Potential role of the steroid receptor pattern in the response of inoperable intra-abdominal desmoid to toremifene after failure of tamoxifen therapy

Altomare, D. F.; Rotelli, Maria Teresa; Rinaldi, Marcella; Bocale, Domenica; Lippolis, Catia; Lobascio, Pierluigi; Cavallini, A

doi:10.1007/s00384-009-0859-z

Cited by 9 publications

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“…A possible explanation is that patients with a more aggressive, fast‐growing tumour are likely to be treated with a multidrug regimen instead of with a single drug regimen. The data available also indicate that tamoxifen [42,43] and toremifene [44] are equally effective, but the latter has been demonstrated to be sometimes effective as a second line of therapy following resistance to tamoxifen [45]. Finally the response to anti‐oestrogens seems to be independent of oestrogen receptor expression.…”

Section: Discussionmentioning

confidence: 99%

“…On the other hand, it is known, in other types of cancer, that the presence of several co‐activators and co‐repressors of oestrogen receptors can modulate the response to anti‐oestrogen therapy. Furthermore, the possible role of a recently identified family of nuclear oestrogen receptor‐related receptors may play a role by binding anti‐oestrogen molecules [45].…”

Section: Discussionmentioning

confidence: 99%

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Anti-oestrogen therapy in the treatment of desmoid tumours: a systematic review

et al. 2011

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Anti-oestrogen therapy in the treatment of desmoid tumours: a systematic review

et al. 2011

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“…In patients who are not candidates to surgery, different therapeutic options could be considered, including radiation or pharmacological therapy [5, 6]. Anti-inflammatory agents, hormonal blockade, cytotoxic chemotherapy and tyrosine kinase inhibitors have all been used, but with inconsistent and unpredictable results [7, 8]. …”

Section: Introductionmentioning

confidence: 99%

Human microRNA expression in sporadic and FAP-associated desmoid tumors and correlation with beta-catenin mutations

et al. 2017

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Desmoid tumors (DT) are rare, benign, fibroblastic neoplasm with challenging histological diagnosis. DTs can occur sporadically or associated with the familial adenomatous polyposis coli (FAP). Most sporadic DTs are associated with β-catenin gene (CTNNB1) mutations, while mutated APC gene causes FAP disease. microRNAs (miRNAs) are involved in many human carcinogenesis.The miRNA profile was analyzed by microarray in formalin-fixed, paraffin-embedded (FFPE) specimens of 12 patients (8 sporadic, 4 FAP-associated) and 4 healthy controls. One hundred and one mRNAs resulted dysregulated, of which 98 in sporadic DTs and 8 in FAP-associated DTs, 5 were shared by both tumors. Twenty-six miRNAs were then validated by RT-qPCR in 23 sporadic and 7 FAP-associated DT samples matched with healthy controls. The qPCR method was also used to evaluate the CTNNB1 mutational status in sporadic DTs. The correlation between sporadic DTs and miRNA expression showed that miR-21-3p increased in mutated versus wild-type DTs, while miR-197-3p was decreased. The mRNA expression of Tetraspanin3 and Serpin family A member 3, as miR-21-3p targets, and L1 Cell Adhesion Molecule, as miR-197-3p target, was also evaluate. CTNNB1 mutations associated to miRNA dysregulation could affect the genesis and the progression of this disease and help histological diagnosis of sporadic DTs.

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“…The effective use of oestrogen blockade has been reported in this tumour type, but not all tumours are responsive (Bus et al , 1999; Altomare et al , 2010). A poor outcome with oestrogen blockade in some aggressive fibromatosis tumours could be related to the role of testosterone in this tumour type.…”

Section: Discussionmentioning

confidence: 99%

Testosterone regulates cell proliferation in aggressive fibromatosis (desmoid tumour)

et al. 2011

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Background:Aggressive fibromatosis (desmoid tumour) is a locally invasive tumour caused by mutations resulting in β-catenin protein stabilisation. Apc1638N mice are predisposed to developing aggressive fibromatosis tumours, and male mice develop greater numbers of tumours than female mice, suggesting a role for androgens in this tumour type.Methods:Human aggressive fibromatosis tumours were examined for the expression of the androgen receptor, and primary human tumour cell cultures were treated with testosterone. Orchidectomised Apc1638N mice were investigated for the development of tumours, and were treated with testosterone to study the effect of tumour formation and the level of β-catenin.Results:Androgen receptors are universally expressed in human aggressive fibromatosis tumours. Testosterone increased the proliferation rate and β-catenin protein level in a dose-dependent manner in human aggressive fibromatosis tumours. Orchiectomy reduced the number and size of tumours that formed in male Apc1638N mice to a similar level as observed in female mice. Testosterone treatment increased the number of tumours that formed in orchidectomised male mice, and resulted in a marked increase in β-catenin protein levels.Conclusion:Testosterone regulates β-catenin protein level and proliferation rate in this mesenchymal tumour. This work identifies the therapeutic use of testosterone blockade in aggressive fibromatosis as an area for further investigation.

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Potential role of the steroid receptor pattern in the response of inoperable intra-abdominal desmoid to toremifene after failure of tamoxifen therapy

Cited by 9 publications

References 0 publications

Anti-oestrogen therapy in the treatment of desmoid tumours: a systematic review

Anti-oestrogen therapy in the treatment of desmoid tumours: a systematic review

Human microRNA expression in sporadic and FAP-associated desmoid tumors and correlation with beta-catenin mutations

Testosterone regulates cell proliferation in aggressive fibromatosis (desmoid tumour)

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