title: ELAM selectin expression in breast carcinomas detected by automated and quantitative immunohistochemical assays.
abstract: ELAM is an E-Selectin adhesion molecule involved in the inflammatory process but it is also thought to potentially participate in the development of blood borne metastases, by facilitating tumour cell adhesion to vessels wall. ELAM expression in tumours was immunohistochemically investigated in 203 breast carcinomas. Frozen tissue sections were probed with monoclonal anti ELAM (Clone 1.2B6) using automated and quantitative immunoperoxidase systems. A positive anti-ELAM immunoreaction was observed in 113 tumours (57%). The mean surface of positive tumours varied from 3% to 50% (mean = 11.75%, SD = 8.7) and was correlated with histoprognostic indicators and tumour expression of various antigens detected according to the same method as ELAM. The results showed that ELAM immunoexpression was independent of the tumour size, grade and type and of the nodal status but significantly increased parallel to patients' age (p<0. 01). ELAM expression was independent of Ki-67/MIB1, anti-P53 and anti-Bcl2, anti-CD44v, anti-c-erbB-2, anti-CD31, anti-RE/RP, anti-PS2, and anti-VLA3 immunoreactions. But ELAM expression correlated with that of the VCAM vascular cell adhesion molecule (p=0.0004), VLA2 (p<0.0001), P-glycoprotein (p=0.025), and of Cathepsin D to a lower degree (p=0.06) and inversely correlated with E-cadherin (p=0.03). The results suggest that endothelial cell activation is independent of tumour cell proliferative activity and of stromal angiogenesis and that the precise role and regulation of ELAM in tumours remains to be elucidated. Also the clinical relevance of ELAM immunohistochemical expression requires further investigation and correlation with patients' follow-up.
authors.affiliation: Laboratoire d'Anatomie Pathologique, Faculté de Médecine Timone, 27 Boulevard Jean Moulin, Marseille Cedex 5, 13385, France.
authors.forename: C
authors.initials: C
authors.lastname: Charpin
authors.forename: D
authors.initials: D
authors.lastname: Bergeret
authors.forename: S
authors.initials: S
authors.lastname: Garcia
authors.forename: L
authors.initials: L
authors.lastname: Andrac
authors.forename: F
authors.initials: F
authors.lastname: Martini
authors.forename: N
authors.initials: N
authors.lastname: Horschowski
authors.forename: R
authors.initials: R
authors.lastname: Choux
authors.forename: M N
authors.initials: MN
authors.lastname: Lavaut
mesh_terms: D020168:ATP Binding Cassette Transporter, Subfamily B, Member 1 / Q000032:analysis; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015703:Antigens, CD / Q000032:analysis; D001331:Automation / Q000379:methods; D001943:Breast Neoplasms / Q000473:pathology* / Q000601:surgery; D015820:Cadherins / Q000032:analysis; D002402:Cathepsin D / Q000032:analysis; D002455:Cell Division; D019040:E-Selectin / Q000032:analysis* / Q000096:biosynthesis; D005260:Female; D006801:Humans; D007124:Immunoenzyme Techniques; D007150:Immunohistochemistry / Q000379:methods; D016023:Integrins / Q000032:analysis; D019394:Ki-67 Antigen / Q000032:analysis; D008207:Lymphatic Metastasis; D008875:Middle Aged; D009389:Neovascularization, Pathologic; D011379:Prognosis; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000032:analysis; D016159:Tumor Suppressor Protein p53 / Q000032:analysis; D019010:Vascular Cell Adhesion Molecule-1 / Q000032:analysis
chemical_list: D020168:ATP Binding Cassette Transporter, Subfamily B, Member 1; D015703:Antigens, CD; D015820:Cadherins; D002402:Cathepsin D; D019040:E-Selectin; D016023:Integrins; D019394:Ki-67 Antigen; D018719:Erb-b2 Receptor Tyrosine Kinases; D016159:Tumor Suppressor Protein p53; D019010:Vascular Cell Adhesion Molecule-1