[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"detail-sidebar-cat-0-en-105":3,"doc-seo-360044-105":59,"doc-detail-360044-en":131},{"code":4,"msg":5,"data":6},0,"success",[7,13,18,23,28,33,38,43,48,51,55],{"id":8,"doc_module":4,"doc_module_name":9,"category_name":10,"show_sort_weight":11,"slug":12},1,"Document","Story & Novel",90,"story-novel",{"id":14,"doc_module":4,"doc_module_name":9,"category_name":15,"show_sort_weight":16,"slug":17},2,"Literature",80,"literature",{"id":19,"doc_module":4,"doc_module_name":9,"category_name":20,"show_sort_weight":21,"slug":22},4,"Exam",70,"exam",{"id":24,"doc_module":4,"doc_module_name":9,"category_name":25,"show_sort_weight":26,"slug":27},5,"Comic",60,"comic",{"id":29,"doc_module":4,"doc_module_name":9,"category_name":30,"show_sort_weight":31,"slug":32},6,"Technology",50,"technology",{"id":34,"doc_module":4,"doc_module_name":9,"category_name":35,"show_sort_weight":36,"slug":37},7,"Healthcare",40,"healthcare",{"id":39,"doc_module":4,"doc_module_name":9,"category_name":40,"show_sort_weight":41,"slug":42},8,"Research & Report",30,"research-report",{"id":44,"doc_module":4,"doc_module_name":9,"category_name":45,"show_sort_weight":46,"slug":47},9,"Religion & Spirituality",20,"religion-spirituality",{"id":46,"doc_module":4,"doc_module_name":9,"category_name":49,"show_sort_weight":46,"slug":50},"World Cup","world-cup",{"id":52,"doc_module":4,"doc_module_name":9,"category_name":53,"show_sort_weight":52,"slug":54},10,"Lifestyle","lifestyle",{"id":56,"doc_module":4,"doc_module_name":9,"category_name":57,"show_sort_weight":24,"slug":58},19,"General","general",{"code":4,"msg":60,"data":61},"ok",{"site_id":62,"language":63,"slug":64,"title":65,"keywords":66,"description":67,"schema_data":68,"social_meta":124,"head_meta":126,"extra_data":128,"updated_unix":130},105,"en","tumor-cell-intrinsic-mechanisms-of-immune-escape","Tumor cell intrinsic mechanisms of immune escape","","Cancer develops through a multistep sequence: mutations accumulate, oncogenes become activated, and tumor-suppressive mechanisms are lost in otherwise normal cells. 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Cell Communication and Signaling (2026) 24:290  \n[https://doi.org/10.1186/s12964-026-02891-3](https://doi.org/10.1186/s12964-026-02891-3)  \nCell Communication and Signaling  \nREVIEW Open Access  \nTumor cell intrinsic mechanisms of immune escape  \nGanapathy Sriram1,2*, Ahmed Aquib3, Robert Glassman4 and Raymond B. Birge3*  \nAbstract  \nCancer arises in a multi-step process involving acquisition of mutations, activation of oncogenes and the loss of tumor suppressive mechanisms in normal cells. Such intrinsic genetic events lead to cellular transformation and gain of aggressive traits including enhanced proliferation and survival, as well as invasion and metastasis of tumor cells. Recent evidence suggests that tumor cell—intrinsic signaling pathways can also lead to suppression of the immune response against tumor cells resulting in failure of cancer cells to be recognized and eliminated by the host immune system. Insights into the tumor-intrinsic mechanisms of immune escape will not only expand our understanding of tumor development and progression but help develop new combinations of therapeutic strategies in immuno-oncology to better align them with targeted therapeutics. Historically, the literature on oncogenes and tumor suppressor mechanisms has focused on signaling pathways leading to tumor cell proliferation, survival, and metastasis. Here, in this special thematic collection published in Cell Communication and Signaling ( [https://link.springer.com/collections/dbbfcgaece](https://link.springer.com/collections/dbbfcgaece)), we featured commentaries, review articles, and primary research articles that highlight recent work focused on the molecular and mechanistic links between intrinsic oncogenic signaling and mechanisms of immune escape. We conclude with commentary and open questions and challenges that remain in this emerging field.  \nKeywords Targeted Therapeutics, Drug Resistance, Cell Intrinsic Immune Evasion  \n*Correspondence: Ganapathy Sriram  \n[Sriram_ganapathy@wheatoncollege.edu](Sriram_ganapathy@wheatoncollege.edu); [sriram.crk@gmail.com](sriram.crk@gmail.com)  \nRaymond B. Birge  \n[birgera@njms.rutgers.edu](birgera@njms.rutgers.edu)  \n1Department of Biological, Chemical and Environmental Sciences, Wheaton College, 26 E Main St, Norton, MA 02766, USA  \n2Department of Biology, Tufts University, Medford, MA, USA 3Department of Microbiology, Biochemistry and Molecular Genetics, Center for Cell Signaling, Rutgers New Jersey Medical School, 205 South Orange Ave, Newark, NJ 07103, USA  \n4Department of Medicine, Division of Hematology & Oncology, Weill Cornell Medicine, 525 East 68th Street, New York, NY 10065, USA  \nNearly a quarter century ago, Hanahan and Weinberg articulated six interrelated disciplines to explain mechanistically how normal cells transform into malignant tumors [1].Such a provisional set of biological principles acquired during tumor development laid the groundwork for multidisciplinary approaches to tackle the cancer problem, as well as the conceptualization and rationalization of newer hallmarks that have subsequently emerged such as onco-metabolism and the role of epigenetic reprograming of tumor cells [2]. Despite the occurrence of more nuanced features of cancer development since their classical tenets, the acquisition of oncogenic mutations and the dominant gain-of-function of driver mutations that initiate malignant transformation is still central to this dogma, including the dominant role of tyrosine kinases that are frequently mutated and/or over-  \n© The Author(s) 2026. Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You ","cbCaigKeD0wOAoZq","https://ap.wps.com/l/cbCaigKeD0wOAoZq","pdf",1844633,15,"English","# Abstract\n## Background and rationale\n## Tumor-intrinsic immune suppression\n## Scope of the thematic collection\n## Conclusions and open questions","[{\"question\":\"How does the document describe the fundamental process of cancer development?\",\"answer\":\"It describes cancer as a multistep process involving acquisition of mutations, activation of oncogenes, and loss of tumor-suppressive mechanisms, leading to transformation and aggressive traits.\"},{\"question\":\"What mechanism of immune escape is emphasized as tumor-intrinsic?\",\"answer\":\"The document emphasizes that tumor cell–intrinsic signaling pathways can suppress the immune response, preventing tumors from being recognized and eliminated by the host immune system.\"},{\"question\":\"What is the purpose of the special thematic collection mentioned in the abstract?\",\"answer\":\"It features commentaries, review articles, and primary research focused on molecular and mechanistic links between intrinsic oncogenic signaling and immune escape, concluding with commentary and open questions.\"}]","Tumor cell intrinsic mechanisms of immune escape | PDF",1790138577,38]