Niche-expressed Galectin-1 is involved in pre-B acute lymphoblastic leukemia relapse through pre-B cell receptor activation

被引：1

作者：

Pelletier, Jeoffrey ^{[1
]}

Balzano, Marielle ^{[1
]}

Destin, Jerome ^{[2
]}

Montersino, Camille ^{[1
]}

Delahaye, Marjorie C. ^{[1
]}

Marchand, Tony ^{[2
]}

Bailly, Anne-Laure ^{[1
]}

Bardin, Florence ^{[1
]}

Coppin, Emilie ^{[1
,7
]}

Goubard, Armelle ^{[1
]}

Castellano, Remy ^{[1
]}

de Bruijn, Marjolein J. W. ^{[3
]}

Rip, Jasper ^{[3
,8
]}

Collette, Yves ^{[1
]}

Dubreuil, Patrice ^{[1
]}

Tarte, Karin ^{[2
]}

Broccardo, Cyril ^{[4
]}

Hendriks, Rudi W. ^{[3
]}

Schiff, Claudine ^{[5
]}

Vey, Norbert ^{[1
,6
]}

Aurrand-Lions, Michel ^{[1
]}

Mancini, Stephane J. C. ^{[1
,2
]}

机构：

[1] Aix Marseille Univ, CNRS, INSERM, Inst Paoli Calmettes,CRCM, Marseille, France

[2] Univ Rennes, INSERM, EFS, UMR S1236, Rennes, France

[3] Erasmus MC, Univ Med Ctr, Dept Pulm Med, Rotterdam, Netherlands

[4] Univ Toulouse III Paul Sabatier, Ctr Rech Cancerol Toulouse, INSERM UMR 1037, Toulouse, France

[5] Aix Marseille Univ, CNRS, INSERM, CIML, Marseille, France

[6] Inst Paoli Calmettes, Dept Hematol, Marseille, France

[7] Leibniz Inst Aging, Fritz Lipmann Inst, Immunol Aging, Jena, Germany

[8] Erasmus MC, Univ Med Ctr, Dept Immunol, Rotterdam, Netherlands

来源：

ISCIENCE | 2023年 / 26卷 / 04期

关键词：

BRUTONS TYROSINE KINASE; STROMAL CELLS; TUMOR-SUPPRESSOR; PROLIFERATION; MECHANISMS; SLP-65; AGENT; MOUSE; MICE;

D O I：

10.1016/j.isci.2023.106385

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

B-cell acute lymphoblastic leukemia (B-ALL) reflects the malignant counterpart of developing B cells in the bone marrow (BM). Despite tremendous progress in B-ALL treatment, the overall survival of adults at diagnosis and patients at all ages after relapse remains poor. Galectin-1 (GAL1) expressed by BM supportive niches delivers proliferation signals to normal pre-B cells through interaction with the pre-B cell receptor (pre-BCR). Here, we asked whether GAL1 gives non-cell autonomous signals to pre-BCR+ pre-B ALL, in addition to cell-autonomous signals linked to genetic alterations. In syngeneic and patient-derived xenograft (PDX) murine models, murine and human pre-B ALL development is influenced by GAL1 produced by BM niches through pre-BCR-dependent signals, similarly to normal pre-B cells. Furthermore, targeting pre-BCR signaling together with cell-autonomous oncogenic pathways in pre-B ALL PDX improved treatment response. Our results show that non-cell autonomous signals transmitted by BM niches represent promising targets to improve B-ALL patient survival.

引用

页数：17

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