Theodore F. Zipf

Children's Hospital of Los Angeles

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Dennis A. Johnston

Baylor University

W. Mark Roberts

Ochsner Medical Center

Zeev Estrov

The University of Texas MD Anderson Cancer Center

Maia V. Ouspenskaia

National Institutes of Health

Sima Jeha

St. Jude Children's Research Hospital

Gamil R. Antoun

University of Ottawa

Kenneth V. I. Rolston

The University of Texas MD Anderson Cancer Center

Michael Rytting

The University of Texas MD Anderson Cancer Center

Craig A. Mullen

University of Rochester

Demetrios Petropoulos

The University of Texas MD Anderson Cancer Center

Cooperative Institutions

The University of Texas MD Anderson Cancer Center

The University of Texas Health Science Center at Houston

Baylor College of Medicine

St. Jude Children's Research Hospital

Anderson Hospital

The University of Texas at Austin

University of Southern California

Children's Cancer Center

Children's Hospital of Los Angeles

Boston Children's Hospital

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Immature and Differentiated Neoplastic Populations in Acute Lymphoid Leukemia of Childhood: Biological and Clinical Implications

Leukemia & lymphoma/Leukemia and lymphoma (1993)

Zeev Estrov Gian Guldo Re Theodore F. Zipf

Despite significant improvement in the therapy for acute lymphoid leukemia (ALL) of childhood, approximately 30% of patients relapse. Unfortunately, since no successful treatment for recurrent disease has been developed, the majority of these patients die. Recently, we presented evidence consistent with the presence of a limited program of differentiation in B-precursor ALL that is reminiscent of normal B-cell development. We found that ALL cell populations consist of both a subpopulation of progenitors with the immunophenotype of normal B-cell precursors that has self-renewal capability and a second subpopulation with a more mature early B-cell immunophenotype that is without self-renewal capability but can proliferate to a limited extent. In our recent studies we were able to grow the progenitor cells in the ALL blast colony assay and establish their leukemic origin using the polymerase chain reaction. Our results suggest that these progenitors are the cells that sustain the disease. We hypothesize that these cells may remain quiescent, for a time, and either eventually die or regain proliferative capability and cause relapse. Further studies aimed both at detecting residual ALL and determining changes in their biology may provide an understanding of the mechanisms of relapse in this disease.

Immunophenotyping

Minimal Residual Disease

Precursor cell

10.3109/10428199309054724

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Citations (7)

Risk classification at the time of diagnosis differentially affects the level of residual disease in children with B-precursor acute lymphoblastic leukemia after completion of therapy

Leukemia Research (2003)

M. Fatih Okcu W. Mark Roberts Dennis A. Johnston Maia V. Ouspenskaia Victor Z. Papusha

Minimal Residual Disease

Residual risk

Group B

10.1016/s0145-2126(02)00324-7

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Citations (1)

Editors’ Notes

Humana Press eBooks (2003)

Theodore F. Zipf Dennis A. Johnston

10.1007/978-1-59259-318-7_15

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Definition of the high-risk acute lymphoblastic leukemia patient by immunological phenotyping with monoclonal antibodies.

PubMed (1981)

Theodore F. Zipf Robert I. Fox Jeanette Dilley Ronald Levy

An accurate method of classification of the surface membrane characteristics of blast cells from patients with acute lymphoblastic leukemia would allow a more definitive study of the nature of this disease. Monoclonal antibodies have been produced to the surface antigens of leukemic blasts form a patient with high-risk acute lymphoblastic leukemia. Two antibodies of interest were obtained from this immunization. These two, in combination with a monoclonal antibody with anti-Ia specificity, have been used to obtain surface phenotypes for patients with childhood acute lymphoblastic leukemia. Preliminary results indicate that the definition of a high-risk group, using these antibodies, possible.

Acute lymphocytic leukemia

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Citations (13)

Outpatient treatment of fever and neutropenia for low risk pediatric cancer patients

Cancer (1999)

Craig A. Mullen Demetrios Petropoulos Walter Roberts Michael Rytting Theodore F. Zipf

Pediatric cancer

10.1002/(sici)1097-0142(19990701)86:1<126::aid-cncr18>3.3.co;2-t

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Citations (12)

Inhibition of acute myelogenous leukemia progenitor proliferation by macrophage inflammatory protein 1-alpha.

PubMed (1994)

Alessandra Ferrajoli Moshe Talpaz Theodore F. Zipf Cheryl Hirsch‐Ginsberg Elihu H. Estey

Macrophage inflammatory protein

Alpha (finance)

Interleukin 3

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Citations (26)

Detection of minimal residual disease in all: biology, methods, and applications

Cancer treatment and research (1996)

W. Mark Roberts Zeev Estrov Geoffrey R. Kitchingman Theodore F. Zipf

Minimal Residual Disease

Spontaneous remission

Cure rate

10.1007/978-1-4613-1261-1_8

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Citations (7)

High-Dose Mercaptopurine and Intermediate-Dose Cytarabine During First Remission of Acute Myeloid Leukemia

Cancer Investigation (1997)

Cengiz Canpolat Sima Jeha Sharon Lockhart Irma Ramirez Theodore F. Zipf

High-dose, continuous infusion of intravenous mercaptopurine (HD 6MP) followed by intermediate-dose continuous cytarabine (ID Ara-C) has been shown to produce remissions in children with relapsed acute myeloid leukemia (AML). The purpose of this pilot study was to explore the feasibility of using this drug regimen as a component of treatment during the first remission of AML. Of 17 children with newly diagnosed AML registered in the study, 14 developed complete remission on conventional induction therapy and subsequently received the HD 6MP and ID Ara-C combination. The dosages of HD 6MP were escalated from 500 mg/m2 to 1250 mg/m2 in 24-hr infusions. The initial dosages of ID Ara-C were escalated from 250 mg/m2 to 650 mg/m2/24 hr and from 1 day to 4 days. Conventional treatment for AML was administered simultaneously. Seven of the 14 children remain in initial complete remission for 15 to 46 months and have completed treatment. Severe pancytopenia was observed in all patients, but there were no toxic deaths and no deaths during remission. The inclusion ofHD 6MP and ID Ara-C in the treatment of AML in first remission appears to be feasible. Evaluation of its efficacy will require a comparative clinical trial.

Mercaptopurine

Dose

Regimen

10.3109/07357909709115764

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Citations (1)

Infrared studies and diffraction-grating measurements : final report; period August, 1952 - August, 1954.

Deep Blue (University of Michigan) (1954)

C. W. Peters P. V. Deibel R. H. Hunt William Knox. Pursley Theodore F. Zipf

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