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Editorials
sia.9,11,12 It is highly probable that the inferior outcome of t-ALL patients may be attributable to the high-risk of cytogenetic abnormalities in these patients rather than the antecedent cancer itself even after considering the possible relapse of the neoplasia after the ALL treatment. In Ph-positive t-ALL the combination of tyrosine kinase inhibitors and chemotherapy, generally followed by alloHSCT, yields similar results to those observed in de novo Ph-positive ALL.16 The presence of ACA to the Ph chromosome does not seem to have an impact on prog- nosis, but the low number of cases cannot drive solid con- clusions.
The current information of t-ALL is based on retrospec- tive studies of patients treated with chemotherapy fol- lowed, when possible, by alloHSCT in first CR. The latter decision is based on the assumption of their poor progno- sis, mirroring what occurs in t-AML or t-MDS. Deep molecular studies as well as the systematic use of MRD in newly diagnosed patients with t-ALL are required in order to increase the knowledge of the precise mechanisms of leukemogenesis and to make an adequate choice of the post-remission therapy. Given the scarce frequency of t- ALL, the response of the relapsed or refractory patients to the modern immunotherapeutic or targeted therapy approaches is largely unknown, and their possible use in first-line therapy has not been evaluated to date. Finally, the identification of prognostic factors, especially genetic biomarkers, predictive for t-ALL or s-ALL in patients with primary malignancies should be pursued in order to pre- vent or anticipate the occurrence of this disease.
References
1. Aldoss I, Stiller T, Tsai NC, et al. Therapy-related acute lymphoblas- tic leukemia has distinct clinical and cytogenetic features compared to de novo acute lymphoblastic leukemia, but outcomes are compa- rable in transplanted patients. Haematologica. 2018. doi: 10.3324/haematol.2018.193599.
2. Bagg A. Therapy-associated lymphoid proliferations. Adv Anat
Pathol. 2011;18(3):199-205.
3. Pagano L, Pulsoni A, Tosti ME, et al. Acute lymphoblastic leukaemia
occurring as second malignancy: report of the GIMEMA archive of adult acute leukaemia. Gruppo Italiano Malattie Ematologiche Maligne dell'Adulto. Br J Haematol. 1999;106(4):1037-1040.
4. Shivakumar R, Tan W, Wilding GE, Wang ES, Wetzler M. Biologic features and treatment outcome of secondary acute lymphoblastic leukemia--a review of 101 cases. Ann Oncol. 2008;19(9):1634-1638.
5. Tang G, Zuo Z, Thomas DA, et al. Precursor B-acute lymphoblastic leukemia occurring in patients with a history of prior malignancies: is it therapy-related? Haematologica. 2012;97(6):919-925.
6. Abdulwahab A, Sykes J, Kamel-Reid S, et al. Therapy-related acute lymphoblastic leukemia is more frequent than previously recognized and has a poor prognosis. Cancer. 2012;118(16):3962-3967.
7. Ganzel C, Devlin S, Douer D, et al. Secondary acute lymphoblastic leukaemia is constitutional and probably not related to prior therapy. Br J Haematol. 2015;170(1):50-55.
8. Matnani R, Parekh V, Borate U, Brazelton J, Reddy V, Peker D. Therapy-related B-lymphoblastic leukemia associated with Philadelphia chromosome and MLL rearrangement: Single institu- tion experience and the review of the literature. Pathol Int. 2015;65(10):536-540.
9. Giri S, Chi M, Johnson B, et al. Secondary acute lymphoblastic leukemia is an independent predictor of poor prognosis. Leuk Res. 2015;39(12):1342-1346.
10. KelleherN,GallardoD,Gonzalez-CamposJ,etal.Incidence,clinical and biological characteristics and outcome of secondary acute lym- phoblastic leukemia after solid organ or hematologic malignancy. Leuk Lymphoma. 2016;57(1):86-91.
11. Rosenberg AS, Brunson A, Paulus JK, et al. Secondary acute lym- phoblastic leukemia is a distinct clinical entity with prognostic sig- nificance. Blood Cancer J. 2017;7(9):e605.
12. Swaika A, Frank RD, Yang D, et al. Second primary acute lym- phoblastic leukemia in adults: a SEER analysis of incidence and out- comes. Cancer Med. 2018;7(2):499-507.
13. KurtH,ZhengL,KantarjianHM,etal.SecondaryPhiladelphiachro- mosome acquired during therapy of acute leukemia and myelodys- plastic syndrome. Mod Pathol. 2018;31(7):1141-1154.
14. Imamura T, Taga T, Takagi M, et al. Leukemia/Lymphoma Committee; Japanese Society of Pediatric Hematology Oncology (JSPHO). Nationwide survey of therapy-related leukemia in child- hood in Japan. Int J Hematol. 2018;108(1):91-97.
15. Aldoss I, Dagis A, Palmer J, et al. Therapy-related ALL: cytogenetic features and hematopoietic cell transplantation outcome. Bone Marrow Transplant. 2015;50(5):746-748.
16. Aldoss I, Stiller T, Song J, et al. Philadelphia chromosome as a recur- rent event among therapy-related acute leukemia. Am J Hematol. 2017;92(2):E18-E19.
eGVHD App: a new tool to improve graft-versus-host disease assessment
Marie Therese Rubio
Service d’Hématologie, CHRU Nancy, Hôpital Brabois, and CNRS UMR 7365, Equipe 6, Biopole de l’Université de Lorraine, Vandoeuvre les Nancy, France
E-mail: mt_rubio@hotmail.com doi:10.3324/haematol.2018.200303
Accurately diagnosing and scoring acute and chron- ic graft-versus-host disease (GvHD) remain chal- lenging for many hematologists. Inconsistency between bone marrow transplant centers has been recog- nized in this field, in particular because of problems in following the latest recommended guidelines.1-3 In this regard, Schoemans et al. present a new electronic tool, the eGVHD application (eGVHD App), designed to improve and harmonize GvHD assessment. 4
The eGVHD app was developed by the UZ Leuven (Belgium) in collaboration with the European Society for Blood and Marrow Transplantation (EBMT) Transplantation Complications Working Party and the National Institute of Health (NIH) (Bethesda, USA). This e-tool is a free, open-source web application, distributed as a normal website or a mobile application (accessible at: www.uzleuven.be/egvhd). The App allows the diagnosis of classic and late acute, as well as classic and overlap
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