Abstract
The distinction between benign and malignant tumors is classically based on the metastatic potential of a tumor type. While desmoid tumors do not metastasize and as such are classified as benign lesions, their clinical behavior, cellular biology, and molecular etiology all share more characteristics with malignancies than benign processes. Research into these aspects of desmoid tumor biology has the potential not only to develop better treatments for desmoid tumors, but also to shed light into fundamental aspects of tumor biology that will have broad ranging applications. Its classification as a benign process could have implications hampering research, advocacy, and management progress.
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References
Weekes RG, McLeod RA, Reiman HM, Pritchard DJ (1985) CT of soft-tissue neoplasms. Am J Roentgenol 144:355–360
Donati D, Colangeli S, Colangeli M, Di Bella C, Bertoni F (2010) Surgical treatment of grade I central chondrosarcoma. Clin Orthop Relat Res 468:581–589
Galiatsatos P, Foulkes WD (2006) Familial adenomatous polyposis. Am J Gastroenterol 101:385–398
Hosalkar HS, Fox EJ, Delaney T, Torbert JT, Ogilvie CM, Lackman RD (2006) Desmoid tumors and current status of management. Orthop Clin North Am 37:53–63
Dormans JP, Spiegel D, Meyer J et al (2001) Fibromatoses in childhood: the desmoid/fibromatosis complex. Med Pediatr Oncol 37:126–131
Alman BA, Goldberg MJ, Naber SP, Galanopoulous T, Antoniades HN, Wolfe HJ (1992) Aggressive fibromatosis. J Pediatr Orthop 12:1–10
Bandipalliam P, Balmana J, Syngal S (2004) Comprehensive genetic and endoscopic evaluation may be necessary to distinguish sporadic versus familial adenomatous polyposis-associated abdominal desmoid tumors. Surgery 135:683–689
Benoit L, Faivre L, Cheynel N et al (2007) 3′ Mutation of the APC gene and family history of FAP in a patient with apparently sporadic desmoid tumors. J Clin Gastroenterol 41:297–300
Maher ER, Morson B, Beach R, Hodgson SV (1992) Phenotypic variation in hereditary nonpolyposis colon cancer syndrome. Association with infiltrative fibromatosis (desmoid tumor). Cancer 69:2049–2051
Gurbuz AK, Giardiello FM, Petersen GM et al (1994) Desmoid tumours in familial adenomatous polyposis. Gut 35:377–381
Eccles DM, van der Luijt R, Breukel C et al (1996) Hereditary desmoid disease due to a frameshift mutation at codon 1924 of the APC gene. Am J Hum Genet 59:1193–1201
Scott RJ, Froggatt NJ, Trembath RC, Evans DG, Hodgson SV, Maher ER (1996) Familial infiltrative fibromatosis (desmoid tumours) (MIM135290) caused by a recurrent 3′ APC gene mutation. Hum Mol Genet 5:1921–1924
Couture J, Mitri A, Lagace R et al (2000) A germline mutation at the extreme 3′ end of the APC gene results in a severe desmoid phenotype and is associated with overexpression of beta-catenin in the desmoid tumor. Clin Genet 57:205–212
Alman BA, Pajerski ME, Diaz-Cano S, Corboy K, Wolfe HJ (1997) Aggressive fibromatosis (desmoid tumor) is a monoclonal disorder. Diagn Mol Pathol 6:98–101
Bridge JA, Sreekantaiah C, Mouron B, Neff JR, Sandberg AA, Wolman SR (1992) Clonal chromosomal abnormalities in desmoid tumors. Implications for histopathogenesis. Cancer 69:430–436
Fletcher JA, Naeem R, Xiao S, Corson JM (1995) Chromosome aberrations in desmoid tumors. Trisomy 8 may be a predictor of recurrence. Cancer Genet Cytogenet 79:139–143
Li M, Cordon-Cardo C, Gerald WL, Rosai J (1996) Desmoid fibromatosis is a clonal process. Hum Pathol 27:939–943
Li C, Bapat B, Alman BA (1998) Adenomatous polyposis coli gene mutation alters proliferation through its beta-catenin-regulatory function in aggressive fibromatosis (desmoid tumor). Am J Pathol 153:709–714
Alman BA, Li C, Pajerski ME, Diaz-Cano S, Wolfe HJ (1997) Increased beta-catenin protein and somatic APC mutations in sporadic aggressive fibromatoses (desmoid tumors). Am J Pathol 151:329–334
Tejpar S, Nollet F, Li C et al (1999) Predominance of beta-catenin mutations and beta-catenin dysregulation in sporadic aggressive fibromatosis (desmoid tumor). Oncogene 18:6615–6620
Tejpar S, Li C, Yu C et al (2001) Tcf-3 expression and beta-catenin mediated transcriptional activation in aggressive fibromatosis (desmoid tumour). Br J Cancer 85:98–101
Gebert C, Hardes J, Kersting C et al (2007) Expression of beta-catenin and p53 are prognostic factors in deep aggressive fibromatosis. Histopathology 50:491–497
Rakheja D, Molberg KH, Roberts CA, Jaiswal VR (2005) Immunohistochemical expression of beta-catenin in solitary fibrous tumors. Arch Pathol Lab Med 129:776–779
Bhattacharya B, Dilworth HP, Iacobuzio-Donahue C et al (2005) Nuclear beta-catenin expression distinguishes deep fibromatosis from other benign and malignant fibroblastic and myofibroblastic lesions. Am J Surg Pathol 29:653–659
Ng TL, Gown AM, Barry TS et al (2005) Nuclear beta-catenin in mesenchymal tumors. Mod Pathol 18:68–74
Saito T, Oda Y, Kawaguchi K et al (2002) Possible association between higher beta-catenin mRNA expression and mutated beta-catenin in sporadic desmoid tumors: real-time semiquantitative assay by TaqMan polymerase chain reaction. Lab Invest 82:97–103
Montgomery E, Lee JH, Abraham SC, Wu TT (2001) Superficial fibromatoses are genetically distinct from deep fibromatoses. Mod Pathol 14:695–701
Saito T, Oda Y, Tanaka K et al (2001) Beta-catenin nuclear expression correlates with cyclin D1 overexpression in sporadic desmoid tumours. J Pathol 195:222–228
Signoroni S, Frattini M, Negri T et al (2007) Cyclooxygenase-2 and platelet-derived growth factor receptors as potential targets in treating aggressive fibromatosis. Clin Cancer Res 13:5034–5040
Jilong Y, Jian W, Xiaoyan Z, Xiaoqiu L, Xiongzeng Z (2007) Analysis of APC/beta-catenin genes mutations and Wnt signalling pathway in desmoid-type fibromatosis. Pathology 39:319–325
Bowley E, O’Gorman DB, Gan BS (2007) Beta-catenin signaling in fibroproliferative disease. J Surg Res 138:141–150
Ferenc T, Sygut J, Kopczynski J et al (2006) Aggressive fibromatosis (desmoid tumors): definition, occurrence, pathology, diagnostic problems, clinical behavior, genetic background. Pol J Pathol 57:5–15
Tajima S, Hironaka M, Oshikawa K et al (2006) Intrathoracic sporadic desmoid tumor with the beta-catenin gene mutation in exon 3 and activated cyclin D1. Respiration 73:558–561
Varallo VM, Gan BS, Seney S et al (2003) Beta-catenin expression in Dupuytren’s disease: potential role for cell-matrix interactions in modulating beta-catenin levels in vivo and in vitro. Oncogene 22:3680–3684
Shitoh K, Konishi F, Iijima T et al (1999) A novel case of a sporadic desmoid tumour with mutation of the beta catenin gene. J Clin Pathol 52:695–696
Miyoshi Y, Iwao K, Nawa G, Yoshikawa H, Ochi T, Nakamura Y (1998) Frequent mutations in the beta-catenin gene in desmoid tumors from patients without familial adenomatous polyposis. Oncol Res 10:591–594
Amary MF, Pauwels P, Meulemans E et al (2007) Detection of beta-catenin mutations in paraffin-embedded sporadic desmoid-type fibromatosis by mutation-specific restriction enzyme digestion (MSRED): an ancillary diagnostic tool. Am J Surg Pathol 31:1299–1309
Carlson JW, Fletcher CD (2007) Immunohistochemistry for beta-catenin in the differential diagnosis of spindle cell lesions: analysis of a series and review of the literature. Histopathology 51:509–514
Cheon SS, Cheah AY, Turley S et al (2002) Beta-Catenin stabilization dysregulates mesenchymal cell proliferation, motility, and invasiveness and causes aggressive fibromatosis and hyperplastic cutaneous wounds. Proc Natl Acad Sci U S A 99:6973–6978
Reya T, Morrison SJ, Clarke MF, Weissman IL (2001) Stem cells, cancer, and cancer stem cells. Nature 414:105–111
Galmozzi E, Facchetti F, La Porta CA (2006) Cancer stem cells and therapeutic perspectives. Curr Med Chem 13:603–607
Gudjonsson T, Magnusson MK (2005) Stem cell biology and the cellular pathways of carcinogenesis. Apmis 113:922–929
Pardal R, Clarke MF, Morrison SJ (2003) Applying the principles of stem-cell biology to cancer. Nat Rev Cancer 3:895–902
Clarke MF, Dick JE, Dirks PB et al (2006) Cancer stem cells--perspectives on current status and future directions: AACR workshop on cancer stem cells. Cancer Res 66:9339–9344
Romano G (2005) The role of adult stem cells in carcinogenesis. Drug News Perspect 18:555–559
Pierce GB, Speers WC (1988) Tumors as caricatures of the process of tissue renewal: prospects for therapy by directing differentiation. Cancer Res 48:1996–2004.
Challen GA, Little MH (2006) A side order of stem cells: the SP phenotype. Stem Cells 24:3–12
Goodell MA, McKinney-Freeman S, Camargo FD (2005) Isolation and characterization of side population cells. Methods Mol Biol 290:343–352
Hirschmann-Jax C, Foster AE, Wulf GG et al (2004) A distinct “side population” of cells with high drug efflux capacity in human tumor cells. Proc Natl Acad Sci U S A 101:14228–14233
Liadaki K, Kho AT, Sanoudou D et al (2005) Side population cells isolated from different tissues share transcriptome signatures and express tissue-specific markers. Exp Cell Res 303:360–374
Alison MR (2003) Tissue-based stem cells: ABC transporter proteins take centre stage. J Pathol 200:547–550
Wu C, Wei Q, Utomo V, Nadesan P, Whetstone H, Kandel R, Wunder JS, Alman BA (2007) Side population cells isolated from mesenchymal neoplasms have tumor initiating potential. Cancer Res 67:8216–8222
Kelly PN, Dakic A, Adams JM, Nutt SL, Strasser A (2007) Tumor growth need not be driven by rare cancer stem cells. Science 317:337
Wu C, Nik-Amini S, Nadesan P, Stanford WL, Alman BA (2010) Aggressive fibromatosis (desmoid tumor) is derived from mesenchymal progenitor cells. Cancer Res 70:7690–7698
Rubio R, Garcia-Castro J, Gutierrez-Aranda I et al (2010) Deficiency in p53 but not retinoblastoma induces the transformation of mesenchymal stem cells in vitro and initiates leiomyosarcoma in vivo. Cancer Res 70:4185–4194
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Alman, B. (2012). Desmoid Tumors: Are They Benign or Malignant?. In: Litchman, C. (eds) Desmoid Tumors. Springer, Dordrecht. https://doi.org/10.1007/978-94-007-1685-8_13
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DOI: https://doi.org/10.1007/978-94-007-1685-8_13
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