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Pazopanib: a novel treatment option for aggressive fibromatosis

Pazopanib: a novel treatment option for aggressive fibromatosis Background: Aggressive fibromatosis (AF), also known as desmoid tumor, is an uncommon soft tissue neoplasm. AF does not metastasize, but it is locally invasive and its propensity for recurrence after conservative resection is well doc- umented. No effective cytotoxic treatment has been reported, hence there is a need for novel treatment strategies. Case presentation: We present the case of an AF successfully treated with an oral tyrosine kinase inhibitor, pazo- panib, with mild side effects. As far as we know, this is the first case of AF with complete response to pazopanib. Conclusion: Pazopanib might be an effective treatment option for AF. Keywords: Pazopanib, Aggressive fibromatosis, Desmoid tumor, Oral tyrosine kinase inhibitor efficacious treatment options, patients might die due to Background local organ dysfunction because of their locally progres- Aggressive fibromatosis (AF) (also called deep fibroma - sive disease. tosis or desmoid tumor) is a proliferation of cytologically Sporadic AF is usually associated with somatic muta- benign-appearing fibrocytes, often resulting in significant tions in codons 41 or 45 of exon 3 of beta-catenin functional loss. The nature of the lesion is controver - (CTNNB1). AF occurring in the background of familial sial: some evidence suggests that it is a reactive process, adenomatous polyposis (FAP) usually contains inactivat- whereas other evidence supports a neoplastic etiology ing germline mutations in the adenomatous polyposis [1]. Although it does not have the propensity of distant coli (APC) gene. CTNNB1 and APC are part of the Wnt organ metastases, AF often exhibits an infiltrative pat - signaling pathway and mutations in either gene resulting tern of spread in an abundant collagen matrix, giving it a in stabilization of the beta-catenin protein and allowing dense, fibrotic character. As a result, this tumor can pro - nuclear translocation and binding of beta-catenin to the duce local tissue destruction leading to significant mor - T cell factor/lymphoid enhancer factor (TCF/Lef ) family bidity and functional loss. of transcription factors, lead to activation of target genes Since the etiology of AF is poorly understood, several that may underlie desmoid tumor biology and clinical medical approaches have been combined with or with- behavior. In the era of molecularly targeted therapeu- out surgical resection with scarce results. These include tics, there is a need to exploit the molecular mechanisms chemotherapy with doxorubicin-based combinations, behind desmoid tumorigenesis and progression in a bet- antiestrogen therapy with tamoxifen, nonsteroidal anti- ter way. Recently, new encouraging data with small mol- inflammatory drugs (NSAIDs) such as indomethacin ecule tyrosine kinase inhibitors (imatinib, sunitinib etc.,) and sulindac, colchicines [2]. However, all of these treat- have been published [3–7]. ment approaches show moderate activity. Due to a lack of These new data support further investigation of the role of novel tyrosine kinases in AF. Pazopanib is one of the latest anti-angiogenic drugs developed to target VEGF *Correspondence: gulcanbulut07@gmail.com Department of Medical Oncology, Ege University Medical School, Tulay and PDGF. It has recently been approved for the treat- Aktas Oncology Hospital, Ege University, Izmir, Turkey ment of advanced renal cancer and soft-tissue sarcomas Full list of author information is available at the end of the article © The Author(s) 2016. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/ publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. Bulut et al. Clin Sarcoma Res (2016) 6:22 Page 2 of 4 by the US Food and Drug Administration (FDA) and by the European Medicines Agency (EMA). [8, 9]. Case report Here we report a case of AF treated successfully with paz- opanib. In 2013, a 50-year-old male was admitted to our University Hospital with recurrent episodes of abdominal pain, and loss of appetite. He did not have any comor- bid disease and was not on any medication. Computed tomography (CT) scan showed an intra-abdominal soft tissue mass of 5 × 4 × 3 cm originating from the retrop- eritoneum. For both diagnostic and therapeutic reasons, he underwent a surgical excision of the mass, including partial resection of transverse colon. Pathological exami- nation revealed aggressive fibromatosis with a low prolif - eration index. The surgical procedure was accepted as R2 resection of the residual mass. In spite of the residual mass after surgery, and consid- ering that the Ki-67 index was 3% and the patient was asymptomatic, no further treatment was offered at that time. A wait-and-see policy is one of the most acceptable options with slowly progressing AFs, since AF can show Fig. 1 The photographs the patient before treatment pazopanib very varying clinical behavior, ranging from spontane- ous regression to rapid progression leading to local organ dysfunction [10]. During his planned follow-up visits, CT scans revealed progression of residual mass and tamoxifen 20  mg/daily was started. After 3  months on tamoxifen, progressive disease was detected by CT scan (Fig.  3a, b). This time, the patient complained of abdominal cramps and his creatinine level was rising due to invasion of bladder by tumoral mass. Since no cytotoxic treatment was reported to have an efficacy for AF, we searched for possible treat - ment options on PubMed. Recently, new data has been released to demonstrate the efficacy of tyrosine kinases for AF [11]. It was suggested that kinase-targeting therapy may be effective against AF as there may be an autocrine/ paracrine loop in AF that sustains platelet-derived growth factor receptor (PDGFR)-α and PDGFR-β activation [12]. Based on the literature that Pazopanib may be an effective treatment option in desmoid tumor/aggressive fibromato - sis, we decided to treat our patient with pazopanib. The schedule was 800 mg/day. He tolerated the drug quite well with mild to moderate GI symptoms, including grade I diarrhea. One month after the initiation of pazopanib, he presented with vitiligo and hair depigmentation (Figs.  1, Fig. 2 One month after the start of pazopanib treatment; Patient 2) which are quite common side effects of pazopanib. presented with loss of hair color and vitiligo On the follow-up period, first response to treatment was documented 4  months after the initiation of treat- Conclusion ment (Fig.  3c). The response to treatment lasted on the Our report demonstrates that pazopanib is an effective follow-up visits, and after 22  months on pazopanib; and well-tolerated treatment option for the treatment of complete response was achieved on patient’s last scan AF. To the best of our knowledge, this is the first reported (Fig. 3d). Bulut et al. Clin Sarcoma Res (2016) 6:22 Page 3 of 4 Fig. 3 Patient CT scans; a before initial treatment of tamoxifen; axial plan CT scan performed in September 2013 demonstrates 2.89 cm diameter homogeneous mass located at the left anterior pararenal space of the retroperitoneal area (yellow arrow). b Post contrast CT images in december 2013; retroperitoneal mass (diameter 4.14 cm) progressed after treatment of tamoxifen (yellow arrow). c 9 months after the initiation of pazopanib treatment; the residual mass regressed on CT scan at same level (yellow arrow). d Post contrast CT images obtained in October 2015 showing com- plete response of the residual mass at 22 months of pazopanib treatment.(yellow arrow) case of AF where a complete response was achieved with French Sarcoma Group has conducted a phase II trial pazopanib. AF has various clinical presentations, from that assesses the efficacy and toxicity of pazopanib in AF spontaneous regression to rapid progression of tumor, (ClinicalTrials.gov identifier NCT01876082). We hope necessitating a precise treatment decision. In our case, that above mentioned clinical trial will confirm the effec - the patient was progressing not only radiologically but tiveness of pazopanib in AF, a challenging atypical tumor. also clinically, which led us to decide in favor of a tar- geted treatment for this case. Abbreviations Angiogenesis is one of the fundamental mechanisms in AF: aggressive fibromatosis; NSAIDs: nonsteroidal anti-inflammatory drugs; cancer and many studies suggest that it also plays a cru- VEGF: vascular endothelial growth factor; PDGF: platelet derivated growth factor; FDA: US Food and Drug Administration; EMA: The European Medicines cial role in soft tissue sarcomas [13]. Based on the results Agency; CT: computed tomography; PET: positron emission tomography. of a phase 3 randomized, placebo-controlled trial pazo- panib was approved by the FDA in 2012 for the treatment Authors’ contributions GB supervised development of work, wrote manuscript and acted as cor- of patients with locally advanced or metastatic soft tissue responding author. AO was responsible for patient’s management, organizing sarcoma after treatment with standard chemotherapy [14]. and reporting data. APE participated in literature search and editing the Owing to low or no cumulative toxicity of pazopanib manuscript. RU supervised manuscript preparation and supplied financial resources. NE helped to evaluate radiological dates. BK participated in data compared to standard chemotherapy may allows an interpretation and manuscript evaluation. All authors took full responsibil- extended treatment duration. However, this observation ity for the content of the final paper. All authors read and approved the final clearly needs to be confirmed in prospective studies. The manuscript. Bulut et al. Clin Sarcoma Res (2016) 6:22 Page 4 of 4 Author details the effect of imatinib on advanced aggressive fibromatosis (desmoid Department of Medical Oncology, Ege University Medical School, Tulay Aktas tumor). J Clin Oncol. 2006;24(7):1195–203. Oncology Hospital, Ege University, Izmir, Turkey. Department of Internal 4. Penel N, Le Cesne A, Bui BN, Perol D, Brain EG, Ray-Coquard I, Guillemet C, Medicine, Ege University Medical School, Ege University Medical School Hos- Chevreau C, Cupissol D, Chabaud S, Jimenez M, Duffaud F, Piperno-Neu- pital, Ege University, Izmir, Turkey. Department of Radiology, Ege University mann S, Mignot L, Blay JY. Imatinib for progressive and recurrent aggres- Medical School, Ege University Medical School Hospital, Ege University, Izmir, sive fibromatosis (desmoid tumors): an FNCLCC/French Sarcoma Group Turkey. phase II trial with a long-term follow-up. Ann Oncol. 2011;22(2):452–7. 5. Martin-Liberal J, Benson C, McCarty H, Thway K, Messiou C, Judson I. Acknowledgements Pazopanib is an active treatment in desmoid tumor/aggressive fibroma- The authors would like to thank all of the participating patients and their tosis. Clin Sarcoma Res. 2013;3(1):13. families. 6. Gounder MM, Lefkowitz RA, Keohan ML, D’Adamo DR, Hameed M, Antonescu CR, Singer S, Stout K, Ahn L, Maki RG. Activity of sorafenib Competing interests against desmoid tumor/aggressive fibromatosis. Clin Cancer Res. The authors declare that they have no competing interests. 2011;17(12):4082–90. 7. Escobar C, Munker R, Thomas JO, Li BD, Burton GV. Update on desmoid Availability of data and supporting materials section tumors. Ann Oncol. 2012;23(3):562–9. This is only a case report and authors have no database for this case report. 8. Votrient (pazopanib) dosing, indications, interactions, adverse effects, and more. Medscape Reference. WebMD. Accessed 27 Jan 2014. Consent for publication 9. VOTRIENT (pazopanib hydrochloride) tablet, film coated (Glaxo Smith The consent was received to publish his PET/CT images and his photographs Kline LLC). DailyMed. 2013. and disease information from the patient with aggressive fibromatosis who 10. Braschi-Amirfarzan M, Abhishek R, et al. Role of imaging in management was reported. of desmoid-type fibromatosis: a primer for radiologists. Radiographics. 2016;36(3):767–82. Received: 2 June 2016 Accepted: 1 November 2016 11. Jo JC, Hong YS, Kim KP, Lee JL, Lee J, Park YS, Kim SY, Ryu JS, Lee JS, Kim TW. A prospective multicenter phase II study of sunitinib in patients with advanced aggressive fibromatosis. Invest New Drugs. 2014;32(2):369–76. 12. Signoroni S, Frattini M, Negri T, Pastore E, Tamborini E, Casieri P, Orsenigo M, Da Riva L, Radice P, Sala P, Gronchi A, Bertario L, Pierotti MA, Pilotti S. Cyclooxygenase-2 and platelet-derived growth factor receptors as References potential targets in treating aggressive fibromatosis. Clin Cancer Res. 1. Alman BA, Pajerski ME, Diaz-Cano S, Corboy K, Wolfe HJ. Aggressive 2007;13(17):5034–40. fibromatosis (desmoid tumor) is a monoclonal disorder. Diagn Mol 13. Martin-Liberal J, Judson I, Benson C. Anti angiogenic approach in soft- Pathol. 1997;6(2):98–101. tissue sarcomas. Expert Rev Anticancer Ther. 2013;13(8):975–82. 2. Hansmann A, Adolph C, Vogel T, Unger A, Moeslein G, Ballo MT, Zagars 14. Van der Graaf WT, Blay JY, Chawla SP, Kim DW, Bui-Nguyen B, Casali GK, Pollack A, Pisters PW, Pollack RA. High-dose tamoxifen and sulindac as PG, et al. Pazopanib for metastatic soft-tissue sarcoma (PALETTE); a first-line treatment for desmoid tumors. Cancer. 2004;100(3):612–20. randomized, double-blind, placebo controlled phase 3 trial. Lancet. 3. Heinrich MC, McArthur GA, Demetri GD, Joensuu H, Bono P, Herrmann 2012;379(9829):1879–86. R, Hirte H, Cresta S, Koslin DB, Corless CL, Dirnhofer S, van Oosterom AT, Nikolova Z, Dimitrijevic S, Fletcher JA. Clinical and molecular studies of Submit your next manuscript to BioMed Central and we will help you at every step: • We accept pre-submission inquiries • Our selector tool helps you to find the most relevant journal • We provide round the clock customer support • Convenient online submission • Thorough peer review • Inclusion in PubMed and all major indexing services • Maximum visibility for your research Submit your manuscript at www.biomedcentral.com/submit http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Clinical Sarcoma Research Springer Journals

Pazopanib: a novel treatment option for aggressive fibromatosis

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Springer Journals
Copyright
Copyright © 2016 by The Author(s)
Subject
Biomedicine; Cancer Research; Oncology; Surgical Oncology
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2045-3329
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10.1186/s13569-016-0061-3
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Abstract

Background: Aggressive fibromatosis (AF), also known as desmoid tumor, is an uncommon soft tissue neoplasm. AF does not metastasize, but it is locally invasive and its propensity for recurrence after conservative resection is well doc- umented. No effective cytotoxic treatment has been reported, hence there is a need for novel treatment strategies. Case presentation: We present the case of an AF successfully treated with an oral tyrosine kinase inhibitor, pazo- panib, with mild side effects. As far as we know, this is the first case of AF with complete response to pazopanib. Conclusion: Pazopanib might be an effective treatment option for AF. Keywords: Pazopanib, Aggressive fibromatosis, Desmoid tumor, Oral tyrosine kinase inhibitor efficacious treatment options, patients might die due to Background local organ dysfunction because of their locally progres- Aggressive fibromatosis (AF) (also called deep fibroma - sive disease. tosis or desmoid tumor) is a proliferation of cytologically Sporadic AF is usually associated with somatic muta- benign-appearing fibrocytes, often resulting in significant tions in codons 41 or 45 of exon 3 of beta-catenin functional loss. The nature of the lesion is controver - (CTNNB1). AF occurring in the background of familial sial: some evidence suggests that it is a reactive process, adenomatous polyposis (FAP) usually contains inactivat- whereas other evidence supports a neoplastic etiology ing germline mutations in the adenomatous polyposis [1]. Although it does not have the propensity of distant coli (APC) gene. CTNNB1 and APC are part of the Wnt organ metastases, AF often exhibits an infiltrative pat - signaling pathway and mutations in either gene resulting tern of spread in an abundant collagen matrix, giving it a in stabilization of the beta-catenin protein and allowing dense, fibrotic character. As a result, this tumor can pro - nuclear translocation and binding of beta-catenin to the duce local tissue destruction leading to significant mor - T cell factor/lymphoid enhancer factor (TCF/Lef ) family bidity and functional loss. of transcription factors, lead to activation of target genes Since the etiology of AF is poorly understood, several that may underlie desmoid tumor biology and clinical medical approaches have been combined with or with- behavior. In the era of molecularly targeted therapeu- out surgical resection with scarce results. These include tics, there is a need to exploit the molecular mechanisms chemotherapy with doxorubicin-based combinations, behind desmoid tumorigenesis and progression in a bet- antiestrogen therapy with tamoxifen, nonsteroidal anti- ter way. Recently, new encouraging data with small mol- inflammatory drugs (NSAIDs) such as indomethacin ecule tyrosine kinase inhibitors (imatinib, sunitinib etc.,) and sulindac, colchicines [2]. However, all of these treat- have been published [3–7]. ment approaches show moderate activity. Due to a lack of These new data support further investigation of the role of novel tyrosine kinases in AF. Pazopanib is one of the latest anti-angiogenic drugs developed to target VEGF *Correspondence: gulcanbulut07@gmail.com Department of Medical Oncology, Ege University Medical School, Tulay and PDGF. It has recently been approved for the treat- Aktas Oncology Hospital, Ege University, Izmir, Turkey ment of advanced renal cancer and soft-tissue sarcomas Full list of author information is available at the end of the article © The Author(s) 2016. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/ publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. Bulut et al. Clin Sarcoma Res (2016) 6:22 Page 2 of 4 by the US Food and Drug Administration (FDA) and by the European Medicines Agency (EMA). [8, 9]. Case report Here we report a case of AF treated successfully with paz- opanib. In 2013, a 50-year-old male was admitted to our University Hospital with recurrent episodes of abdominal pain, and loss of appetite. He did not have any comor- bid disease and was not on any medication. Computed tomography (CT) scan showed an intra-abdominal soft tissue mass of 5 × 4 × 3 cm originating from the retrop- eritoneum. For both diagnostic and therapeutic reasons, he underwent a surgical excision of the mass, including partial resection of transverse colon. Pathological exami- nation revealed aggressive fibromatosis with a low prolif - eration index. The surgical procedure was accepted as R2 resection of the residual mass. In spite of the residual mass after surgery, and consid- ering that the Ki-67 index was 3% and the patient was asymptomatic, no further treatment was offered at that time. A wait-and-see policy is one of the most acceptable options with slowly progressing AFs, since AF can show Fig. 1 The photographs the patient before treatment pazopanib very varying clinical behavior, ranging from spontane- ous regression to rapid progression leading to local organ dysfunction [10]. During his planned follow-up visits, CT scans revealed progression of residual mass and tamoxifen 20  mg/daily was started. After 3  months on tamoxifen, progressive disease was detected by CT scan (Fig.  3a, b). This time, the patient complained of abdominal cramps and his creatinine level was rising due to invasion of bladder by tumoral mass. Since no cytotoxic treatment was reported to have an efficacy for AF, we searched for possible treat - ment options on PubMed. Recently, new data has been released to demonstrate the efficacy of tyrosine kinases for AF [11]. It was suggested that kinase-targeting therapy may be effective against AF as there may be an autocrine/ paracrine loop in AF that sustains platelet-derived growth factor receptor (PDGFR)-α and PDGFR-β activation [12]. Based on the literature that Pazopanib may be an effective treatment option in desmoid tumor/aggressive fibromato - sis, we decided to treat our patient with pazopanib. The schedule was 800 mg/day. He tolerated the drug quite well with mild to moderate GI symptoms, including grade I diarrhea. One month after the initiation of pazopanib, he presented with vitiligo and hair depigmentation (Figs.  1, Fig. 2 One month after the start of pazopanib treatment; Patient 2) which are quite common side effects of pazopanib. presented with loss of hair color and vitiligo On the follow-up period, first response to treatment was documented 4  months after the initiation of treat- Conclusion ment (Fig.  3c). The response to treatment lasted on the Our report demonstrates that pazopanib is an effective follow-up visits, and after 22  months on pazopanib; and well-tolerated treatment option for the treatment of complete response was achieved on patient’s last scan AF. To the best of our knowledge, this is the first reported (Fig. 3d). Bulut et al. Clin Sarcoma Res (2016) 6:22 Page 3 of 4 Fig. 3 Patient CT scans; a before initial treatment of tamoxifen; axial plan CT scan performed in September 2013 demonstrates 2.89 cm diameter homogeneous mass located at the left anterior pararenal space of the retroperitoneal area (yellow arrow). b Post contrast CT images in december 2013; retroperitoneal mass (diameter 4.14 cm) progressed after treatment of tamoxifen (yellow arrow). c 9 months after the initiation of pazopanib treatment; the residual mass regressed on CT scan at same level (yellow arrow). d Post contrast CT images obtained in October 2015 showing com- plete response of the residual mass at 22 months of pazopanib treatment.(yellow arrow) case of AF where a complete response was achieved with French Sarcoma Group has conducted a phase II trial pazopanib. AF has various clinical presentations, from that assesses the efficacy and toxicity of pazopanib in AF spontaneous regression to rapid progression of tumor, (ClinicalTrials.gov identifier NCT01876082). We hope necessitating a precise treatment decision. In our case, that above mentioned clinical trial will confirm the effec - the patient was progressing not only radiologically but tiveness of pazopanib in AF, a challenging atypical tumor. also clinically, which led us to decide in favor of a tar- geted treatment for this case. Abbreviations Angiogenesis is one of the fundamental mechanisms in AF: aggressive fibromatosis; NSAIDs: nonsteroidal anti-inflammatory drugs; cancer and many studies suggest that it also plays a cru- VEGF: vascular endothelial growth factor; PDGF: platelet derivated growth factor; FDA: US Food and Drug Administration; EMA: The European Medicines cial role in soft tissue sarcomas [13]. Based on the results Agency; CT: computed tomography; PET: positron emission tomography. of a phase 3 randomized, placebo-controlled trial pazo- panib was approved by the FDA in 2012 for the treatment Authors’ contributions GB supervised development of work, wrote manuscript and acted as cor- of patients with locally advanced or metastatic soft tissue responding author. AO was responsible for patient’s management, organizing sarcoma after treatment with standard chemotherapy [14]. and reporting data. APE participated in literature search and editing the Owing to low or no cumulative toxicity of pazopanib manuscript. RU supervised manuscript preparation and supplied financial resources. NE helped to evaluate radiological dates. BK participated in data compared to standard chemotherapy may allows an interpretation and manuscript evaluation. All authors took full responsibil- extended treatment duration. However, this observation ity for the content of the final paper. All authors read and approved the final clearly needs to be confirmed in prospective studies. The manuscript. Bulut et al. Clin Sarcoma Res (2016) 6:22 Page 4 of 4 Author details the effect of imatinib on advanced aggressive fibromatosis (desmoid Department of Medical Oncology, Ege University Medical School, Tulay Aktas tumor). J Clin Oncol. 2006;24(7):1195–203. Oncology Hospital, Ege University, Izmir, Turkey. Department of Internal 4. Penel N, Le Cesne A, Bui BN, Perol D, Brain EG, Ray-Coquard I, Guillemet C, Medicine, Ege University Medical School, Ege University Medical School Hos- Chevreau C, Cupissol D, Chabaud S, Jimenez M, Duffaud F, Piperno-Neu- pital, Ege University, Izmir, Turkey. Department of Radiology, Ege University mann S, Mignot L, Blay JY. Imatinib for progressive and recurrent aggres- Medical School, Ege University Medical School Hospital, Ege University, Izmir, sive fibromatosis (desmoid tumors): an FNCLCC/French Sarcoma Group Turkey. phase II trial with a long-term follow-up. Ann Oncol. 2011;22(2):452–7. 5. Martin-Liberal J, Benson C, McCarty H, Thway K, Messiou C, Judson I. Acknowledgements Pazopanib is an active treatment in desmoid tumor/aggressive fibroma- The authors would like to thank all of the participating patients and their tosis. Clin Sarcoma Res. 2013;3(1):13. families. 6. Gounder MM, Lefkowitz RA, Keohan ML, D’Adamo DR, Hameed M, Antonescu CR, Singer S, Stout K, Ahn L, Maki RG. Activity of sorafenib Competing interests against desmoid tumor/aggressive fibromatosis. Clin Cancer Res. The authors declare that they have no competing interests. 2011;17(12):4082–90. 7. Escobar C, Munker R, Thomas JO, Li BD, Burton GV. Update on desmoid Availability of data and supporting materials section tumors. Ann Oncol. 2012;23(3):562–9. This is only a case report and authors have no database for this case report. 8. Votrient (pazopanib) dosing, indications, interactions, adverse effects, and more. Medscape Reference. WebMD. Accessed 27 Jan 2014. Consent for publication 9. VOTRIENT (pazopanib hydrochloride) tablet, film coated (Glaxo Smith The consent was received to publish his PET/CT images and his photographs Kline LLC). DailyMed. 2013. and disease information from the patient with aggressive fibromatosis who 10. Braschi-Amirfarzan M, Abhishek R, et al. Role of imaging in management was reported. of desmoid-type fibromatosis: a primer for radiologists. Radiographics. 2016;36(3):767–82. Received: 2 June 2016 Accepted: 1 November 2016 11. Jo JC, Hong YS, Kim KP, Lee JL, Lee J, Park YS, Kim SY, Ryu JS, Lee JS, Kim TW. A prospective multicenter phase II study of sunitinib in patients with advanced aggressive fibromatosis. Invest New Drugs. 2014;32(2):369–76. 12. Signoroni S, Frattini M, Negri T, Pastore E, Tamborini E, Casieri P, Orsenigo M, Da Riva L, Radice P, Sala P, Gronchi A, Bertario L, Pierotti MA, Pilotti S. Cyclooxygenase-2 and platelet-derived growth factor receptors as References potential targets in treating aggressive fibromatosis. Clin Cancer Res. 1. Alman BA, Pajerski ME, Diaz-Cano S, Corboy K, Wolfe HJ. Aggressive 2007;13(17):5034–40. fibromatosis (desmoid tumor) is a monoclonal disorder. Diagn Mol 13. Martin-Liberal J, Judson I, Benson C. Anti angiogenic approach in soft- Pathol. 1997;6(2):98–101. tissue sarcomas. Expert Rev Anticancer Ther. 2013;13(8):975–82. 2. Hansmann A, Adolph C, Vogel T, Unger A, Moeslein G, Ballo MT, Zagars 14. Van der Graaf WT, Blay JY, Chawla SP, Kim DW, Bui-Nguyen B, Casali GK, Pollack A, Pisters PW, Pollack RA. High-dose tamoxifen and sulindac as PG, et al. Pazopanib for metastatic soft-tissue sarcoma (PALETTE); a first-line treatment for desmoid tumors. Cancer. 2004;100(3):612–20. randomized, double-blind, placebo controlled phase 3 trial. Lancet. 3. Heinrich MC, McArthur GA, Demetri GD, Joensuu H, Bono P, Herrmann 2012;379(9829):1879–86. R, Hirte H, Cresta S, Koslin DB, Corless CL, Dirnhofer S, van Oosterom AT, Nikolova Z, Dimitrijevic S, Fletcher JA. Clinical and molecular studies of Submit your next manuscript to BioMed Central and we will help you at every step: • We accept pre-submission inquiries • Our selector tool helps you to find the most relevant journal • We provide round the clock customer support • Convenient online submission • Thorough peer review • Inclusion in PubMed and all major indexing services • Maximum visibility for your research Submit your manuscript at www.biomedcentral.com/submit

Journal

Clinical Sarcoma Research – Springer Journals

Published: Dec 1, 2016

There are no references for this article.