Therapy-related myelodysplastic syndrome after allogeneic BMT: successful treatment by donor lymphocyte infusions

Roos‐Weil, Damien; Nguyen, Son Truong; Uzunov, Madalina; Bories, D.; Chapiro, Élise; Nguyen‐Khac, Florence; Jp, Vernant; Dhédin, Nathalie

doi:10.1038/bmt.2009.369

Cited by 6 publications

(8 citation statements)

References 8 publications

(14 reference statements)

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“…1,2 Some cases demonstrate progression of disease, and occasional cases develop host cell-derived therapy-related secondary acute leukemia or MDS resulting from a complication of pretransplantation chemotherapy and/or conditioning treatment. 3,4 In rare cases, secondary leukemia/MDS is derived from donor cells, thus being designated donor cell leukemia (DCL). First described in 1971 by Fialkow et al, 34 DCL has been reported mostly as case reports.…”

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confidence: 99%

Donor Cell–Derived Leukemias/Myelodysplastic Neoplasms in Allogeneic Hematopoietic Stem Cell Transplant Recipients

Wang

Hutchinson

Huang

et al. 2011

American Journal of Clinical Pathology

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We report 10 cases of donor cell leukemia (DCL). All cases except the case of chronic lymphocytic leukemia had anemia, neutropenia, and/or thrombocytopenia when DCL was diagnosed. Eight cases with sex-mismatched hematopoietic stem cell transplant (HCT) showed donor gonosomal complements, suggesting DCL. Clonal cytogenetic abnormalities were detected in 8 cases: 6 were monosomy 7/del(7q). In all 10 cases, engraftment studies confirmed donor cell origin. Retrospective fluorescence in situ hybridization in archived donor cells in 4 cases showed a low level of abnormalities in 2. Of 7 patients with clinical follow-up of 5 months or more, 1 (with acute myeloid leukemia) died of disease; 6 are alive, including 1 with myelodysplastic syndrome with spontaneous remission. Similar to reported cases, we found disproportional sex-mismatched HCTs, suggesting probable underdetection of DCL in sex-matched HCTs. The latency between HCT and DCL ranged from 1 to 193 months (median, 24 months), in keeping with the literature. Analyzing our cases, pooled with reported cases, with survival models showed much shorter latency for malignancy as primary disease, for T-cell large granular lymphocyte leukemia as type of DCL, and for umbilical cord blood as stem cell source.

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confidence: 99%

Donor Cell–Derived Leukemias/Myelodysplastic Neoplasms in Allogeneic Hematopoietic Stem Cell Transplant Recipients

Wang

Hutchinson

Huang

et al. 2011

American Journal of Clinical Pathology

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“…Immune restoration with lymphocyte infusions has been used predominantly in leukemia where donor lymphocytes are given to deliver an antitumor effect while limiting graft-versus-host disease, and lymphocyte infusions have been used to restore immunity in a number of conditions (29). We evaluate full T-cell immune reconstitution with CD3 + T cells where the alloreactive cells have been removed (“pruning”) as a therapeutic strategy to prevent pancreatic islet allograft rejection while maintaining the ability to reject third-party grafts across a major MHC mismatch in diabetic mice.…”

Section: Introductionmentioning

confidence: 99%

Selective Depletion of Alloreactive T Cells Leads to Long-Term Islet Allograft Survival across a Major Histocompatibility Complex Mismatch in Diabetic Mice

Zhang

et al. 2013

Cell Transplant

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Islet cell transplantation as a therapy for type 1 diabetes has been limited by progressive graft loss. Significant immunosuppression including T-cell ablation has been used in an attempt to limit islet rejection. Here, we show that CD3+ lymphocytes depleted of alloreactive T cells selected from a mixed lymphocyte reaction (MLR), where responder BALB/c splenocytes stained with carboxyfluorescein succinimidyl ester (CFSE) were stimulated with irradiated C57BL/6 splenocytes for 5 days, infused into diabetic immunodeficient mice are capable of restoring a broad T-cell repertoire and specifically do not reject islet transplants from the strain (C57BL/6) used in the original depletion. These mice demonstrate reconstitution with CD4 + and CD8 + T cells, the capacity to reject third-party grafts (CBA), and restoration of interferon-g (IFN-g) responses to third-party alloantigens. Over time, both forkhead box P3-positive (Foxp3 + ) T regulatory cells (Tregs) and gd T cells expand, suggesting a role for peripheral tolerance, in addition to the initial depletion of alloreactive T cells, in long-term islet graft survival. Our results suggest that immune restoration with CD3 + lymphocytes where alloreactive T cells are removed can restore cognate immunity without islet allograft loss and recurrence of diabetes.

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“…46,XX,add(2)(q31),add(2)(q? ),add(7)(q22),add(9)(q34) [9]/other complex abnormal clone [5] /46,XY [5] Alive/t-MDS relapse after second CBT (7) Yamamoto et al …”

Section: Conflict Of Interestmentioning

confidence: 99%

“…Roos-Weil et al reported that t-MDS with complex karyotypes involving chromosome 7 and developing 1 year after BMT could be successfully treated with donor lymphocyte infusions (DLIs). 5 They suggested that early treatment with DLIs might be an effective and well-tolerated therapeutic option. Yoshihara et al also reported the case of a patient with ALL who showed numerous aberrant chromosomal changes in the recipient cells after allogeneic BMT with TBI regimen and was effectively treated by DLIs 14 months after BMT.…”

mentioning

confidence: 99%

Therapy-related myelodysplastic syndrome of recipient origin in a juvenile myelomonocytic leukemia patient 17 years after allogeneic BMT

Yabe

Morimoto

Shimizu

et al. 2010

Bone Marrow Transplant

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Therapy-related myelodysplastic syndrome after allogeneic BMT: successful treatment by donor lymphocyte infusions

Cited by 6 publications

References 8 publications

Donor Cell–Derived Leukemias/Myelodysplastic Neoplasms in Allogeneic Hematopoietic Stem Cell Transplant Recipients

Donor Cell–Derived Leukemias/Myelodysplastic Neoplasms in Allogeneic Hematopoietic Stem Cell Transplant Recipients

Selective Depletion of Alloreactive T Cells Leads to Long-Term Islet Allograft Survival across a Major Histocompatibility Complex Mismatch in Diabetic Mice

Therapy-related myelodysplastic syndrome of recipient origin in a juvenile myelomonocytic leukemia patient 17 years after allogeneic BMT

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