Spontaneous Remission in Diffuse Large Cell Lymphoma

A Case Report

J. Snijder; N. Mihyawi; A. Frolov; A. Ewton; G. Rivero

Disclosures

J Med Case Reports. 2019;13(28) 

In This Article

Abstract and Introduction

Abstract

Background: Spontaneous 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 description: Here, 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.

Conclusion: 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 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.

Introduction

Diffuse large b cell lymphoma (DLBCL) is an immunologic and genetic heterogeneous disease. Anthracycline-based chemotherapies combined with rituximab, such as the regimen of rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP) are normally administered for therapy.[1] However, spontaneous remission (SR) rarely occurs.[2] SR is defined as the complete or partial resolution of the tumor without administration of immunochemotherapy. SR is not exclusively observed in lymphomas and has been increasingly described in various malignancies, such as leukemia, malignant melanoma, Kaposi sarcoma, and neuroblastoma.[3] Although the mechanisms leading to SR remain uncharacterized, its infrequent occurrence highlights the possibility that tumor-associated molecular and patient-induced immunologic mechanisms cooperate to induce tumor regression. Previously, it has been hypothesized that a "favorable adaptive immunity" against concurrent bacterial or viral infection and even post biopsy trauma could render an "enhanced anti-tumor effect." Understanding mechanisms leading to SR could improve cellular and immunotherapy challenges for treatment of lymphoma. In this study, we present an elderly patient diagnosed with DLBCL who experienced SR. In addition, to gain insight into the histologic, immunophenotypic, cytogenetic, and molecular features of patients experiencing SR, we examined 16 additional cases reported in the English literature. 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 SR.

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