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Tumor-Infiltrating Macrophages in Post-Transplant, Relapsed Classical Hodgkin Lymphoma Are Donor-Derived.

ABSTRACT: Tumor-associated inflammatory cells in classical Hodgkin lymphoma (CHL) typically outnumber the neoplastic Hodgkin/Reed-Sternberg (H/RS) cells. The composition of the inflammatory infiltrate, particularly the fraction of macrophages, has been associated with clinical behavior. Emerging work from animal models demonstrates that most tissue macrophages are maintained by a process of self-renewal under physiologic circumstances and certain inflammatory states, but the contribution from circulating monocytes may be increased in some disease states. This raises the question of the source of macrophages involved in human disease, particularly that of CHL. Patients with relapsed CHL following allogeneic bone marrow transplant (BMT) provide a unique opportunity to begin to address this issue. We identified 4 such patients in our archives. Through molecular chimerism and/or XY FISH studies, we demonstrated the DNA content in the post-BMT recurrent CHL was predominantly donor-derived, while the H/RS cells were derived from the patient. Where possible to evaluate, the cellular composition of the inflammatory infiltrate, including the percentage of macrophages, was similar to that of the original tumor. Our findings suggest that the H/RS cells themselves define the inflammatory environment. In addition, our results demonstrate that tumor-associated macrophages in CHL are predominantly derived from circulating monocytes rather than resident tissue macrophages. Given the association between tumor microenvironment and disease progression, a better understanding of macrophage recruitment to CHL may open new strategies for therapeutic intervention.

SUBMITTER: Crane GM

PROVIDER: S-EPMC5042490 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundThe prognosis of Hodgkin lymphoma (HL) relapsing post autologous transplant (AuSCT) is poor. Even with novel therapies, only approximately 20%-25% of patients attain complete remissions, with a median progression-free survival (PFS) of approximately 5-15 months. Lenalidomide has been shown to have activity in relapsed HL. We retrospectively analyzed the outcomes of patients with relapsed HL post AuSCT treated with lenalidomide alone or in combination with dexamethasone at our center.Patients and methodsRecords of 143 patients transplanted from November 2007 to October 2021 were reviewed. Of these patients, 41 (28%) relapsed, and 16 (39%) received lenalidomide alone or in combination with dexamethasone. Data collected included demographic, pathological, staging, and prior therapy details. Lenalidomide was administered at 10-25 mg/day on an intermittent or continuous schedule alone or in combination with dexamethasone (20-40 mg weekly). Response was assessed using PET-CT scan in accordance with Lugano criteria. Standard definitions were used for response, PFS, and overall survival (OS). Toxicities were graded using Common Terminology Criteria for Adverse Events version 5.0. Statistical analysis was done using SPSS Version 21.ResultsThe median age of the patients was 25.5 years, and 10 were males. Eleven (69%) had advanced disease, and 7 (44%) were refractory to last systemic therapy. Nine patients received lenalidomide alone and 7 with dexamethasone. Four (25%) had complete response, and another four (25%) had partial response, with an overall response rate of 50%. The 3-year PFS and OS were 31% and 38%, respectively. Grade III/IV toxicities were only hematological, neutropenia and thrombocytopenia in four and three patients, respectively. No therapy-related deaths were recorded.ConclusionsLenalidomide alone or in combination with dexamethasone is a safe and effective therapy for relapsed HL post AuSCT and results in durable response and long-term survival in approximately one-third of the patients. However, these results needs verification in larger prospective studies.

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Tumor-Infiltrating Macrophages in Post-Transplant, Relapsed Classical Hodgkin Lymphoma Are Donor-Derived.

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