Tumours of the thymic region. Symptomatology, diagnosis, treatment, and prognosis.

Bertelsen, S; Malmstrøm, Jørgen; Heerfordt, J; Pedersen, Hans Chr.

doi:10.1136/thx.30.1.19

Cited by 11 publications

(2 citation statements)

References 27 publications

(29 reference statements)

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“…Although our study do not support that the endothelium could serve as the original cell of HB-neovascularization, this high uniformity of Twist1 expression response to inactivation of the VHL gene, indicating that Twist1-mediated angiogenic signaling mechanism is conserved in the process of HB-neovascularization, at least in the process of the cell with CD34 expression. Combined with our previous studies of HB-vasculogenesis 9 , 12 , a possible explanation may be that this angiogenic mechanism may play an accessorial role in development of HB-neovascularization, and might be responsible for the incorporation into foci of this vascular network, and sequential remodeling as well as expansion 34 .…”

Section: Discussionmentioning

confidence: 55%

Endothelial cells by inactivation of VHL gene direct angiogenesis, not vasculogenesis via Twist1 accumulation associated with hemangioblastoma neovascularization

Wáng

Chen

et al. 2017

Sci Rep

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Inactivation of the VHL tumour suppressor gene is a highly frequent genetic event in the carcinogenesis of central nervous system-(CNS) hemangioblastomas (HBs). The patterning of the similar embryonicvasculogenesis is an increasing concern in HB-neovascularization, and the classic vascular endothelial growth factor (VEGF)-mediated angiogenesis driven by VHL loss-of-function from human endothelium have been questioned. With this regard, we identify a distinct, VHL silencing-driven mechanism in which human vascular endothelial cells by means of increasing cell proliferation and decreasing cell apoptosis, is concomitant with facilitating accumulation of Twist1 protein in vascular endothelial cells in vitro. Importantly, this molecular mechanism is also pinpointed in CNS-HBs, and associated with the process of HB-neovascularization. In contrast with recent studies of HB-neovascularization, these modified cells did not endow with the typical features of vasculogenesis, indicating that this is a common angiogenesis implementing the formation of the vascular network. Taken together, these findings suggest that vasculogenesis and angiogenesis may constitute complementary mechanisms for HB-neovascularization, and could provide a rational recognition of single anti-angiogenic intervention including targeting to the Twist1 signalling for HBs.Hemangioblastomas (HBs) are high-vascularized neoplasms commonly arising in the cerebellum or brainstem [1][2][3][4] . The cytological origin and process of neovascularization remains tremendously controversial. Etiologically, HBs are divided into two subtypes, the sporadic HBs (takes up 75%) and familial HBs (VHL disease) (takes up 25%). Histologic examination showed numerous small capillary channels and abundant vacuolated 'stromal cells' in sporadic HBs and VHL-HBs 2 . Currently, surgical complete resection is the only curative treatment for sporadic HBs; however, surgical treatment of brain-stem HBs is a great challenge to neurosurgeons because of the location of HBs. Moreover, as an inherited multisystem disorder, VHL-HBs are difficult to be cured. So a better understanding of HB biological mechanisms may further provide useful insights into its therapeutic strategies.The cytological origin of HBs (including its neovascularization) and its evolutionary process remain controversial for nearly a century. The related studies are associated with the vascular progenitors including embryonic cells, reactive endothelial cells, stromal cells, and mast cells etc 5,6 . In recent years, increasing evidence has showed that many mesodermal makers were expressed in both sporadic and inherited HBs 7,8 , suggesting that HB-neovascularization is a similar embryologic vasculogenesis [9][10][11][12] . Then, as the classic hypothesis of HB-angiogenesis, the vascular endothelial growth factor (VEGF) secreted by stromal cells may bind to endothelial cells and trigger an intracellular signaling pathway in the endothelial cells that eventually results in cell proliferation and vascular formation 13 . In ...

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Section: Discussionmentioning

confidence: 55%

Endothelial cells by inactivation of VHL gene direct angiogenesis, not vasculogenesis via Twist1 accumulation associated with hemangioblastoma neovascularization

Wáng

Chen

et al. 2017

Sci Rep

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“…The mass was a well-demarcated nodule in the left lobe of the thymus. There are three reports of six thymic hemangiomas for which no pathology reports and specific clinical data were available [ 1 , 5 , 6 ].…”

Section: Discussionmentioning

confidence: 99%

Cavernous hemangioma of thymus misdiagnosed as thymoma: a case report

Shen

Liang

et al. 2014

World J Surg Onc

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IntroductionCavernous hemangioma in the thymus is a rare presentation in mediastinal hemangiomas. The diagnosis is difficult to make promptly because both invasive and noninvasive examinations usually fail to distinguish it from other tumors of the mediastinum. Their clinical presentations depends on their size and their involvement with adjacent mediastinal structures.Case presentationWe treated a 52-year-old man with thymic cavernous hemangioma that was incidentally detected by chest radiography during a routine health check, and had been misdiagnosed as thymoma before the operation. The tumor was completely resected by thymectomy via video-assisted thoracic surgery. The pathological tissue was diagnosed as a cavernous hemangioma, and no phlebolith was observed in the center.ConclusionsWe reported this case of thymic cavernous hemangioma for its extremely rare occurrence in the thymus. The preoperative diagnosis remains a challenge both clinically and radiologically. It is still difficult to distinguish this tumor from other tumors in the thymus. Furthermore, biopsies might not result in a definitive diagnosis. Finally, surgical resection provides material for histopathologic diagnosis. To facilitate the preoperative diagnosis of such a rare tumor, more cases will need to be reported.

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Malignant thymoma in an eight‐month‐old boy

Deshpande

Fisher

Jewett

et al. 1981

Journal of Surgical Oncology

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A case of locally invasive malignant thymoma is presented. This 8‐month‐old child presented with respiratory distress and superior vena cava syndrome. Histology revealed malignant lymphocytic thymoma infiltrating the great vessels, pericardium, and regional lymph node. He was successfully treated with surgical removal, radiotherapy, and aggressive chemotherapy. We believe he is the youngest child with thymoma reported in medical literature.

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Tumours of the thymic region. Symptomatology, diagnosis, treatment, and prognosis.

Cited by 11 publications

References 27 publications

Endothelial cells by inactivation of VHL gene direct angiogenesis, not vasculogenesis via Twist1 accumulation associated with hemangioblastoma neovascularization

Endothelial cells by inactivation of VHL gene direct angiogenesis, not vasculogenesis via Twist1 accumulation associated with hemangioblastoma neovascularization

Cavernous hemangioma of thymus misdiagnosed as thymoma: a case report

Malignant thymoma in an eight‐month‐old boy

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