Angiosarcoma: State of the art and perspectives

Penel, Nicolas; Marréaud, Sandrine; Robin, Y.; Hohenberger, Peter

doi:10.1016/j.critrevonc.2010.10.007

Cited by 104 publications

(129 citation statements)

References 56 publications

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“…Besides undifferentiated sarcomas angiosarcomas are most frequent. Angiosarcomas are derived from endothelial cells and encompass a heterogeneous group of tumors with variable histologic characteristics and several clinical forms besides cardiac angiosarcomas, such as the skin and scalp angiosarcomas, angiosarcomas arising in irradiated fields, and hepatica angiosarcomas related to occupational causes (2)(3)(4). Cardiac angiosarcomas are characterized by a high proliferation rate and a marked propensity to metastasize, mostly to the lung (5,6).…”

Section: Introductionmentioning

confidence: 99%

A Recurrent Activating PLCG1 Mutation in Cardiac Angiosarcomas Increases Apoptosis Resistance and Invasiveness of Endothelial Cells

et al. 2014

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Primary cardiac angiosarcomas are rare tumors with unfavorable prognosis. Pathogenic driver mutations are largely unknown. We therefore analyzed a collection of cases for genomic aberrations using SNP arrays and targeted next-generation sequencing (tNGS) of oncogenes and tumor-suppressor genes. Recurrent gains of chromosome 1q and a small region of chromosome 4 encompassing KDR and KIT were identified by SNP array analysis. Repeatedly mutated genes identified by tNGS were KDR with different nonsynonymous mutations, MLL2 with different nonsense mutations, and PLCG1 with a recurrent nonsynonymous mutation (R707Q) in the highly conserved autoinhibitory SH2 domain in three of 10 cases. PLCg1 is usually activated by Y783 phosphorylation and activates protein kinase C and Ca 2þ -dependent second messengers, with effects on cellular proliferation, migration, and invasiveness. Ectopic expression of the PLCg1-R707Q mutant in endothelial cells revealed reduced PLCg1-Y783 phosphorylation with concomitant increased c-RAF/MEK/ ERK1/2 phosphorylation, increased IP3 amounts, and increased Ca 2þ -dependent calcineurin activation compared with ectopic expressed PLCg1-wild-type. Furthermore, cofilin, whose activation is associated with actin skeleton reorganization, showed decreased phosphorylation, and thus activation after expression of PLCg1-R707Q compared with PLCg1-wild-type. At the cellular level, expression of PLCg1-R707Q in endothelial cells had no influence on proliferation rate, but increased apoptosis resistance and migration and invasiveness in in vitro assays. Together, these findings indicate that the PLCg1-R707Q mutation causes constitutive activation of PLCg1 and may represent an alternative way of activation of KDR/PLCg1 signaling besides KDR activation in angiosarcomas, with implications for VEGF/KDR targeted therapies. Cancer Res; 74(21); 6173-83. Ó2014 AACR.

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Section: Introductionmentioning

confidence: 99%

A Recurrent Activating PLCG1 Mutation in Cardiac Angiosarcomas Increases Apoptosis Resistance and Invasiveness of Endothelial Cells

et al. 2014

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“…The exact pathogenesis remains unclear although previous radiotherapy and chronic lymphoedema are two well established risk factors. 1 The relative risk for developing an angiosarcoma is approximately six times higher after radiotherapy 2 and angiosarcomas in irradiated fields represent approximately 3-10% of all angiosarcomas. 3,4 Angiosarcoma following radiotherapy tends to occur within an eight-year window although it is a far more common finding in radiotherapy for breast cancer and lymphoma.…”

Section: Discussionmentioning

confidence: 99%

“…Radiotherapy and lymphoedema are well established risk factors for angiosarcoma. 1 We present a case of angiosarcoma of the pharynx occurring approximately three years after curative multimodal treatment for a T2N2bM0 oropharyngeal squamous cell carcinoma with surgery and chemoradiotherapy. On reviewing the literature, we are not aware of any similar case of post-treatment pharyngeal angiosarcoma.…”

mentioning

confidence: 99%

Pharyngeal angiosarcoma following multimodal treatment for oropharyngeal squamous cell carcinoma

Ball

Kwong

Young

et al. 2014

annals

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It is well established that angiosarcoma can develop following radiotherapy. We present an unusual case of angiosarcoma of the pharynx that developed three years after treatment with surgery and adjuvant chemoradiotherapy for a T2N2bM0 squamous cell carcinoma of the oropharynx. The patient was tumour free until developing dysphagia, which was found to be caused by an angiosarcoma. The patient underwent surgery of the pharyngeal angiosarcoma by laryngopharyngectomy, tongue base resection, selective neck dissection and radial forearm microvascular free flap reconstruction. Angiosarcoma following head and neck malignancy is rare but must be considered as part of the differential diagnosis in patients with new symptoms after radiotherapy.

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“…For metastatic disease, palliative chemotherapy is the treatment of choice for the majority of the diseases and anti-angiogenic drugs, such as sorafenib and sunitinib, have shown some efficiency in angiosarcomas 25 .…”

Section: Chemotherapymentioning

confidence: 99%

Radiation Induced Second Malignancies (RISM): Risk, Diagnosis, Treatments and Review of Literature

Haque¹,

Chowdhury²,

Ali³

2016

Faridpur Med Coll J

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Abstract:Information concerning radiation-induced malignancies comes from the A-bomb survivors and from medically exposed individuals, including second malignancies in radiation therapy patients. The A-bomb survivors show an excess incidence of carcinomas in tissues such as the gastrointestinal tract, breast, thyroid, and bladder, which is linear with dose up to about 2.5 Sv. There is great uncertainty concerning the dose-response relationship for radiationinduced carcinogenesis at higher doses. Some animal and human data suggest a decrease at higher doses, usually attributed to cell killing; other data suggest a plateau in dose. Modern treatment modalities such as passive proton therapy and intensity modulated radiation therapy (IMRT) produce large amounts of scatter, leakage and neutron radiation, which has been found to be directly proportional to the risk of second malignancy incidence. Organs closer to the target typically receive higher and less homogeneous doses of cell killing and repopulation effects play an increasing role. The most common type of cancer caused by radiation is sarcoma, which is typically a cancer of muscle, bone, or blood vessel origin. We reviewed the literature with key words "Radiation induced second malignancies, second primary tumour, second cancer" to find relevant articles describing risk, diagnosis and treatments of radiation induced second malignancies.

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Angiosarcoma: State of the art and perspectives

Cited by 104 publications

References 56 publications

A Recurrent Activating PLCG1 Mutation in Cardiac Angiosarcomas Increases Apoptosis Resistance and Invasiveness of Endothelial Cells

A Recurrent Activating PLCG1 Mutation in Cardiac Angiosarcomas Increases Apoptosis Resistance and Invasiveness of Endothelial Cells

Pharyngeal angiosarcoma following multimodal treatment for oropharyngeal squamous cell carcinoma

Radiation Induced Second Malignancies (RISM): Risk, Diagnosis, Treatments and Review of Literature

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