Radioimmunotherapy for Treatment of Acute Leukemia

Bodet-Milin, Caroline; Kraeber-Bodéré, Françoise; Eugène, Thomas; Guérard, François; Gaschet, Joëlle; Bailly, Clément; Mougin, Marie; Bourgeois, Mickaël; Faivre-Chauvet, Alain; Chérel, Michel; Chevallier, Patrice

doi:10.1053/j.semnuclmed.2015.10.007

Cited by 31 publications

(24 citation statements)

References 58 publications

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“…On the basis of our results, we can consider pan CD66 good candidate for immunotherapy in B-ALL and AML due to its high frequency of expression and molecular stability after induction therapy. However, anti-CD66 radioimmunotherapy may not be the optimal radioimmunoconjugate as its mechanism is indirect with no direct fixation on the leukemic blasts as it was tried earlier [37].…”

Section: Discussionmentioning

confidence: 99%

Membranous Expression of pan CD66, CD66a, CD66b, and CD66c and their Clinical Impact in Acute Leukemia: Cross Sectional Longitudinal Cohort Study in Saudi Arabia

Ismail¹,

Zaghloul²,

Ab³

et al. 2017

J Leuk

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the early phases of many cancers including colon, prostate, liver, and breast cancers, and it is thought to be a tumour suppressor protein [13]. However, CECAM1-L, CD66a isoforms is overexpressed in other types of aggressive cancers, such as melanoma, gastric, thyroid, bladder cancers [14] and metastatic colon cancer [15], thus demonstrating its role in metastasis [14]. CD66b is highly expressed on the surface of peripheral blood eosinophils [16]. It is expressed by promyelocytes and early myelocytes, reaches maximal expression at the late myelocyte and metamyelocyte stages and then decreases at the band and segmented neutrophil stages [11]. CD66c is expressed on granulocytes and their precursors [16]. In contrast to CD66b, CD66c expression is highest at the promyelocyte stage and progressively declines during maturation [11]. It inhibits anoikis, a form of programmed cell death [17], and modulating its expression alters the malignant phenotype of cancer cells. Its deregulation was first noticed in chronic myeloid leukaemia [9] and childhood B-acute lymphoblastic leukaemia [18]. CD66c might be the most specific marker for some aggressive cancers [13].

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Section: Discussionmentioning

confidence: 99%

Membranous Expression of pan CD66, CD66a, CD66b, and CD66c and their Clinical Impact in Acute Leukemia: Cross Sectional Longitudinal Cohort Study in Saudi Arabia

Ismail¹,

Zaghloul²,

Ab³

et al. 2017

J Leuk

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“…Apart from this standard approach, novel treatment methods have been also proposed in the recent decade, including monoclonal antibodies [42], immuno-chemotherapy [43], interferon-α-maintenance therapy [44], radio-immunotherapy [45], and stem cell transplantation [46]. Despite promising results, most of these methods are in preclinical or clinical trials.…”

Section: Discussionmentioning

confidence: 99%

Induction of Apoptosis in U937 Cells by Using a Combination of Bortezomib and Low-Intensity Ultrasound

et al. 2016

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BackgroundWe scrutinized the feasibility of apoptosis induction in blood cancer cells by means of low-intensity ultrasound and the proteasome inhibitor bortezomib (Velcade).Material/MethodsHuman leukemic monocyte lymphoma U937 cells were subjected to ultrasound in the presence of bortezomib and the echo contrast agent Sonazoid. Two types of acoustic intensity (0.18 W/cm2 and 0.05 W/cm2) were used for the experiments. Treated U937 cells were analyzed for viability and levels of early and late apoptosis. In addition, scanning electron microscopy analysis of treated cells was performed.ResultsThe percentage of cells that underwent early apoptosis in the group treated with ultrasound and Sonazoid was 8.0±1.31% (intensity 0.18 W/cm2) and 7.0±1.69% (0.05 W/cm2). However, coupling of bortezomib and Sonazoid resulted in an increase in the percentage of cells in the early apoptosis phase, up to 32.50±3.59% (intensity 0.18 W/cm2) and 33.0±4.90% (0.05 W/cm2). The percentage of U937 cells in the late apoptosis stage was not significantly different from that in the group treated with bortezomib only.ConclusionsOur findings indicate the feasibility of apoptosis induction in blood cancer cells by using a combination of bortezomib, ultrasound contrast agents, and low-intensity ultrasound.

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“…188 Rhe-labeled CD66 antibody. [71][72][73][74] Unfortunately, these antibodies usually produce substantial hematologic toxicities, including prolonged cytopenia (long-term aplasia) which is due to the accumulation of these agents in various hematopoietic tissues thereby affecting also normal hematopoietic stem and progenitor cells by cross-radiation. As a result, such antibodies have to be applied in conjunction with a subsequent HSCT.…”

Section: Antigen CDmentioning

confidence: 99%

Cell-based and antibody-mediated immunotherapies directed against leukemic stem cells in acute myeloid leukemia: Perspectives and open issues

Valent

Bauer

Sadovnik

et al. 2020

Stem Cells Translational Medicine

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Despite new insights in molecular features of leukemic cells and the availability of novel treatment approaches and drugs, acute myeloid leukemia (AML) remains a major clinical challenge. In fact, many patients with AML relapse after standard therapy and eventually die from progressive disease. The basic concept of leukemic stem cells (LSC) has been coined with the goal to decipher clonal architectures in various leukemia-models and to develop curative drug therapies by eliminating LSC. Indeed, during the past few years, various immunotherapies have been tested in AML, and several of these therapies follow the strategy to eliminate relevant leukemic subclones by introducing LSC-targeting antibodies or LSC-targeting immune cells. These therapies include, among others, new generations of LSC-eliminating antibody-constructs, checkpoint-targeting antibodies, bi-specific antibodies, and CART or CAR-NK cell-based strategies. However, responses are often limited and/or transient which may be due to LSC resistance. Indeed, AML LSC exhibit multiple forms of resistance against various drugs and immunotherapies. An additional problems are treatment-induced myelotoxicity and other side effects. The current article provides a short overview of immunological targets expressed on LSC in AML. Moreover, cell-based therapies and immunotherapies tested in AML are discussed. Finally, the article provides an overview about LSC resistance and strategies to overcome resistance.

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Radioimmunotherapy for Treatment of Acute Leukemia

Cited by 31 publications

References 58 publications

Membranous Expression of pan CD66, CD66a, CD66b, and CD66c and their Clinical Impact in Acute Leukemia: Cross Sectional Longitudinal Cohort Study in Saudi Arabia

Membranous Expression of pan CD66, CD66a, CD66b, and CD66c and their Clinical Impact in Acute Leukemia: Cross Sectional Longitudinal Cohort Study in Saudi Arabia

Induction of Apoptosis in U937 Cells by Using a Combination of Bortezomib and Low-Intensity Ultrasound

Cell-based and antibody-mediated immunotherapies directed against leukemic stem cells in acute myeloid leukemia: Perspectives and open issues

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