Abstract
BackgroundSpontaneous remission in solid malignancies has been documented. However, spontaneous remission in aggressive diffuse large b cell lymphoma is exceedingly rare. Previous reports of lymphoma remission suggest that not yet fully characterized tumor-intrinsic and microenvironment mechanisms cooperate with spontaneous regression.Case descriptionHere, we report the case of an 88-year-old white woman with diffuse large b cell lymphoma (follicular lymphoma transformed) who achieved morphologic spontaneous remission 3 months after her diagnostic core biopsy. We examined 16 similar cases of diffuse large b cell lymphoma suggesting that spontaneous remission is preferentially observed in elderly patients soon after their biopsy microtrauma, especially if malignancies are Epstein–Barr virus driven and activated B-cell type.ConclusionOur case and reported analysis highlight that anti-tumor adaptive T cell responses are potentially augmented in a subset of patients leading to lymphoma regression. In these patients, it is possible that “primed” innate anti-tumor T cell immunity is enhanced in immunogenic lymphoma subtypes after tissue biopsy. Our case and analysis not only reinforce the role of innate T cell anticancer immunity, but also originates potential proof of concept for investigation of unexplored pathways that could favorably impact T cell therapy.
Highlights
ConclusionOur case and reported analysis highlight that anti-tumor adaptive T cell responses are potentially augmented in a subset of patients leading to lymphoma regression
Diffuse large b cell lymphoma (DLBCL) is an immunologic and genetic heterogeneous disease
We found that advanced age, limited stage, and activated B-cell (ABC) phenotype associated with Epstein–Barr virus (EBV) are potentially linked with a subgroup of patients with propensity for spontaneous remission (SR)
Summary
Our case and reported analysis highlight that anti-tumor adaptive T cell responses are potentially augmented in a subset of patients leading to lymphoma regression. In these patients, it is possible that “primed” innate anti-tumor T cell immunity is enhanced in immunogenic lymphoma subtypes after tissue biopsy. Our case and analysis reinforce the role of innate T cell anticancer immunity, and originates potential proof of concept for investigation of unexplored pathways that could favorably impact T cell therapy
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