Efficacy of inotuzumab ozogamicin in patients with Philadelphia chromosome-positive relapsed/refractory acute lymphoblastic leukemia.


Journal

Cancer
ISSN: 1097-0142
Titre abrégé: Cancer
Pays: United States
ID NLM: 0374236

Informations de publication

Date de publication:
15 03 2021
Historique:
received: 09 06 2020
revised: 30 08 2020
accepted: 25 09 2020
pubmed: 25 11 2020
medline: 15 10 2021
entrez: 24 11 2020
Statut: ppublish

Résumé

Patients with relapsed/refractory (R/R) Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia (ALL) have a poor prognosis and limited treatment options. The efficacy of inotuzumab ozogamicin (InO), a humanized anti-CD22 monoclonal antibody conjugated to the cytotoxic antibiotic calicheamicin, was evaluated in R/R ALL patients in the phase 1/2 study 1010 (NCT01363297) and open-label, randomized, phase 3 study 1022 (INO-VATE; NCT01564784). This analysis focused specifically on Ph+ R/R ALL patients. In study 1022, Ph+ patients were randomly assigned 1:1 to InO (n = 22) or standard intensive chemotherapy (SC) (n = 27) and 16 Ph+ patients in study 1010 received InO. In study 1022, rates of complete remission/complete remission with incomplete hematologic recovery (CR/CRi) and minimal residual disease (MRD) negativity (patients achieving CR/CRi) were higher with InO (CR/CRi = 73%; MRD = 81%) versus SC (CR/CRi = 56%; MRD = 33%). The corresponding rates in study 1010 were 56% (CR/CRi) and 100% (MRD). The hematopoietic stem cell transplantation (HSCT) rate in study 1022 was 41% versus 19% for InO versus SC; however, there was no benefit in overall survival (median OS: 8.7 vs 8.4 months; hazard ratio, 1.17 [95% CI, 0.64-2.14]). The probability of being event-free (progression-free survival) at 12 months was greater with InO versus SC (20.1% vs 4.8%). Given the substantial improvement in responses and rates of HSCT, InO is an important treatment option for patients with R/R Ph+ ALL. Future studies need to consider better characterization of disease characteristics, more sensitive MRD measurements, MRD-directed therapy before HSCT, and potentially combination therapies, including tyrosine kinase inhibitors.

Sections du résumé

BACKGROUND
Patients with relapsed/refractory (R/R) Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia (ALL) have a poor prognosis and limited treatment options.
METHODS
The efficacy of inotuzumab ozogamicin (InO), a humanized anti-CD22 monoclonal antibody conjugated to the cytotoxic antibiotic calicheamicin, was evaluated in R/R ALL patients in the phase 1/2 study 1010 (NCT01363297) and open-label, randomized, phase 3 study 1022 (INO-VATE; NCT01564784). This analysis focused specifically on Ph+ R/R ALL patients. In study 1022, Ph+ patients were randomly assigned 1:1 to InO (n = 22) or standard intensive chemotherapy (SC) (n = 27) and 16 Ph+ patients in study 1010 received InO.
RESULTS
In study 1022, rates of complete remission/complete remission with incomplete hematologic recovery (CR/CRi) and minimal residual disease (MRD) negativity (patients achieving CR/CRi) were higher with InO (CR/CRi = 73%; MRD = 81%) versus SC (CR/CRi = 56%; MRD = 33%). The corresponding rates in study 1010 were 56% (CR/CRi) and 100% (MRD). The hematopoietic stem cell transplantation (HSCT) rate in study 1022 was 41% versus 19% for InO versus SC; however, there was no benefit in overall survival (median OS: 8.7 vs 8.4 months; hazard ratio, 1.17 [95% CI, 0.64-2.14]). The probability of being event-free (progression-free survival) at 12 months was greater with InO versus SC (20.1% vs 4.8%).
CONCLUSION
Given the substantial improvement in responses and rates of HSCT, InO is an important treatment option for patients with R/R Ph+ ALL. Future studies need to consider better characterization of disease characteristics, more sensitive MRD measurements, MRD-directed therapy before HSCT, and potentially combination therapies, including tyrosine kinase inhibitors.

Identifiants

pubmed: 33231879
doi: 10.1002/cncr.33321
pmc: PMC7983935
doi:

Substances chimiques

Inotuzumab Ozogamicin P93RUU11P7

Banques de données

ClinicalTrials.gov
['NCT01363297', 'NCT01564784']

Types de publication

Journal Article Randomized Controlled Trial Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

905-913

Subventions

Organisme : Pfizer Inc

Informations de copyright

© 2020 The Authors. Cancer published by Wiley Periodicals LLC on behalf of American Cancer Society.

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Auteurs

Wendy Stock (W)

Section of Hematology/Oncology, Department of Medicine, and University of Chicago Comprehensive Cancer Center, University of Chicago, Chicago, Illinois.

Giovanni Martinelli (G)

Istituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori IRCCS, Meldola, Italy.

Matthias Stelljes (M)

Universitätsklinikum Münster, Münster, Germany.

Daniel J DeAngelo (DJ)

Dana-Farber Cancer Institute, Boston, Massachusetts.

Nicola Gökbuget (N)

Goethe University, Frankfurt, Germany.

Anjali S Advani (AS)

Cleveland Clinic Taussig Cancer Institute, Cleveland, Ohio.

Susan O'Brien (S)

Chao Family Comprehensive Cancer Center, University of California Irvine, Orange, California.

Michaela Liedtke (M)

Stanford Cancer Institute, Stanford, California.

Akil A Merchant (AA)

Cedars Sinai Medical Center, Los Angeles, California.

Ryan D Cassaday (RD)

University of Washington School of Medicine and Fred Hutchinson Cancer Research Center, Seattle, Washington.

Tao Wang (T)

Pfizer Inc, Cambridge, Massachusetts.

Hui Zhang (H)

Pfizer Inc, Shanghai, China.

Erik Vandendries (E)

Pfizer Inc, Cambridge, Massachusetts.

Elias Jabbour (E)

University of Texas MD Anderson Cancer Center, Houston, Texas.

David I Marks (DI)

University Hospitals Bristol, Bristol, UK.

Hagop M Kantarjian (HM)

University of Texas MD Anderson Cancer Center, Houston, Texas.

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Classifications MeSH