ESMO Congress 2026

Using T cells and immune effectors against sarcoma is not without biological grounding. As early as 1975, researchers isolated tumor necrosis factor (TNF) from the serum of BCG-primed mice given endotoxin; it caused hemorrhagic necrosis of transplanted tumors such as sarcoma Meth A, and the factor was inferred to come from host cells, probably macrophages ^[5]. In 2015, a mouse sarcoma model further showed that glucose consumption by tumors metabolically restricts T cells, dampening mTOR activity, glycolytic capacity, and IFN-γ production, while clinically used CTLA-4, PD-1, and PD-L1 blocking antibodies restore glucose in the tumor microenvironment and permit T-cell glycolysis and function ^[4]. On the pathogen and immune background, Kaposi's sarcoma is listed as an 'opportunistic neoplasm' of AIDS accompanying depletion of a CD4-positive T-cell subset ^[6], and KSHV sequences homologous to, yet distinct from, gammaherpesviruses were detected in more than 90 percent of AIDS-associated Kaposi's sarcoma tissues ^[1]. Together these lines of evidence point to the conclusion that sarcoma is not inherently resistant to T-cell-mediated attack; the bottleneck is bringing that efficacy to more patients.

At this ESMO26 in Madrid, T-cell therapies in sarcoma are the most closely watched storyline. Per the on-site summary by @PestanaRC, Sandra P. D'Angelo presented on T-cell therapies in sarcoma: TCRs clearly work for cancer-testis antigens in select patients, with more TIL data to be presented on Monday; but patient selection remains a hard constraint—target expression, HLA subtype, and even geography restrict who can benefit, and afami-cell is approved only by the FDA, with no other agent approved. A second item of news the same day: OncoDaily launched OncoDailySarcoma at the meeting, Prof. Robin Jones mandated faster progress and 'clever designs' to expand options, and pointed to iNKT–myeloid crosstalk (MiNK, under Agenus) as possibly broadening activity; the post also tagged Deciphera, PharmaMar and others.

Relative to existing knowledge, this meeting moves the question from 'can T cells treat sarcoma' to 'who is eligible and how to broaden coverage': the TCR approach is explicitly considered effective for cancer-testis antigens in selected patients, but the eligible population is boxed in by three gates—target expression, HLA subtype, and geography—with only one approved agent; and the proposed solutions go beyond polishing the TCR itself, as the meeting also raised mechanism directions such as iNKT–myeloid crosstalk that may broaden activity, along with Jones's call for faster and 'cleverer' trial designs.

The limitations should be stated plainly: the on-site posts give no efficacy or safety numbers from any specific trial, the TIL data will only be presented on Monday, and broadened activity via iNKT was raised only as a question—everything so far is qualitative information from during the conference, and conclusions await confirmation by formal reports.