Development of mycosis fungoides after bone marrow transplantation for chronic myeloid leukaemia: transmission from an allogeneic donor

Fahy, Caoimhe M. R.; Fortune, Anne; Quinn, Fiona; McMenamin, Máirín; Browne, Paul; Langabeer, S. E.; McCarron, Sarah L.; Hayden, PJ; Marren, P.; Chonghaile, M. Ni; Irvine, Alan D.; Vandenberghe, Elisabeth; Barnes, Louise

doi:10.1111/bjd.12647

Cited by 10 publications

(10 citation statements)

References 18 publications

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“…53 In MF, the source of those dermotropic neoplastic T-cell clones remains unknown, although there is some evidence that bone marrow may play such a role. [11][12][13] Research showed that the bone marrow niche provides shelter for different types of malignant cells (e.g. breast or prostate cancers) and that the bone marrow pool of cancer might be responsible for relapses after therapy.…”

Section: Discussionmentioning

confidence: 99%

“…by electron beam radiation therapy or psoralen ultraviolet A therapy [PUVA]) almost never results in a cure but only in a short-term responses. [7][8][9][10] Third, cells sharing molecular characteristics of malignant T-cells in MF have been found in the bone marrow of the patients years before the emergence of skin lesions of the disease 11 and CTCL can be transmitted via the bone marrow transplant from asymptomatic donors 12,13 . Fourth, MF may share the common precursor with other lymphomas (e.g.…”

Section: Introductionmentioning

confidence: 99%

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Skin colonization by circulating neoplastic clones in cutaneous T-cell lymphoma

Iyer

Hennessey

OʼKeefe

et al. 2019

Preprint

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Mycosis fungoides (MF) is a mature T-cell lymphoma currently thought to develop primarily in the skin by a clonal expansion of a transformed, resident memory T-cell. However, this concept does not explain the key characteristics of MF such as the debut with multiple, widespread skin lesions or inability of skin directed therapies to provide cure. The testable inference of the mature T-cell theory is the clonality of MF with respect to all rearranged T-cell receptor (TCR) genes. Here we have used whole exome sequencing approach to detect and quantify TCRα, -β and -γ clonotypes in tumor cell clusters microdissected from MF lesions. This method allows us to calculate the tumor cell fraction of the sample and therefore an unequivocal identification of the TCR clonotypes as neoplastic. Analysis of TCR sequences from 29 patients with MF stage I-IV proved existence of multiple T-cell clones within the tumor cell fraction, with a considerable variation between patients and between lesions from the same patient (median 11 clones, range 2-80 clones/sample). We have also detected multiple neoplastic clones in the peripheral blood in all examined patients. Based on these findings we propose that circulating neoplastic T-cell clones continuously replenish the lesions of MF thus increasing their heterogeneity by a mechanism analogous to the consecutive tumor seeding. We hypothesize that circulating neoplastic clones might be a promising target for therapy and could be exploited as a potential biomarker in MF.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Skin colonization by circulating neoplastic clones in cutaneous T-cell lymphoma

Iyer

Hennessey

OʼKeefe

et al. 2019

Preprint

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“…Even more rare, but recognized, is EBV-negative PTLD that are also donor-derived but most often of T and NK cell origin that typically present after one year post-transplant [2] , [3] , [4] . While patients with PTLD of T-cell origin are well-documented post solid organ transplantion, there has only been a handful of reports of T-cell lymphoma following alloHSCT since the early 2000s [5] . Most recently a few cases of CTCL following alloHSCT were described [ Table 1 ].…”

Section: Discussionmentioning

confidence: 99%

“…Dermatitis, in an otherwise asymptomatic patient, presented from three to eight years following alloHSCT [2] , [5] , [6] . In the two matched-related donor cases, the patient's sibling donor also developed rash and was diagnosed with mycosis fungoides at around the time of diagnosis of the recipient; the recipient was found to have 100% donor engraftment [5] , [6] . In the matched-unrelated donor case, the patient also developed a rash three years after alloHSCT.…”

Section: Discussionmentioning

confidence: 99%

Sezary syndrome manifesting as posttransplant lymphoproliferative disorder

Afiat

Zhang

et al. 2018

Leukemia Research Reports

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“…Two previous case reports describe the development of CTCL following allotransplant transmitted from allogeneic donor [ 23 , 24 ]. In our case, the skin lesions were thought to be recurrence of her old CTCL lesions.…”

Section: Discussionmentioning

confidence: 99%

Skin Recurrence of Transformed Mycosis Fungoides Postumbilical Cord Blood Transplant despite Complete Donor Chimerism

Pawar

Kumar

Woodroof

et al. 2014

Case Reports in Hematology

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Background. Allogeneic stem cell transplant is the treatment of choice for systemic cutaneous T-cell lymphoma (CTCL) which provides graft-versus-lymphoma effect. Herein we discuss a case of recurrence of CTCL skin lesions after cord blood transplant in a patient who continued to have 100% donor chimerism in bone marrow. Case Presentation. A 48-year-old female with history of mycosis fungoides (MF) presented with biopsy proven large cell transformation of MF. PET scan revealed multiple adenopathy in abdomen and chest suspicious for lymphoma and skin biopsy showed large cell transformation. She was treated with multiple cycles of chemotherapy. Posttherapy PET scan showed resolution of lymphadenopathy. Later she underwent ablative preparative regimen followed by single cord blood transplant. Bone marrow chimerism studies at day +60 after transplant showed 100% donor cells without presence of lymphoma. However 5 months after transplant she had recurrence of MF with the same genotype as prior skin lesion. Bone marrow chimerism study continued to show 100% donor cells. Conclusion. A differential graft-versus-lymphoma effect in our case prevented lymphoma recurrence systemically but failed to do so in skin. We hypothesize that this response may be due to presence of other factors in the bone marrow and lymph node microenvironments preventing recurrence in these sites.

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Development of mycosis fungoides after bone marrow transplantation for chronic myeloid leukaemia: transmission from an allogeneic donor

Cited by 10 publications

References 18 publications

Skin colonization by circulating neoplastic clones in cutaneous T-cell lymphoma

Skin colonization by circulating neoplastic clones in cutaneous T-cell lymphoma

Sezary syndrome manifesting as posttransplant lymphoproliferative disorder

Skin Recurrence of Transformed Mycosis Fungoides Postumbilical Cord Blood Transplant despite Complete Donor Chimerism

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