Late mortality in survivors of autologous hematopoietic-cell transplantation: report from the Bone Marrow Transplant Survivor Study

Bhatia, Smita; Robison, Leslie L.; Francisco, Liton; Carter, Andrea; Liu, Yan; Grant, Marcia; Baker, K. Scott; Fung, Henry C.; Gurney, James G.; McGlave, Philip B.; Nademanee, Auayporn; Ramsay, Norma K.C.; Stein, Anthony S.; Weisdorf, Daniel J.; Forman, Stephen J.

doi:10.1182/blood-2005-01-0035

Cited by 227 publications

(205 citation statements)

References 43 publications

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“…2,12 In our analysis, there was no difference in late mortality based on the use of TBI conditioning.…”

Section: Study Populationmentioning

confidence: 78%

“…1,16 Survivors of allogeneic HSCT have been shown to be at a 12-fold increased risk of developing another malignancy when compared with the general population. 12 Although the risk for the development of a second malignant neoplasm increases with increasing time from HSCT, we did not find new malignancies to be a major cause of late mortality despite a median follow-up of 10.0 years. The reason for the difference between adults and children post-HSCT is yet to be explained.…”

Section: Study Populationmentioning

confidence: 86%

“…2,11 Studies that include mainly adults have demonstrated a much higher incidence of late NRM than observed in our study. 1,12 These studies did not report the causes and risk for NRM in patients who underwent HSCT during childhood separately. Conflicting results regarding the effect of age at transplant on mortality have been published.…”

Section: Study Populationmentioning

confidence: 99%

“…Studies in adults have reported a similarly high risk for death due to late relapse, but the risk for NRM is substantially higher in adult cohorts. For example, Bhatia et al 12 reported that 31.2% of 854 patients (90% of whom were 418 years of age at time of HSCT) died 2 or more years after autologous HSCT for a hematologic malignancy. Although relapse accounted for the majority of deaths, 13.7% of the cohort experienced NRM, a rate 10 times higher than our cohort.…”

Section: Study Populationmentioning

confidence: 99%

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Late mortality after hematopoietic SCT for a childhood malignancy

Schechter

Pole

Darmawikarta

et al. 2013

Bone Marrow Transplant

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Hematopoietic SCT (HSCT) has been used as a curative therapy for pediatric malignancies. Survivors of HSCT are at risk for disease recurrence, late morbidity and mortality. We assessed late mortality (X2 years post-HSCT) in a population-based cohort of children who underwent HSCT for a malignancy. Mortality outcomes were determined by linking a clinical transplant database with the Canadian province of Ontario's pediatric cancer mortality files. Seven hundred and fifty-four children underwent HSCT (371 allogeneic, 383 autologous). Of the 479 (63.5%) who were alive X2 years post HSCT, 98 (20.5%) suffered a late death. Late mortality in the allogeneic HSCT group was 14.9% (median follow-up 10.0 years; range: 2.0-25.6 years), mainly due to relapse of the primary malignancy (64.7%). Chronic GVHD and second malignancies were not major causes of late mortality. A total of 25.5% suffered a late death following autologous HSCT (median follow-up 6.7 years; range: 2.0-22.2 years). Recurrence of the primary malignancy accounted for 87.5% of these deaths. Recurrence of the primary malignancy is the predominant cause of late mortality after HSCT. In contrast to studies of adult patients, non-relapse mortality is less common in children, and death due to chronic GVHD and secondary malignancies is uncommon.

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“…2,12 In our analysis, there was no difference in late mortality based on the use of TBI conditioning.…”

Section: Study Populationmentioning

confidence: 78%

Section: Study Populationmentioning

confidence: 86%

Section: Study Populationmentioning

confidence: 99%

Section: Study Populationmentioning

confidence: 99%

See 2 more Smart Citations

Late mortality after hematopoietic SCT for a childhood malignancy

Schechter

Pole

Darmawikarta

et al. 2013

Bone Marrow Transplant

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“…3,6–8 SN are typically grouped into three categories: B- and T-cell malignancies (including post-transplant lymphoproliferative disorder [PTLD]), myelodysplastic syndrome/acute myeloid leukemia (MDS/AML), and solid tumors. The time course for development of SN after HCT is variable, with lymphomas and leukemias developing relatively early, whereas solid tumors tend to have a longer latency.…”

Section: Background and Purposementioning

confidence: 99%

National Institutes of Health Hematopoietic Cell Transplantation Late Effects Initiative: The Subsequent Neoplasms Working Group Report

Morton

Saber

Baker

et al. 2017

Biology of Blood and Marrow Transplantation

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Subsequent neoplasms (SN) following hematopoietic cell transplantation (HCT) cause significant patient morbidity and mortality. Risks for specific SN types vary substantially, with particularly elevated risks for post-transplant lymphoproliferative disorders, myelodysplastic syndrome/acute myeloid leukemia, and squamous cell malignancies. This consensus document provides an overview of the current state of knowledge regarding SN after HCT and recommends priorities and approaches to overcome challenges and gaps in understanding. Numerous factors have been suggested to impact risk, including patient-related (e.g., age), primary disease-related (e.g., disease type, pre-HCT therapies), and HCT-related characteristics (e.g., type and intensity of conditioning regimen, stem cell source, development of graft-versus-host disease). However, gaps in understanding remain for each of these risk factors, particularly for patients receiving HCT in the current era due to substantial advances in clinical transplantation practices. Additionally, the influence of non-transplant-related risk factors (e.g., germline genetic susceptibility, oncogenic viruses, lifestyle factors) is poorly understood. Clarification of the magnitude of SN risks and identification of etiologic factors will require large-scale, long-term, systematic follow-up of HCT survivors with detailed clinical data. Most investigations of the mechanisms of SN pathogenesis after HCT have focused on immune drivers. Expansion of our understanding in this area will require interdisciplinary laboratory collaborations utilizing measures of immune function and availability of archival tissue from SN diagnoses. Consensus-based recommendations for optimal preventative, screening, and therapeutic approaches have been developed for certain SN after HCT, whereas for other SN, general population guidelines are recommended. Further evidence is needed to specifically tailor preventative, screening, and therapeutic guidelines for SN after HCT, particularly for unique patient populations. Accomplishment of this broad research agenda will require increased investment in systematic data collection with engagement from patients, clinicians, and interdisciplinary scientists in order to reduce the burden of SN in the rapidly growing population of HCT survivors.

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