Skip to main content
Key Specialties
Cardiology Diabetology Endocrinology Gastroenterology Geriatrics and Gerontology Gynecology and Obstetrics Hematology Infectious Disease Internal Medicine Nephrology Neurology Oncology Pediatrics Respiratory Medicine Rheumatology Surgery
Congress Coverage
2024 ACC Congress 2023 ESMO Congress 2023 EASD Congress 2023 ERS Congress 2023 ESC Congress
Clinical Collections
Advances in Alzheimer’s

Keynote webinar | Spotlight on medication adherence

LIVE: Thursday 27th June 2024, 18:00-19:30 (CEST)
Join our expert panel to discover why you need to understand the drivers of non-adherence in your patients, and how you can optimize medication adherence in your clinics to drastically improve patient outcomes.
ADVANCED SEARCH
Log in
Top
Familial Cancer
Published in: Familial Cancer 4/2009

01-12-2009

FAP-associated desmoid invasiveness correlates with in vitro resistance to doxorubicin

Authors: David E. Joyner, Sylvia H. Trang, Albert J. Aboulafia, Timothy A. Damron, R. Lor Randall

Published in: Familial Cancer | Issue 4/2009

Login to get access

Abstract

Desmoid tumors are locally invasive myofibroblastic lesions that arise predominantly in the abdominal wall or shoulder girdle and are prone to aggressive local recurrences without metastases. We hypothesized the intrinsic invasiveness and drug resistance displayed by cells derived from a familial adenomatous polyposis (FAP)-associated desmoid tumor would surpass the response shown by cells derived from sporadic desmoid tumors. In vitro cell motility and expression of motility-associated genes were quantified using Boyden Chambers and Enzyme-Linked ImmunoSorbent Assays, respectively. Doxorubicin resistance was quantified by Trypan Blue dye exclusion. cDNA microarrays identified genes responsive to doxorubicin. FAP-associated tumor cells were significantly more invasive and refractory to doxorubicin than were cells extracted from sporadic tumors. Pro-MMP1 protein predominated over MMP3 in FAP-associated cell culture supernatants, while MMP3 was the dominant antigen in sporadic tumor cell supernatants. Three genes associated with apoptosis were identified by microarray, two prosurvival genes overexpressed in FAP-associated cell cultures (NTN1, TNFRSF10C) and one proapoptosis gene overexpressed in sporadic tumor cell cultures (FOXL2).
Literature
1.
Alman BA, Pajerski ME, Diaz-Cano S et al (1997) Aggressive fibromatosis (desmoid tumor) is a monoclonal disorder. Diagn Mol Pathol 6:98–101CrossRefPubMed
2.
Angiero F, Benedicenti S, Stefani M (2008) Fibromatosis of the head and neck: morphological, immunohistochemical and clinical features. Anticancer Res 28:1725–1732PubMed
3.
4.
Burke AP, Sobin LH, Shekitka KM (1990) Mesenteric fibromatosis. A follow-up study. Arch Pathol Lab Med 114:832–835PubMed
5.
Cheng S, Tada M, Hida Y et al (2008) High MMP-1 mRNA expression is a risk factor for disease-free and overall survivals in patients with invasive breast carcinoma. J Surg Res 146:104–109CrossRefPubMed
6.
Cohen S, Ad-El D, Benjaminov O et al (2008) Post-traumatic soft tissue tumors: case report and review of the literature a propos a post-traumatic paraspinal desmoid tumor. World J Surg Oncol 6:28CrossRefPubMed
7.
Debatin KM (1999) Activation of apoptosis pathways by anticancer drugs. Adv Exp Med Biol 457:237–244PubMed
8.
De Cian F, Delay E, Rudigoz RC et al (1999) Desmoid tumor arising in a cesarean section scar during pregnancy: monitoring and management. Gynecol Oncol 75:145–148CrossRefPubMed
9.
Denys H, De Wever O, Nusgens B et al (2004) Invasion and MMP expression profile in desmoid tumours. Br J Cancer 90:1443–1449CrossRefPubMed
10.
Dimanche-Boitrel MT, Genne P, Duchamp O, Chauffert B (1994) Confluence dependent resistance (CDR) to doxorubicin and E-cadherin expression in murine mammary cells. Cancer Lett 85:171–176CrossRefPubMed
11.
Dobbin K, Shih JH, Simon R (2003) Statistical design of reverse dye microarrays. Bioinformatics 19:803–810CrossRefPubMed
12.
Ezumi K, Yamamoto H, Takemasa I et al (2008) Dacarbazine–Doxorubicin therapy ameliorated an extremely aggressive mesenteric desmoid tumor associated with familial adenomatous polyposis: report of a case. Jpn J Clin Oncol 38:222–226CrossRefPubMed
13.
Fallen T, Wilson M, Morlan B et al (2006) Desmoid tumors—a characterization of patients seen at Mayo Clinic 1976–1999. Fam Cancer 5:191–194CrossRefPubMed
14.
Fang Y, Sullivan R, Graham CH (2007) Confluence-dependent resistance to doxorubicin in human MDA-MB-231 breast carcinoma cells requires hypoxia-inducible factor-1 activity. Exp Cell Res 313:866–877CrossRef
15.
Ferenc T, Sygut J, Kopczyński J et al (2006) Aggressive fibromatosis (desmoid tumors): definition, occurrence, pathology, diagnostic problems, clinical behavior, genetic background. Pol J Pathol 57:5–15PubMed
16.
Fitamant J, Guenebeaud C, Coissieux MM et al (2008) Netrin-1 expression confers a selective advantage for tumor cell survival in metastatic breast cancer. Proc Natl Acad Sci USA 105:4850–4855CrossRefPubMed
17.
Gouazé V, Mirault ME, Carpentier S, Salvayre R, Levade T, Andrieu-Abadie N (2001) Glutathione peroxidase-1 overexpression prevents ceramide production and partially inhibits apoptosis in doxorubicin-treated human breast carcinoma cells. Mol Pharmacol 60:488–496PubMed
18.
Hosalkar HS, Torbert JT, Fox EJ et al (2008) Musculoskeletal desmoid tumors. J Am Acad Orthop Surg 16:188–198PubMed
19.
Jilong Y, Jian W, Xiaoyan Z et al (2007) Analysis of APC/beta-catenin genes mutations and Wnt signalling pathway in desmoid-type fibromatosis. Pathology 39:319–325CrossRefPubMed
20.
Joyner DE, Albritton KH, Bastar JD et al (2006) G3139 antisense oligonucleotide directed against antiapoptotic Bcl-2 enhances doxorubicin cytotoxicity in the FU-SY-1 synovial sarcoma cell line. J Orthop Res 24:474–480CrossRefPubMed
21.
Knudsen AL, Bülow S (2001) Desmoid tumour in familial adenomatous polyposis. A review of literature. Fam Cancer 1:111–119CrossRefPubMed
22.
Kong Y, Poon R, Nadesan P et al (2004) Matrix metalloproteinase activity modulates tumor size, cell motility, and cell invasiveness in murine aggressive fibromatosis. Cancer Res 64:5795–5803CrossRefPubMed
23.
Kotiligam D, Lazar AJ, Pollock RE et al (2008) Desmoid tumor: a disease opportune for molecular insights. Histol Histopathol 23:117–126PubMed
24.
Kudoh K, Ramanna M, Ravatn R et al (2000) Monitoring the expression profiles of doxorubicin induced and doxorubicin-resistant cancer cells by cDNA microarray. Cancer Res 60:4161–4166PubMed
25.
Lee K, Pisarska MD, Ko JJ et al (2005) Transcriptional factor FOXL2 interacts with DP103 and induces apoptosis. Biochem Biophys Res Commun 336:876–881CrossRefPubMed
26.
Leithner A, Gapp M, Leithner K et al (2004) Margins in extra-abdominal desmoid tumors: a comparative analysis. J Surg Oncol 86:152–156CrossRefPubMed
27.
Lund-Johansen M, Bjerkvig R, Humphrey PA et al (1990) Effect of epidermal growth factor on glioma cell growth, migration, and invasion in vitro. Cancer Res 50:6039–6044PubMed
28.
Mace J, Sybil Biermann J, Sondak V, McGinn C, Hayes C, Thomas D, Baker L (2002) Response of extraabdominal desmoid tumors to therapy with imatinib mesylate. Cancer 95:2373–2379CrossRefPubMed
29.
30.
Mills BG, Frausto A, Brien E (2000) Cytokines associated with the pathophysiology of aggressive fibromatosis. J Orthop Res 18:655–662CrossRefPubMed
31.
Momparler RL, Karon M, Siegel SE et al (1976) Effect of adriamycin on DNA, RNA, and protein synthesis in cell-free systems and intact cells. Cancer Res 36:2891–2895PubMed
32.
Muller C, Laurent G, Ling V (1995) P-glycoprotein stability is affected by serum deprivation and high cell density in multidrug-resistant cells. J Cell Physiol 163:538–544CrossRefPubMed
33.
34.
Pryczynicz A, Guzińska-Ustymowicz K, Kemona A et al (2008) Expression of EGF and EGFR strongly correlates with metastasis of pancreatic ductal carcinoma. Anticancer Res 28:1399–1404PubMed
35.
Pulukuri SM, Rao JS (2008) Matrix metalloproteinase-1 promotes prostate tumor growth and metastasis. Int J Oncol 32:757–765PubMed
36.
Rosenzweig BA, Pine PS, Domon OE et al (2004) Dye bias correction in dual-labeled cDNA microarray gene expression measurements. Environ Health Perspect 112:480–487PubMed
37.
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 82:97–103PubMed
38.
Sturt NJ, Gallagher MC, Bassett P, Philp CR, Neale KF, Tomlinson IP, Silver AR, Phillips RK (2004) Evidence for genetic predisposition to desmoid tumours in familial adenomatous polyposis independent of the germline APC mutation. Gut 53:1832–1836CrossRefPubMed
39.
40.
Tejpar S, Michils G, Denys H et al (2005) Analysis of Wnt/Beta catenin signalling in desmoid tumors. Acta Gastroenterol Belg 68:5–9PubMed
41.
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 18:6615–6620CrossRefPubMed
42.
Tolan S, Shanks JH, Loh MY et al (2007) Fibromatosis: benign by name but not necessarily by nature. Clin Oncol (R Coll Radiol) 19:319–326
43.
Wang S, Konorev EA, Kotamraju S, Joseph J, Kalivendi S, Kalyanaraman B (2004) Doxorubicin induces apoptosis in normal and tumor cells via distinctly different mechanisms. intermediacy of H(2)O(2)- and p53-dependent pathways. J Biol Chem 279:25535–25543CrossRefPubMed
44.
Wang YD, Yang F, Chen WD, Huang X, Lai L, Forman BM, Huang W (2008) Farnesoid X receptor protects liver cells from apoptosis induced by serum deprivation in vitro and fasting in vivo. Mol Endocrinol 22:1622–1632CrossRefPubMed
45.
Zhang XD, Nguyen T, Thomas WD et al (2000) Mechanisms of resistance of normal cells to TRAIL induced apoptosis vary between different cell types. FEBS Lett 482:193–199CrossRefPubMed
Metadata
Title
FAP-associated desmoid invasiveness correlates with in vitro resistance to doxorubicin
Authors
David E. Joyner
Sylvia H. Trang
Albert J. Aboulafia
Timothy A. Damron
R. Lor Randall
Publication date
01-12-2009
Publisher
Springer Netherlands
Published in
Familial Cancer / Issue 4/2009
Print ISSN: 1389-9600
Electronic ISSN: 1573-7292
DOI
https://doi.org/10.1007/s10689-009-9288-y

Other articles of this Issue 4/2009

Familial Cancer 4/2009 Go to the issue

OriginalPaper

Functional characterization of rare missense mutations in MLH1 and MSH2 identified in Danish colorectal cancer patients

OriginalPaper

Cancer genetic predisposition: information needs of patients irrespective of risk level

BriefCommunication

Epitope-positive truncating MLH1 mutation and loss of PMS2: implications for IHC-directed genetic testing for lynch syndrome

OriginalPaper

The RNF146 and ECHDC1 genes as candidates for inherited breast and ovarian cancer in Jewish Ashkenazi women

OriginalPaper

Genetic polymorphism in ornithine decarboxylase and risk of breast cancer

BriefCommunication

CHEK2*1100delC does not contribute to risk to breast cancer among Malay, Chinese and Indians in Malaysia
Webinar | 19-02-2024 | 17:30 (CET)

Keynote webinar | Spotlight on antibody–drug conjugates in cancer

Watch now

Antibody–drug conjugates (ADCs) are novel agents that have shown promise across multiple tumor types. Explore the current landscape of ADCs in breast and lung cancer with our experts, and gain insights into the mechanism of action, key clinical trials data, existing challenges, and future directions.

Dr. Véronique Diéras
Prof. Fabrice Barlesi
Developed by: Springer Medicine
Image Credits