Epidemiological, Clinical and Pathological Features of Primary Cardiac Hemangiosarcoma in Dogs: A Review of 51 Cases

Yamamoto, Shinya; Hoshi, Katsuichiro; Hirakawa, Atsushi; Chimura, Syuuichi; Kobayashi, Masayuki; Motomura, Noboru

doi:10.1292/jvms.13-0064

Cited by 68 publications

(101 citation statements)

References 29 publications

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“…Generating survival curves using the product limit method of Kaplan and Meier, 67 we compared our longevity results to those obtained by Yamamoto et al, the group that has published the best results to date. 68 We then individually compared survival curves for G6PD inhibition against each of the Yamamoto treatment groups using the logrank test of Mantel-Cox, generating the statistical data shown in Table 1. Dogs with CCH treated by inhibition of G6PD had complete or near-complete resolution of their tumor (Figure 4), and dramatically extended longevity compared to the dogs in the Yamamoto study.…”

Section: Hypersensitivity To G6pd Inhibition In a Subset Of Canine Tumentioning

confidence: 99%

Species specificity of an adrenal androgen-mediated kill-switch triggered by p53 inactivation

Nyce¹

2017

Transl Med Rep

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Glucose-6-phosphate dehydrogenase (G6PD) is an oncoprotein that is regulated by the p53 tumor suppressor. Mutant p53 loses the ability to inhibit G6PD, and loss of G6PD control clearly plays a role in oncogenesis. The steroid hormone precursor dehydroepiandrosterone (DHEA) is an endogenous uncompetitive inhibitor of G6PD. In humans, and a few other species, the sulfated circulatory form of DHEA (DHEAS) is present at extremely high concentrations -much higher than can be accounted for by DHEA's function as a precursor to steroid hormones. Uncompetitive inhibition is extremely rare in natural systems because it is irreversible in the presence of high concentrations of substrate and inhibitor. What has gone unappreciated is that such uncompetitive inhibition can quickly lead to cell death when the target is an obligatory housekeeping gene such as G6PD. Cells with inactivated p53 not only lose control over G6PD, but also over hexokinase (HK), the enzyme that converts glucose into glucose-6-phosphate (G6P), the substrate of G6PD. Furthermore, loss of p53 function de-represses NFκB activity, resulting in the upregulation of steroid sulfatase (SS) which converts circulating DHEAS into active DHEA. We propose that inactivation of p53 rapidly elevates G6P and DHEA concentrations in affected cells, driving uncompetitive inhibition of G6PD to lethal irreversibility. In animals with circulating DHEAS, this kill-switch mechanism may prevent most cases of p53 inactivation from becoming tumorigenic. Tumors would thus represent instances in which this mechanism had not been triggered, but which might still be triggered by application of DHEA sufficient to uncompetitively inhibit tumor G6PD. To test this hypothesis, we performed a pilot study in which dogs with cardiac hemangiosarcoma were treated with high dose (HD) DHEA supplemented with isoprene precursors to maintain geranylation of Rac GTPase. Tumor regression and longevity observed in these dogs supported the concept that some tumors retain extraordinary sensitivity to uncompetitive inhibition by DHEA.

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Section: Hypersensitivity To G6pd Inhibition In a Subset Of Canine Tumentioning

confidence: 99%

Species specificity of an adrenal androgen-mediated kill-switch triggered by p53 inactivation

Nyce¹

2017

Transl Med Rep

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“…Hemangiossarcoma é uma neoplasia originada tanto de células do endotélio vascular quanto de células precursoras do endotélio, maligna e agressiva (LAMERATO-KOZICKI et al, 2006;YAMAMOTO et al, 2013). Cães são frequentemente acometidos por essa neoplasia (FLORES et al, 2012;GÖRITZ et al, 2013;YAMAMOTO et al, 2013;CHIKAZAWA et al, 2013;SOARES et al, 2017) que pode ser encontrada em baço, coração, rins, fígado, bexiga, pulmão, intestinos, pele de diversas regiões do corpo, subcutâneo e cavidade oral (FLORES et al, 2012;GÖRITZ et al, 2013;YAMAMOTO et al, 2013;SOARES et al, 2017).…”

Section: Introductionunclassified

“…Cães são frequentemente acometidos por essa neoplasia (FLORES et al, 2012;GÖRITZ et al, 2013;YAMAMOTO et al, 2013;CHIKAZAWA et al, 2013;SOARES et al, 2017) que pode ser encontrada em baço, coração, rins, fígado, bexiga, pulmão, intestinos, pele de diversas regiões do corpo, subcutâneo e cavidade oral (FLORES et al, 2012;GÖRITZ et al, 2013;YAMAMOTO et al, 2013;SOARES et al, 2017). Macroscopicamente, o hemangiossarcoma cutâneo ou subcutâneo se apresenta como uma massa única, bem delimitada, de coloração vermelha a preta, consistência macia a firme, fluindo sangue ao corte.…”

Section: Introductionunclassified

Ocorrência Simultânea De Hemangiossarcoma Subcutâneo E Quimiodectoma Em Cadela – Relato De Caso

Viscone¹,

Rodrigues²,

Oliveira³

et al. 2017

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RESUMOHemangiossarcomas são neoplasias de origem do endotélio vascular ou de células precursoras do endotélio, que pode ocorrer em qualquer parte vascularizada do organismo sendo de ocorrência comum em cães. Quimiodectoma é uma neoplasia de quimiorreceptores que pode se desenvolver nos corpos aórtico e carotídeo, levando a sintomas clínicos de descompensação cardiorrespiratória ou não apresentando nenhum sinal clínico. Esse trabalho teve como objetivo relatar um caso de ocorrência simultânea de hemangiossarcoma subcutâneo e quimiodectoma em uma cadela da raça Boxer, 13 anos, encaminhada para necropsia no setor de Patologia Animal do Hospital Veterinário da Universidade Federal de Uberlândia -MG. Macroscopicamente, o animal apresentava uma massa em região de osso frontal, com crescimento progressivo, próximo ao globo ocular direito. O animal apresentava tremores, incoordenação, fraqueza e perda de peso progressiva. Foi realizada radiografia do crânio onde constatou-se lise óssea. Ainda, massa em corpo aórtico. Ao exame histopatológico, diagnosticou-se hemangiossarcoma na massa da cabeça e quimiodectoma na massa em base do coração. PALAVRAS -CHAVE: endotélio, neoplasia , quimiorreceptores. SIMULTANEOUS OCCURRENCE OF SUBCUTANEOUS HEMANGIOSARCOMA AND CHEMODECTOMA IN DOG -CASE REPORTABSTRACT Hemangiosarcoma of endotelial origin, metastatic, with aggressive biological behavior, can occur in any vascular site in the body and is common in dogs. Chemodectomas are tumors formed from chemoreceptors present at the heart's base involving the aortic and carotid body, can cause cardiorespiratory failure or be asymptomatic. The aim of these study was report an occurrence of hemangiosarcoma and chemodectoma at same time in a Boxer dog, thirteen years old, wich was necropsied at Animal Pathology Department, Federal University of Uberlândia. Macroscopy, there was at frontal bone mass, progressive growth, near to right eye, the animal had neurologycal signs. At skull radiograph showed osteolysis caused by the mass. Furthermore, was found a mass at aortic body. Histopathologyc diagnosis was hemangiosarcoma, at head, and chemodectoma at heart bases.

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“…The mean age range of occurrence in dogs is 8 to 13 years, and German shepherds, golden retrievers and Labrador retrievers are overrepresented [13-15]. Echocardiography and computed tomography (CT) are considered to be good diagnostic tools; however, histological evaluation is necessary for a definitive diagnosis [3]. Treatment usually includes partial pericardiectomy or tumor resection for cardiac HSA [3].…”

Section: Introductionmentioning

confidence: 99%

“…Echocardiography and computed tomography (CT) are considered to be good diagnostic tools; however, histological evaluation is necessary for a definitive diagnosis [3]. Treatment usually includes partial pericardiectomy or tumor resection for cardiac HSA [3]. To the authors’ knowledge, this is the first case report in a dog to describe primary cranial mediastinal HSA.…”

Section: Introductionmentioning

confidence: 99%

Primary cranial mediastinal hemangiosarcoma in a young dog

2014

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Primary cranial mediastinal hemangiosarcomas are uncommon tumors. A 30-kg, 2-year-old, intact female German shepherd was presented for evaluation of cachexia and respiratory distress of a few days’ duration. Lateral radiographic projection of the thorax revealed significant pleural effusion. Computed tomography revealed a cranial mediastinal mass effect adjacent to the heart. On surgical exploration, a pedunculated mass attached to the esophagus, trachea, brachiocephalic trunk, left subclavian artery and cranial vena cava without attachment to the right atrium and auricular appendage was removed and debrided by use of blunt dissection and dry gauzes, respectively. Histopathology results described the cranial mediastinal mass as hemangiosarcoma. At 8 months and 5 days post-operatively, the patient died. Primary cranial mediastinal hemangiosarcomas, although a seemingly rare cause of thoracic pathology in young dogs, should be considered in the differential diagnosis for pleural effusion and soft tissue mass effect in the cranial mediastinum. This is the first case report in a dog to describe primary cranial mediastinal hemangiosarcoma.

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Epidemiological, Clinical and Pathological Features of Primary Cardiac Hemangiosarcoma in Dogs: A Review of 51 Cases

Cited by 68 publications

References 29 publications

Species specificity of an adrenal androgen-mediated kill-switch triggered by p53 inactivation

Species specificity of an adrenal androgen-mediated kill-switch triggered by p53 inactivation

Ocorrência Simultânea De Hemangiossarcoma Subcutâneo E Quimiodectoma Em Cadela – Relato De Caso

Primary cranial mediastinal hemangiosarcoma in a young dog

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