_](https://www.nature.com/bjc) (2026) [Cite this article](https://www.nature.com/articles/s41416-026-03635-3#citeas) Save article [ View saved research ](https://www.nature.com/saved-research) ## Abstract ### Background The tumour immune microenvironment influences neoadjuvant chemoradiotherapy success in esophageal adenocarcinoma (EAC). Complete responders show higher treatment-naïve intratumoral CD8+ T cell levels before treatment than non-complete responders. Understanding mechanisms driving CD8+ T cells exclusion from the TIME is essential to improving outcomes. ### Methods We performed spatial transcriptomics on treatment-naive CD8-low and high EACs (_N_ = 12). Regions of interest (ROIs) were selected based on tumour annotation by a pathologist. Cancer (CK+) cells and immune (CD45+) cells were analysed within the same ROI. Findings were validated using bulk transcriptome data (TCGA) and metabolic profiling (SCENITH) of fresh tumour specimen (_n_ = 5). ### Results Whole transcriptomic profiling showed cancer cell clustering based on T cell infiltration. Cancer cell transcriptomes of CD8-low tumours exhibited reduced antigen presentation and upregulated lipid and mitochondrial metabolism, while CD8-high tumours showed increased cytokine signalling and apoptotic pathways. In CD45+ compartments, CD8-low tumours were enriched for the PGC-1α pathway, linked to mitochondrial biogenesis and immunosuppressive myeloid populations. These findings were supported by TCGA data. SCENITH confirmed mitochondrial dependence of macrophages in CD8-low tumours. ### Conclusion Our results suggest that mitochondrial metabolism and impaired antigen presentation contribute to T cell exclusion in EAC. These findings raise the hypothesis that targeting mitochondrial metabolism in these cancers can modulate the anti-tumour immune response and thereby improve the response to chemoradiotherapy. ### Explore related subjects Discover the latest articles and news in related subjects. * [Cancer microenvironment](https://www.nature.com/subjects/cancer-microenvironment) * [Immunosuppression](https://www.nature.com/subjects/immunosuppression) * [Oesophageal cancer](https://www.nature.com/subjects/oesophageal-cancer) * [Transcriptomics](https://www.nature.com/subjects/transcriptomics) ## Background Esophageal adenocarcinoma (EAC) is a deadly disease with a dismal prognosis causing ~400.000 deaths annually [[1](https://www.nature.com/articles/s41416-026-03635-3#ref-CR1 "Sung H, Ferlay J, Siegel RL, Laversanne M, Soerjomataram I, Jemal A, et al. Global cancer statistics 2020: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA Cancer J Clin. 2021;71:209–49."), [2](https://www.nature.com/articles/s41416-026-03635-3#ref-CR2 "Al-Kaabi A, van der Post RS, van der Werf LR, Wijnhoven BPL, Rosman C, Hulshof MCCM, et al. Impact of pathological tumor response after CROSS neoadjuvant chemoradiotherapy followed by surgery on long-term outcome of esophageal cancer: a population-based study. Acta Oncol. 2021;60:497–504.")]. Even in the absence of overt metastases, when patients may be treated with neoadjuvant chemoradiotherapy (nCRT) followed by a surgical resection, around 50% of patients suffer from recurrent disease which is associated with poor prognosis. While 19% of EACs have a complete histopathological response after nCRT, 18–35% do not respond to nCRT, which immediately impacts survival negatively [[2](https://www.nature.com/articles/s41416-026-03635-3#ref-CR2 "Al-Kaabi A, van der Post RS, van der Werf LR, Wijnhoven BPL, Rosman C, Hulshof MCCM, et al. Impact of pathological tumor response after CROSS neoadjuvant chemoradiotherapy followed by surgery on long-term outcome of esophageal cancer: a population-based study. Acta Oncol. 2021;60:497–504."), [3](https://www.nature.com/articles/s41416-026-03635-3#ref-CR3 "Henckens SPG, Liu D, Gisbertz SS, Kalff MC, Anderegg MCJ, Crull D, et al. Prognostic value of Mandard score and nodal status for recurrence patterns and survival after multimodal treatment of oesophageal adenocarcinoma. Br J Surg. 2024;111:znae034. https://doi.org/10.1093/bjs/znae034 .")]. The CheckMate 577 trial showed clear additive effect of adjuvant immune checkpoint blockade (ICB) in case of residual disease [[4](https://www.nature.com/articles/s41416-026-03635-3#ref-CR4 "Kelly RJ, Ajani JA, Kuzdzal J, Zander T, Van Cutsem E, Piessen G, et al. Adjuvant nivolumab in resected esophageal or gastroesophageal junction cancer. N Engl J Med. 2021;384:1191–203.")] evidenced by an improvement of progression-free survival from 11 months to 22 months. Also in the metastatic setting, the addition of ICB to first-line chemotherapy has resulted in a clear improvement in overall survival. The CheckMate 649 trial showed a median overall survival of 11 months in the chemotherapy treated group, compared to 14 months in patients treated with chemotherapy and nivolumab in gastric and EACs with a PD-L1 combined positivity score of CPS > 5 [[5](https://www.nature.com/articles/s41416-026-03635-3#ref-CR5 "Janjigian YY, Shitara K, Moehler M, Garrido M, Salman P, Shen L, et al. Nivolumab plus chemotherapy versus chemotherapy as first line treatment for advanced gastric cancer/gastroesophageal junction cancer/oesophageal adenocarcinoma \(CheckMate 649\): a multicentre, randomised, open-label, phase 3 trial HHS Public Access. Lancet. 2021;398:27–40.")]. Although these studies indicate a clear potential for ICB in gastroesophageal adenocarcinoma, clinical efficacy is still limited when compared to the effect of ICB in other cancer types such as melanoma where application of ICB in advanced disease increases OS to >60 months [[6](https://www.nature.com/articles/s41416-026-03635-3#ref-CR6 "Larkin J, Chiarion-Sileni V, Gonzalez R, Grob JJ, Rutkowski P, Lao CD, et al. Five-year survival with combined nivolumab and ipilimumab in advanced melanoma. N Engl J Med. 2019;381:1535–46.")]. It is not clear which biological processes underlie the limited response, but increasing evidence points towards the composition of the tumour immune microenvironment (TIME), and the level of infiltrating T cells in particular [[7](https://www.nature.com/articles/s41416-026-03635-3#ref-CR7 "Kamran SC, Lennerz JK, Margolis CA, Liu D, Reardon B, Wankowicz SA, et al. Integrative molecular characterization of resistance to neoadjuvant chemoradiation in rectal cancer. Clin Cancer Res. 2019;25:5561–71."), [8](https://www.nature.com/articles/s41416-026-03635-3#ref-CR8 "Goedegebuure RSA, Harrasser M, de Klerk LK, van Schooten TS, van Grieken NCT, Eken M, et al. Pre-treatment tumor-infiltrating T cells influence response to neoadjuvant chemoradiotherapy in esophageal adenocarcinoma. Oncoimmunology. 2021;10:1954807.")]. Previous studies by us and others have shown that the TIME of EACs is heterogeneous and often suppressed [[8](https://www.nature.com/articles/s41416-026-03635-3#ref-CR8 "Goedegebuure RSA, Harrasser M, de Klerk LK, van Schooten TS, van Grieken NCT, Eken M, et al. Pre-treatment tumor-infiltrating T cells influence response to neoadjuvant chemoradiotherapy in esophageal adenocarcinoma. Oncoimmunology. 2021;10:1954807."),[9](https://www.nature.com/articles/s41416-026-03635-3#ref-CR9 "Derks S, de Klerk LK, Xu X, Fleitas T, Liu KX, Liu Y, et al. Characterizing diversity in the tumor-immune microenvironment of distinct subclasses of gastroesophageal adenocarcinomas. Ann Oncol. 2020;31:1011–20."),[10](https://www.nature.com/articles/s41416-026-03635-3#ref-CR10 "Yamamoto K, Makino T, Sato E, Noma T, Urakawa S, Takeoka T, et al. Tumor-infiltrating M2 macrophage in pretreatment biopsy sample predicts response to chemotherapy and survival in esophageal cancer. Cancer Sci. 2020;111:1103–12."),[11](https://www.nature.com/articles/s41416-026-03635-3#ref-CR11 "Carroll TM, Chadwick JA, Owen RP, White MJ, Kaplinsky J, Peneva I, et al. Tumor monocyte content predicts immunochemotherapy outcomes in esophageal adenocarcinoma. Cancer Cell. 2023;41:1222–.e7.")]. The immune infiltrate is characterised by high levels of monocytic myeloid-derived suppressor cells (MDSCs), neutrophils and macrophages, while T cells are often not present or limited to the invasive margin [[9](https://www.nature.com/articles/s41416-026-03635-3#ref-CR9 "Derks S, de Klerk LK, Xu X, Fleitas T, Liu KX, Liu Y, et al. Characterizing diversity in the tumor-immune microenvironment of distinct subclasses of gastroesophageal adenocarcinomas. Ann Oncol. 2020;31:1011–20.")]. It is not fully understood what drives the T cell excluded state in EAC, but the answer can likely be found in the cancer cells. Cancer cells can orchestrate the TIME by expression of immune suppressive proteins such as programmed death-ligand (PD-L)1 and PD-L2 in EAC [[12](https://www.nature.com/articles/s41416-026-03635-3#ref-CR12 "Derks S, Nason KS, Liao X, Stachler MD, Liu KX, Liu JB, et al. Epithelial PD-L2 expression marks Barrett’s esophagus and esophageal Adenocarcinoma. Cancer Immunol Res. 2015;3:1123–9.")]. In addition, activation of oncogenic pathways such as the WNT/β-catenin signalling pathway and signalling through oncogenic KRAS are associated with immune suppression, characterised by limited CD8+ T cell infiltration and increased levels of Tregs, MDSCs and pro-tumoral macrophages [[13](https://www.nature.com/articles/s41416-026-03635-3#ref-CR13 "Luke JJ, Bao R, Sweis RF, Spranger S, Gajewski TF. WNT/b-catenin pathway activation correlates with immune exclusion across human cancers. Clin Cancer Res. 2019;25:3074–83."), [14](https://www.nature.com/articles/s41416-026-03635-3#ref-CR14 "Hamarsheh S, Groß O, Brummer T, Zeiser R. Immune modulatory effects of oncogenic KRAS in cancer. Nat Commun. 2020;11:5439.")]. In EACs specifically, expression of genes related to cell cycle progression, the unfolded protein response and metabolic pathways are associated with a ‘cold’ immune phenotype [[9](https://www.nature.com/articles/s41416-026-03635-3#ref-CR9 "Derks S, de Klerk LK, Xu X, Fleitas T, Liu KX, Liu Y, et al. Characterizing diversity in the tumor-immune microenvironment of distinct subclasses of gastroesophageal adenocarcinomas. Ann Oncol. 2020;31:1011–20.")]. Next to transcriptional differences, structural genomic features, such as high levels of aneuploidy, are associated with T cell exclusion [[15](https://www.nature.com/articles/s41416-026-03635-3#ref-CR15 "Davoli T, Uno H, Wooten EC, Elledge SJ. Tumor aneuploidy correlates with markers of immune evasion and with reduced response to immunotherapy. Science. 2017;355:1979.")] which has also been observed for EAC specifically [[9](https://www.nature.com/articles/s41416-026-03635-3#ref-CR9 "Derks S, de Klerk LK, Xu X, Fleitas T, Liu KX, Liu Y, et al. Characterizing diversity in the tumor-immune microenvironment of distinct subclasses of gastroesophageal adenocarcinomas. Ann Oncol. 2020;31:1011–20.")]. However, most of these observations in EAC are based on bulk sequencing data which does not take the complex architecture of the EAC immune microenvironment into account. To further expand our knowledge about cancer cell-intrinsic drivers of T cell exclusion in EAC, we performed spatial whole transcriptome analyses in cancer cells and immune cells in T cell-rich and T cell-poor tumour areas in tumours of patients who were scheduled to undergo nCRT. Using this strategy, we identified that the main differences between these areas were related to tumour-associated metabolic pathways, which was confirmed by publicly available transcriptomic data and fresh tumour tissues. Our findings suggest that (re)activation of the antitumor immune response in EAC, needed to improve the efficacy of chemoradiotherapy, may require a metabolic intervention. ## Methods ### Patient selection based on CD8+ T cell infiltration EAC tissues with high and low intratumoral CD8+ T cell densities were selected from a prev
## Related Clinical Research

- [Real-world outcomes with nivolumab-relatlimab in advanced melanoma: multicenter Israeli study](https://medichelpline.com/clinical-feed/pubmed-42735459.md) (DOI: 10.1016/j.ejca.2026.117047)
- [53L10 T‑cell engager tribody for immunotherapy of multiple solid tumors — Frontiers in Immunology](https://medichelpline.com/clinical-feed/frontiers-in-immunology-11-53l10-t-cell-engager-tribody-for-immunotherapy-of-multiple-solid-tumors.md)
- [Immune-pressure redistribution as a framework for resistance to PD-1/PD-L1 blockade](https://medichelpline.com/clinical-feed/pubmed-42763389.md) (DOI: 10.1186/s12943-026-02786-4)
- [Targeting VISTA for Skin Cancer Immunotherapy: Source Article Not Available](https://medichelpline.com/clinical-feed/frontiers-in-immunology-17-targeting-vista-as-a-novel-immunotherapy-for-skin-cancer.md)
- [Personalized mRNA vaccine plus pembrolizumab lowers melanoma recurrence in phase 3 trial](https://medichelpline.com/clinical-feed/medical-news-today-0-novel-mrna-vaccine-plus-immunotherapy-reduces-melanoma-relapse-in-phase-3-trial.md)

## Navigation
- [← Back to Oncology Feed](https://medichelpline.com/clinical-feed/oncology.md)
- [← All Clinical Specialties](https://medichelpline.com/clinical-feed.md)
## Medical & Regulatory Disclaimer

> [!CAUTION]
> MedicHelpline content is structured for research, educational, and professional discovery purposes. It does not constitute individual medical advice, clinical diagnosis, or treatment recommendations.
> Always verify dosing, contraindications, and regulatory alerts against official product labeling and primary regulatory sources before clinical decision-making.