title: Analysis of pRb, p16INK4A proteins and proliferating antigens: PCNA, Ki-67 and MCM5 expression in aggressive fibromatosis (desmoid tumor).
abstract: Aggressive fibromatosis (desmoid tumor) is a mesenchymal lesion originating from fascial, aponeurotic and muscular connective tissue. It rarely becomes histologically malignant. In this study we analyzed the cell cycle regulation proteins: pRb, p16, and proliferating antigens: Ki-67, PCNA, MCM5 with immunohistochemical method in archival material derived from 27 extra-abdominal (E-AD), 18 abdominal (AD) and 5 intra-abdominal (I-AD) cases of desmoid tumor. None of the examined cases (n=50) of aggressive fibromatosis was pRb-immunonegative. Heterogeneous expression of pRb was observed in 51.85% (14/27) of Group AD cases and in 5.56% (1/18) of Group E-AD cases; positive expression in 48,15% (13/27) of Group AD cases, in 94.44% (17/18) of Group E-AD cases, and in 100% (5/5) of Group I-AD cases. There were no negative cases for p16 staining in any of the examined groups. The number of heterogeneous cases in individual groups was: 33.33% (9/27) in Group AD, 50% (9/18) in Group E-AD and 40% (2/5) in Group I-AD, and positive cases: 66.67% (18/27), 50% (9/18) and 60% (3/5), respectively. Overexpression of PCNA was noted in 98% (49/50) of cases. The positive staining for Ki-67 protein was noted in 25.93% (7/27) in Group AD, in 16.67% (3/18) in Group E-AD and in 60% (3/5) in Group I-AD. None of the examined cases was immunopositive for MCM5 protein. The noted levels of pRb and p16 expression in desmoid cells reflect their function in cell cycle regulation. Probably the unsettled cell cycle progression, especially in G1 phase, is not the cause of aggressive fibromatosis pathogenesis.
authors.affiliation: Department of Biology and Genetics, Medical University, Lodz, Poland. liliana.stalinska@gmail.com
authors.forename: Liliana
authors.initials: L
authors.lastname: Stalinska
authors.forename: Maria
authors.initials: M
authors.lastname: Turant
authors.forename: Dariusz
authors.initials: D
authors.lastname: Tosik
authors.forename: Jacek
authors.initials: J
authors.lastname: Sygut
authors.forename: Andrzej
authors.initials: A
authors.lastname: Kulig
authors.forename: Janusz
authors.initials: J
authors.lastname: Kopczynski
authors.forename: Adam
authors.initials: A
authors.lastname: Dziki
authors.forename: Tomasz
authors.initials: T
authors.lastname: Ferenc
mesh_terms: D018797:Cell Cycle Proteins / Q000032:analysis* / Q000235:genetics / Q000378:metabolism; D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000032:analysis* / Q000235:genetics / Q000378:metabolism; D018221:Fibromatosis, Abdominal / Q000378:metabolism* / Q000473:pathology; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D007150:Immunohistochemistry; D019394:Ki-67 Antigen / Q000032:analysis* / Q000235:genetics / Q000378:metabolism; D018809:Proliferating Cell Nuclear Antigen / Q000032:analysis* / Q000235:genetics / Q000378:metabolism; D016160:Retinoblastoma Protein / Q000032:analysis* / Q000235:genetics / Q000378:metabolism
chemical_list: D018797:Cell Cycle Proteins; D019941:Cyclin-Dependent Kinase Inhibitor p16; D019394:Ki-67 Antigen; C489423:MCM5 protein, human; D018809:Proliferating Cell Nuclear Antigen; D016160:Retinoblastoma Protein