CD9 expression indicates a poor outcome in acute lymphoblastic leukemia

Peng, Liang; Miao, Miao; Liu, Zhuogang; Wang, Hongtao; Jiang, Wei; Ma, Shi-yu; Li, Chuan; Hu, Rong

doi:10.3233/cbm-170422

Cited by 17 publications

(13 citation statements)

References 20 publications

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“…Liu et al showed a significant expression of CD9 in AML with NPM1 mutation and, therefore, a favorable prognosis, which is consistent with our findings. In contrast, CD9 seems to be associated with a worse prognosis in ALL treated with intensive chemotherapy, as it was demonstrated in a cohort of 87 patients . These different results are probably explained by the association of CD9 in TEMs with different partners in ALL and AML.…”

Section: Discussionmentioning

confidence: 81%

CD9 in acute myeloid leukemia: Prognostic role and usefulness to target leukemic stem cells

et al. 2019

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CD9 is a cell surface protein and belongs to the tetraspanin family. Its role in carcinomagenesis has been widely studied in solid tumors but remains controversial, depending on the cancer type. Although CD9 seems to be associated with unfavorable outcome and disease progression in acute lymphoblastic leukemia (ALL), this marker has not yet been studied in acute myeloid leukemia (AML). First, we explored its prognostic role and its association with biological factors in a cohort of 112 AML patients treated with intensive chemotherapy. CD9 was expressed in 40% of AML and was associated with a favorable outcome (event‐free survival and relapse‐free survival) in univariate (P = 0.009 and P = 0.048, respectively) and multivariate (P = 0.004 and P = 0.039, respectively) analyses. Interestingly, CD9 expression was different between the more immature physiologic and AML cells (CD34+CD38−) as it was also expressed in AML on putative leukemic stem cells (LSCs) but not on hematopoietic stem cells (HSCs). Hence, CD9 could be a very relevant marker for minimal residual disease (MRD) monitoring in AML based on LSC targeting.

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Section: Discussionmentioning

confidence: 81%

CD9 in acute myeloid leukemia: Prognostic role and usefulness to target leukemic stem cells

et al. 2019

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“…However, CD9 is not strictly recognized as a metastasis suppressor gene because in some tumors, inverse activity is observed. For example, in acute lymphoblastic leukemia, CD9 expression indicates a poor outcome ( 76 ). The various roles of tetraspanins in tumor progression may be the result of specific tetraspanin abundance in exosomes.…”

Section: Cd9 Is Involved In Various Diseasesmentioning

confidence: 99%

CD9 Tetraspanin: A New Pathway for the Regulation of Inflammation?

et al. 2018

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CD9 belongs to the tetraspanin superfamily. Depending on the cell type and associated molecules, CD9 has a wide variety of biological activities such as cell adhesion, motility, metastasis, growth, signal transduction, differentiation, and sperm–egg fusion. This review focuses on CD9 expression by hematopoietic cells and its role in modulating cellular processes involved in the regulation of inflammation. CD9 is functionally very important in many diseases and is involved either in the regulation or in the mediation of the disease. The role of CD9 in various diseases, such as viral and bacterial infections, cancer and chronic lung allograft dysfunction, is discussed. This review focuses also on its interest as a biomarker in diseases. Indeed CD9 is primarily known as a specific exosome marker however, its expression is now recognized as an anti-inflammatory marker of monocytes and macrophages. It was also described as a marker of murine IL-10-competent Breg cells and IL-10-secreting CD9+ B cells were associated with better allograft outcome in lung transplant patients, and identified as a new predictive biomarker of long-term survival. In the field of cancer, CD9 was both identified as a favorable prognostic marker or as a predictor of metastatic potential depending on cancer types. Finally, this review discusses strategies to target CD9 as a therapeutic tool. Because CD9 can have opposite effects depending on the situation, the environment and the pathology, modulating CD9 expression or blocking its effects seem to be a new promising therapeutic strategy.

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“…The association between tetraspanin expression and cancer prognostic is found in many kinds of cancers (Table 1 ). In B lymphoma, aberrant expression of CD9, CD81, and CD82 was linked to B-acute lymphoblastic leukemia ( 30 – 32 ). Increased CD37 expression was found in B cell malignancies and thus CD37 antibodies were developed to deplete malignant B cells for the treatment of chronic lymphocytic leukemia ( 33 ).…”

Section: Functions Of Tetraspanins In B Cellsmentioning

confidence: 99%

Expression and Function of Tetraspanins and Their Interacting Partners in B Cells

et al. 2018

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Tetraspanins are transmembrane proteins that modulate multiple diverse biological processes, including signal transduction, cell–cell communication, immunoregulation, tumorigenesis, cell adhesion, migration, and growth and differentiation. Here, we provide a systematic review of the involvement of tetraspanins and their partners in the regulation and function of B cells, including mechanisms associated with antigen presentation, antibody production, cytokine secretion, co-stimulator expression, and immunosuppression. Finally, we direct our focus to the signaling mechanisms, evolutionary conservation aspects, expression, and potential therapeutic strategies that could be based on tetraspanins and their interacting partners.

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CD9 expression indicates a poor outcome in acute lymphoblastic leukemia

Abstract: CD9 expression predicts some clinical characteristics and indicates an unfavorable prognosis in ALL patients.

Cited by 17 publications

References 20 publications

CD9 in acute myeloid leukemia: Prognostic role and usefulness to target leukemic stem cells

CD9 in acute myeloid leukemia: Prognostic role and usefulness to target leukemic stem cells

CD9 Tetraspanin: A New Pathway for the Regulation of Inflammation?

Expression and Function of Tetraspanins and Their Interacting Partners in B Cells

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