title: B7-H3 protein expression in acute myeloid leukemia.
abstract: Costimulatory molecules are essential regulators of the immunological synapse and enable the fine-tuning of the immune response. These mechanisms are subverted by cancer cells to evade immunosurveillance. The B7 family of costimulatory molecules comprises several ligands that may contribute to immunoescape. B7-H3 [B7-homolog 3 or CD276] remains poorly investigated in hematological malignancies. To determine the role B7-H3, we analyzed the expression of this molecule in blast cells from a cohort of 111 acute myeloid leukemia (AML) patients. B7-H3 was expressed in blast cells with a mean fluorescence intensity ratio >3 in 30 (27%) of the 111 patients. B7-H3 expression was higher in the M3 and M5 FAB subtypes and in cases with mutated NPM1 and wild type CEBPA. There were no significant differences found for the FLT3-ITD or cytogenetic risk groups. The complete remission (CR) rate between the 17 B7-H3-positive and 58 negative patients who were treated intensively was not different. The event free survival was longer in B7-H3-positive patients (P = 0.014), and there was a trend toward better overall survival. However, this difference was not statistically significant (P = 0.053). In conclusion, B7-H3 is one of the most strongly expressed B7-family molecules in AML and merits further investigation.
authors.affiliation: Laboratoire d'Hématologie, CHRU, Lille, France.
authors.forename: Thomas
authors.initials: T
authors.lastname: Guery
authors.affiliation: Laboratoire d'Hématologie, CHRU, Lille, France.|INSERM, UMR 1172, Lille, France.
authors.forename: Christophe
authors.initials: C
authors.lastname: Roumier
authors.affiliation: INSERM, UMR 1172, Lille, France.|Service des Maladies du Sang, CHRU, Lille, France.
authors.forename: Celine
authors.initials: C
authors.lastname: Berthon
authors.affiliation: Laboratoire d'Hématologie, CHRU, Lille, France.|INSERM, UMR 1172, Lille, France.
authors.forename: Aline
authors.initials: A
authors.lastname: Renneville
authors.affiliation: Laboratoire d'Hématologie, CHRU, Lille, France.|INSERM, UMR 1172, Lille, France.|Université de Lille, Lille, France.
authors.forename: Claude
authors.initials: C
authors.lastname: Preudhomme
authors.affiliation: INSERM, UMR 1172, Lille, France.|Service des Maladies du Sang, CHRU, Lille, France.|Université de Lille, Lille, France.
authors.forename: Bruno
authors.initials: B
authors.lastname: Quesnel
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D060887:B7 Antigens / Q000235:genetics / Q000378:metabolism*; D015415:Biomarkers; D002471:Cell Transformation, Neoplastic / Q000235:genetics / Q000378:metabolism; D002648:Child; D002675:Child, Preschool; D005260:Female; D015870:Gene Expression; D006801:Humans; D016130:Immunophenotyping; D007223:Infant; D007231:Infant, Newborn; D015470:Leukemia, Myeloid, Acute / Q000175:diagnosis / Q000235:genetics / Q000276:immunology / Q000378:metabolism* / Q000401:mortality; D008297:Male; D008875:Middle Aged; D000090243:Nucleophosmin; D055815:Young Adult
chemical_list: D060887:B7 Antigens; D015415:Biomarkers; C423237:CD276 protein, human; C000716967:NPM1 protein, human; D000090243:Nucleophosmin
keywords: AML; B7-H3; CD276; CEBPA; NPM1; prognosis