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Letters to the Editor
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Figure 2. Clinical outcomes. (A) Overall survival (OS) and progression-free survival (PFS) and (B) cumulative incidence of non-relapse mortality (NRM) and relapse for the entire cohort. (C) OS and (D) PFS according to the risk group.
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41% among 16 patients who received alloHCT in CR/PR, and 17% for nine patients with progressive disease. In a series of single-center studies, Kharfan-Dabaja et al.11 (n=10, all patients were in CR/PR) reported 4-year OS and PFS 50%; Tsimberidou et al.9 (n=17) reported 3-year OS 75% for seven patients who received alloHCT as postremission therapy and 21% for 13 patients who received allo- or autoHCT as salvage therapy. For patients with RT who do not achieve remission, CAR-T cell ther- apy is a newer option, with recently reported results in a small series (n=9) with limited follow-up by Kittai et al.15 Further and larger studies with longer follow-up are war- ranted to evaluate the efficacy of this therapy on its own or as a bridge to alloHCT.
This study has some limitations owing to its single- center retrospective design with a small sample size of 28 patients, which nonetheless is the largest study to date. Another limitation is the absence of data on clonal rela- tionship between RT and CLL. Published literature,16 however, shows that the majority (~80%) of RT is clon- ally related to the preceding CLL, particularly in heavily pretreated patients like these, suggesting that most RT patients in this study were clonally related.
With availability of less toxic/reduced induced intensi- ty conditioning regimens, improved human leukocyte antigen typing, and better GvHD prophylaxis strategies, alloHCT has become a viable and safe treatment option for patients with high risk hematologic cancers, even with advanced age. Our study results show that a size- able proportion of patients with RT in remission can achieve durable remissions, and that alloHCT should be considered as a treatment option for patients with RT who are fit and have controlled disease.
Haesook T. Kim,1 Peter O. Baker,2 Erin Parry,2 Matthew Davids,2 Edwin P. Alyea,3 Vincent T. Ho,2 Corey Cutler,2 John Koreth,2 Mahasweta Gooptu,2 Rizwan Romee,2 Sarah Nikiforow,2 Joseph H. Antin,2 Jerome Ritz,2 Robert J. Soiffer,2 Catherine J. Wu2#
and Jennifer R. Brown2#
1Department of Data Science, Dana Farber Cancer Institute, Harvard School of Public Health, Boston, MA; 2Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA and 3Duke Cancer Institute, Duke Medical School, Durham, NC, USA
#CJW and JRB contributed equally as co-senior authors. Correspondence:
JENNIFER R. BROWN - jennifer_brown@dfci.harvard.edu HAESOOK T. KIM - htkimc@jimmy.harvard.edu doi:10.3324/haematol.2021.279033
Received: April 19, 2021. Accepted: August 17, 2021. Pre-published: August 26, 2021.
Disclosures: JRB has served as a consultant for Abbvie, Acerta, Astra-Zeneca, Beigene, Catapult, Dynamo Therapeutics, Juno/Celgene, Kite, MEI Pharma, Nextcea, Novartis, Octapharma, Pfizer, Sunesis, TG Therapeutics, Verastem; received honoraria from Janssen and Teva; received research funding from Gilead, Loxo, Sun and Verastem; and served on data safety monitoring committees for Morphosys and Invectys, outside the submitted work. CJW holds equi- ty in BioNTech, Inc, and receives research funding from Pharmacyclics, Inc, outside the submitted work. JR has received research funding from Amgen, Equillium, Kite Pharma and Novartis; and served as a con- sultant for Avrobio, Celgene, Clade Therapeutics, Garuda
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