Desmoid tumor pathophysiology: Difference between revisions

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[[File:Desmoid immuno.jpg|thumb|250px|none|Immunological features of desmoid tumors in the middle section of the left thigh of a 35-year-old woman with femur involvement (a–d). (a) β-catenin staining of desmoid tumors (EnVision × 200). (b) Vimentin staining of desmoid tumors (EnVision × 200). (c) Desmin staining of desmoid tumors (EnVision × 200). (d) Ki-67 staining of desmoid tumors (EnVision × 200).[https://openi.nlm.nih.gov/detailedresult?img=PMC4329213_12957_2015_450_Fig4_HTML&query=desmoid%20tumor&it=xg&req=4&npos=7 Source: Wang YF. et al, Musculoskeletal Tumor Center, Peking University People’s Hospital, Beijing, 100044 P.R. China]]]
[[File:Desmoid immuno.jpg|thumb|250px|none|Immunological features of desmoid tumors in the middle section of the left thigh of a 35-year-old woman with femur involvement (a–d). (a) β-catenin staining of desmoid tumors (EnVision × 200). (b) Vimentin staining of desmoid tumors (EnVision × 200). (c) Desmin staining of desmoid tumors (EnVision × 200). (d) Ki-67 staining of desmoid tumors (EnVision × 200).[https://openi.nlm.nih.gov/detailedresult?img=PMC4329213_12957_2015_450_Fig4_HTML&query=desmoid%20tumor&it=xg&req=4&npos=7 Source: Wang YF. et al, Musculoskeletal Tumor Center, Peking University People’s Hospital, Beijing, 100044 P.R. China]]]
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[[File:Extraabdomianl desmoid histo.png|thumb|250px|none|Extra-Abdominal Fibromatosis (Desmoid Tumor): A Rare Tumor of the Lower Extremity Arising from the Popliteal Fossa. Desmoid fibromatosis showing fascicular arrangement of bland fibroblasts, which are interrupted by thin-walled, compressed vascular channels resulting in an appearance akin to a hypocellular scar. Note entrapped muscle fibers. No mitotic activity or nuclear pleomorphism is present (H&E, original magnification, 40x). [https://openi.nlm.nih.gov/detailedresult?img=PMC3420745_CRIM.VASMED2011-184906.002&query=&req=4 Source: Ali Kaygain M. et al, Department of Cardiovascular Surgery, Erzurum Regional Training and Research Hospital, 25020 Erzurum, Turkey]]]
[[File:Extraabdomianl desmoid histo.png|thumb|250px|none|Extra-Abdominal Fibromatosis (Desmoid Tumor): A Rare Tumor of the Lower Extremity Arising from the Popliteal Fossa. Desmoid fibromatosis showing fascicular arrangement of bland fibroblasts, which are interrupted by thin-walled, compressed vascular channels resulting in an appearance akin to a hypocellular scar. Note entrapped muscle fibers. No mitotic activity or nuclear pleomorphism is present (H&E, original magnification, 40x). [https://openi.nlm.nih.gov/detailedresult?img=PMC3420745_CRIM.VASMED2011-184906.003&query=&req=4 Source: Ali Kaygain M. et al, Department of Cardiovascular Surgery, Erzurum Regional Training and Research Hospital, 25020 Erzurum, Turkey]]]
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Revision as of 02:59, 25 March 2019

Desmoid tumor Microchapters

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Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Desmoid tumor from other Diseases

Epidemiology and Demographics

Risk Factors

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

CT

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sara Mohsin, M.D.[2]Faizan Sheraz, M.D. [3]

Overview

Desmoid tumors are benign tumors arising from monoclonal proliferation of well-differentiated fibroblasts. They appear as firm overgrowths of fibrous tissue with marked cellularity and aggressive local infiltration. The exact etiology remains uncertain, however, they are seem to be associated with antecedent surgical or accidental trauma at the tumor site and various mutations at the molecular level including beta-catenin gene, CTNNB1 or APC gene involved in Wnt/beta-cateninsignaling pathway. Pediatric desmoids have AKT1 E17K, BRAF V600E and TP53 R273H mutations in addition to CTNNB1 mutation. Immunohistochemistry shows an elevated beta-catenin protein level in all tumors, regardless of the mutational status. Associated conditions include Turcot syndrome, Gardner syndrome, Familial adenomatous polyposis and estrogen therapy. Desmoid tumors arise from connective tissue, fasciae and aponeuroses and appear as dense scar tissuewith most common sites of abdominal involvement being abdominal wall, root of the mesentery and retroperitoneum. Histologically, desmoid tumors consist of linearly arranged elongated fibroblasts and myofibroblas surrounded and separated from each other by collagen. These tumors show a tendency to evolve over time.

Pathophysiology

Genetics

Normal function of CTNNB1 and APC genes

Mutations in adults

 
 
 
Binding of an activating external/Wnt ligand to a receptor complex (a member of a seven-transmembrane-domain receptor of the frizzled family) and a LRP5/6 co-receptor(LDL-receptor-related protein family)[22][9]
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Canonical Wnt (Wingless) signaling pathway activation
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Inhibition of kinase activity of APC complex (which tightly binds and regulates Beta-catenin levels by its phosphorylation in proteasome at serine and threonine sites encoded in exon 3, leading to ubiquitin-mediated protein degradation)
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Elevated Beta-catenin levels in cytoplasm (due to non-phosphorylation)
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Beta-catenin translocates to nucleus
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
B-catenin together with TCF/LEF transcription factors, acts to activate transcription of genes such as CYCD1 and MYC
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Promotion of proliferation and enhanced survival
 
 
 

Additional mutations in pediatric desmoids

Immunohistochemistry

Associated Diseases

Gross Pathology

Location

Frequent locations in the abdomen are:

Rapid progression of a pregnancy-associated intra-abdominal desmoid tumor in the post-partum period: A case report. (A) Intra-operative view of intra-abdominal desmoid tumor with adherent portion of small bowel. (B) Desmoid tumor after surgical resection.Source: Hanna D. et al, University of Maryland School of Medicine, 655 W. Baltimore Street, Baltimore, MD 21201, United States
Breast Desmoid Tumor after Ductal Carcinoma Treatment: Salvaging a DIEP Flap Reconstruction. Chest wall defect after desmoid tumor resection (A) and resected desmoid tumor (B). Source: Zavlin D. et al, *Institute for Reconstructive Surgery, Houston Methodist Hospital, Weill Cornell Medicine, Houston, Tex.; and †College of Medicine, Texas A&M University College of Medicine, Houston, Tex.
Extra-Abdominal Fibromatosis (Desmoid Tumor): A Rare Tumor of the Lower Extremity Arising from the Popliteal Fossa. Gross cross-sectional view of pathologyic resected specimen. The gross lesion is poorly circumscribed and usually measures between 5 and 15 cm. On cut section, it is hard and tan-white. The lesion is poorly circumscribed and is centered in skeletal muscle and the adjacent fascia. There often are infiltration and obliteration of adjacent structures. Source: Ali Kaygain M. et al, Department of Cardiovascular Surgery, Erzurum Regional Training and Research Hospital, 25020 Erzurum, Turkey

Microscopic Pathology

Histologically, desmoid tumors consist of:[45]

Stages of evolution of desmoid tumors

Vandevenne et al described three stages of evolution of desmoid tumors as follows:

Stages of evolution of desmoid tumors
Stage Histological features
First stage
Second stage
Third stage
  • Increased fibrous composition
  • Decreased cellularity
  • Decreased water content
Histological features of desmoid tumors in the proximal part of the left thigh of a 29-year-old woman (arrows) (a–d). (a) Desmoid tumors invaded into the skeletal striated muscle aggressively. Degeneration of skeletal muscle cells could be seen (HE × 100). (b) Budding-like protrusion of the lesions invading into the muscles could be seen on the juncture of tumors and muscles (HE × 40). (c) Isolated small lesions in muscles were found away from the main part of the tumor (HE × 40). (d) Microscopically, desmoid tumors were poorly circumscribed on tumor-ligament boundary (HE × 40).Source: Wang YF. et al, Musculoskeletal Tumor Center, Peking University People’s Hospital, Beijing, 100044 P.R. China
Histological features of postoperative recurrent desmoid tumors in the right forearm of a 15-year-old man (arrows) (a–d). (a) Lesions with adipose tissue involvement (HE × 40). (b) Desmoid tumors around vessels could not invade into the vessel wall to form tumor thrombus (HE × 40). (c) Desmoid tumors invaded into the connective tissue and perineurium around nerve tissue (HE × 40). (d) Desmoid tumors with bone involvement penetrated into the periosteum and cortical bone and invaded into the bone marrow cavity along the bone trabecula (HE × 40).Source: Wang YF. et al, Musculoskeletal Tumor Center, Peking University People’s Hospital, Beijing, 100044 P.R. China
Immunological features of desmoid tumors in the middle section of the left thigh of a 35-year-old woman with femur involvement (a–d). (a) β-catenin staining of desmoid tumors (EnVision × 200). (b) Vimentin staining of desmoid tumors (EnVision × 200). (c) Desmin staining of desmoid tumors (EnVision × 200). (d) Ki-67 staining of desmoid tumors (EnVision × 200).Source: Wang YF. et al, Musculoskeletal Tumor Center, Peking University People’s Hospital, Beijing, 100044 P.R. China
Extra-Abdominal Fibromatosis (Desmoid Tumor): A Rare Tumor of the Lower Extremity Arising from the Popliteal Fossa. Desmoid fibromatosis showing fascicular arrangement of bland fibroblasts, which are interrupted by thin-walled, compressed vascular channels resulting in an appearance akin to a hypocellular scar. Note entrapped muscle fibers. No mitotic activity or nuclear pleomorphism is present (H&E, original magnification, 40x). Source: Ali Kaygain M. et al, Department of Cardiovascular Surgery, Erzurum Regional Training and Research Hospital, 25020 Erzurum, Turkey

Reference

  1. ↑ Leal RF, Silva PV, Ayrizono Mde L, Fagundes JJ, Amstalden EM, Coy CS (2010). "Desmoid tumor in patients with familial adenomatous polyposis". Arq Gastroenterol. 47 (4): 373–8. PMID 21225148.
  2. ↑ Desmoid tumor. Dr Tim Luijkx and Radswiki et al. Radiopedia 2015 http://radiopaedia.org/articles/aggressive-fibromatosis. Accessed on January 20, 2015
  3. ↑ De Wever I, Dal Cin P, Fletcher CD, Mandahl N, Mertens F, Mitelman F; et al. (2000). "Cytogenetic, clinical, and morphologic correlations in 78 cases of fibromatosis: a report from the CHAMP Study Group. CHromosomes And Morphology". Mod Pathol. 13 (10): 1080–5. doi:10.1038/modpathol.3880200. PMID 11048801.
  4. ↑ Middleton SB, Frayling IM, Phillips RK (2000). "Desmoids in familial adenomatous polyposis are monoclonal proliferations". Br J Cancer. 82 (4): 827–32. doi:10.1054/bjoc.1999.1007. PMC 2374411. PMID 10732754.
  5. ↑ 5.0 5.1 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 (3): 709–14. PMC 1853030. PMID 9736021.
  6. ↑ Escobar C, Munker R, Thomas JO, Li BD, Burton GV (2012). "Update on desmoid tumors". Ann Oncol. 23 (3): 562–9. doi:10.1093/annonc/mdr386. PMID 21859899.
  7. ↑ 7.0 7.1 Giarola M, Wells D, Mondini P, Pilotti S, Sala P, Azzarelli A; et al. (1998). "Mutations of adenomatous polyposis coli (APC) gene are uncommon in sporadic desmoid tumours". Br J Cancer. 78 (5): 582–7. PMC 2063069. PMID 9744495.
  8. ↑ 8.0 8.1 8.2 Tejpar S, Nollet F, Li C, Wunder JS, Michils G, dal Cin P; et al. (1999). "Predominance of beta-catenin mutations and beta-catenin dysregulation in sporadic aggressive fibromatosis (desmoid tumor)". Oncogene. 18 (47): 6615–20. doi:10.1038/sj.onc.1203041. PMID 10597266.
  9. ↑ 9.0 9.1 Pinson KI, Brennan J, Monkley S, Avery BJ, Skarnes WC (2000). "An LDL-receptor-related protein mediates Wnt signalling in mice". Nature. 407 (6803): 535–8. doi:10.1038/35035124. PMID 11029008.
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  13. ↑ Aitken SJ, Presneau N, Kalimuthu S, Dileo P, Berisha F, Tirabosco R; et al. (2015). "Next-generation sequencing is highly sensitive for the detection of beta-catenin mutations in desmoid-type fibromatoses". Virchows Arch. 467 (2): 203–10. doi:10.1007/s00428-015-1765-0. PMID 25838078.
  14. ↑ Heinrich MC, McArthur GA, Demetri GD, Joensuu H, Bono P, Herrmann R; et al. (2006). "Clinical and molecular studies of the effect of imatinib on advanced aggressive fibromatosis (desmoid tumor)". J Clin Oncol. 24 (7): 1195–203. doi:10.1200/JCO.2005.04.0717. PMID 16505440.
  15. ↑ Abraham SC, Reynolds C, Lee JH, Montgomery EA, Baisden BL, Krasinskas AM; et al. (2002). "Fibromatosis of the breast and mutations involving the APC/beta-catenin pathway". Hum Pathol. 33 (1): 39–46. PMID 11823972.
  16. ↑ Signoroni S, Frattini M, Negri T, Pastore E, Tamborini E, Casieri P; et al. (2007). "Cyclooxygenase-2 and platelet-derived growth factor receptors as potential targets in treating aggressive fibromatosis". Clin Cancer Res. 13 (17): 5034–40. doi:10.1158/1078-0432.CCR-07-0336. PMID 17785554.
  17. ↑ Cheon S, Poon R, Yu C, Khoury M, Shenker R, Fish J; et al. (2005). "Prolonged beta-catenin stabilization and tcf-dependent transcriptional activation in hyperplastic cutaneous wounds". Lab Invest. 85 (3): 416–25. doi:10.1038/labinvest.3700237. PMID 15654359.
  18. ↑ Merchant NB, Lewis JJ, Woodruff JM, Leung DH, Brennan MF (1999). "Extremity and trunk desmoid tumors: a multifactorial analysis of outcome". Cancer. 86 (10): 2045–52. PMID 10570430.
  19. ↑ Kim HS, Kim J, Nam KH, Kim WH (2016). "Clinical significance of midkine expression in sporadic desmoid tumors". Oncol Lett. 11 (3): 1677–1684. doi:10.3892/ol.2016.4129. PMC 4774436. PMID 26998061.
  20. ↑ Kotiligam D, Lazar AJ, Pollock RE, Lev D (2008). "Desmoid tumor: a disease opportune for molecular insights". Histol Histopathol. 23 (1): 117–26. doi:10.14670/HH-23.117. PMID 17952864.
  21. ↑ Crago AM, Chmielecki J, Rosenberg M, O'Connor R, Byrne C, Wilder FG; et al. (2015). "Near universal detection of alterations in CTNNB1 and Wnt pathway regulators in desmoid-type fibromatosis by whole-exome sequencing and genomic analysis". Genes Chromosomes Cancer. 54 (10): 606–15. doi:10.1002/gcc.22272. PMC 4548882. PMID 26171757.
  22. ↑ Bhanot P, Brink M, Samos CH, Hsieh JC, Wang Y, Macke JP; et al. (1996). "A new member of the frizzled family from Drosophila functions as a Wingless receptor". Nature. 382 (6588): 225–30. doi:10.1038/382225a0. PMID 8717036.
  23. ↑ 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 (2): 329–34. PMC 1857985. PMID 9250146.
  24. ↑ Bertario L, Russo A, Sala P, Eboli M, Giarola M, D'amico F; et al. (2001). "Genotype and phenotype factors as determinants of desmoid tumors in patients with familial adenomatous polyposis". Int J Cancer. 95 (2): 102–7. PMID 11241320.
  25. ↑ Schiessling S, Kihm M, Ganschow P, Kadmon G, Büchler MW, Kadmon M (2013). "Desmoid tumour biology in patients with familial adenomatous polyposis coli". Br J Surg. 100 (5): 694–703. doi:10.1002/bjs.9053. PMID 23334997.
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  29. ↑ Bertario L, Russo A, Sala P, Varesco L, Giarola M, Mondini P; et al. (2003). "Multiple approach to the exploration of genotype-phenotype correlations in familial adenomatous polyposis". J Clin Oncol. 21 (9): 1698–707. doi:10.1200/JCO.2003.09.118. PMID 12721244.
  30. ↑ Friedl W, Caspari R, Sengteller M, Uhlhaas S, Lamberti C, Jungck M; et al. (2001). "Can APC mutation analysis contribute to therapeutic decisions in familial adenomatous polyposis? Experience from 680 FAP families". Gut. 48 (4): 515–21. PMC 1728231. PMID 11247896.
  31. ↑ Wallis YL, Morton DG, McKeown CM, Macdonald F (1999). "Molecular analysis of the APC gene in 205 families: extended genotype-phenotype correlations in FAP and evidence for the role of APC amino acid changes in colorectal cancer predisposition". J Med Genet. 36 (1): 14–20. PMC 1762945. PMID 9950360.
  32. ↑ Church J, Xhaja X, LaGuardia L, O'Malley M, Burke C, Kalady M (2015). "Desmoids and genotype in familial adenomatous polyposis". Dis Colon Rectum. 58 (4): 444–8. doi:10.1097/DCR.0000000000000316. PMID 25751801.
  33. ↑ Halling KC, Lazzaro CR, Honchel R, Bufill JA, Powell SM, Arndt CA; et al. (1999). "Hereditary desmoid disease in a family with a germline Alu I repeat mutation of the APC gene". Hum Hered. 49 (2): 97–102. doi:10.1159/000022852. PMID 10077730.
  34. ↑ Hong H, Nadesan P, Poon R, Alman BA (2011). "Testosterone regulates cell proliferation in aggressive fibromatosis (desmoid tumour)". Br J Cancer. 104 (9): 1452–8. doi:10.1038/bjc.2011.107. PMC 3101926. PMID 21468052.
  35. ↑ 35.0 35.1 Lazar AJ, Tuvin D, Hajibashi S, Habeeb S, Bolshakov S, Mayordomo-Aranda E; et al. (2008). "Specific mutations in the beta-catenin gene (CTNNB1) correlate with local recurrence in sporadic desmoid tumors". Am J Pathol. 173 (5): 1518–27. doi:10.2353/ajpath.2008.080475. PMC 2570141. PMID 18832571.
  36. ↑ 36.0 36.1 Mullen JT, DeLaney TF, Rosenberg AE, Le L, Iafrate AJ, Kobayashi W; et al. (2013). "β-Catenin mutation status and outcomes in sporadic desmoid tumors". Oncologist. 18 (9): 1043–9. doi:10.1634/theoncologist.2012-0449. PMC 3780636. PMID 23960186.
  37. ↑ 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 (2): 139–43. PMID 7889507.
  38. ↑ Kouho H, Aoki T, Hisaoka M, Hashimoto H (1997). "Clinicopathological and interphase cytogenetic analysis of desmoid tumours". Histopathology. 31 (4): 336–41. PMID 9363449.
  39. ↑ Bridge JA, Swarts SJ, Buresh C, Nelson M, Degenhardt JM, Spanier S; et al. (1999). "Trisomies 8 and 20 characterize a subgroup of benign fibrous lesions arising in both soft tissue and bone". Am J Pathol. 154 (3): 729–33. doi:10.1016/S0002-9440(10)65319-9. PMC 1866419. PMID 10079250.
  40. ↑ Qi H, Dal Cin P, Hernández JM, Garcia JL, Sciot R, Fletcher C; et al. (1996). "Trisomies 8 and 20 in desmoid tumors". Cancer Genet Cytogenet. 92 (2): 147–9. PMID 8976373.
  41. ↑ Mertens F, Willén H, Rydholm A, Brosjö O, Carlén B, Mitelman F; et al. (1995). "Trisomy 20 is a primary chromosome aberration in desmoid tumors". Int J Cancer. 63 (4): 527–9. PMID 7591262.
  42. ↑ Meazza C, Belfiore A, Busico A, Settanni G, Paielli N, Cesana L; et al. (2016). "AKT1 and BRAF mutations in pediatric aggressive fibromatosis". Cancer Med. 5 (6): 1204–13. doi:10.1002/cam4.669. PMC 4924379. PMID 27062580.
  43. ↑ Tanaka K, Toiyama Y, Okugawa Y, Hiro J, Kawamoto A, Inoue Y; et al. (2012). "Cytoreductive strategy for multiple intra-abdominal and abdominal wall desmoid tumors in familial adenomatous polyposis: report of three cases". Clin J Gastroenterol. 5 (5): 361–6. doi:10.1007/s12328-012-0330-5. PMID 26181076.
  44. ↑ Ferenc T, Sygut J, Kopczyński J, Mayer M, Latos-Bieleńska A, Dziki A; et al. (2006). "Aggressive fibromatosis (desmoid tumors): definition, occurrence, pathology, diagnostic problems, clinical behavior, genetic background". Pol J Pathol. 57 (1): 5–15. PMID 16739877.
  45. ↑ Economou, Athanasios; Pitta, Xanthi; Andreadis, Efstathios; Papapavlou, Leonidas; Chrissidis, Thomas (2011). "Desmoid tumor of the abdominal wall: a case report". Journal of Medical Case Reports. 5 (1): 326. doi:10.1186/1752-1947-5-326. ISSN 1752-1947.

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