GLUT1: A newly discovered immunohistochemical marker for juvenile hemangiomas

North, Paula E.; Waner, Milton; Mizeracki, Adam; Mihm, Martín C.

doi:10.1016/s0046-8177(00)80192-6

Cited by 766 publications

(559 citation statements)

References 41 publications

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“…This hypothesis originated from immunohistochemical staining of several markers uniquely colocalized to placental and hemangioma EC (12,14). We were able to confirm Fc␥RII␤ (12) and IGF2 (19).…”

Section: Discussionmentioning

confidence: 55%

“…At least seven markers of hemangioma vessels are uniquely coexpressed in placental vessels. In addition to the four markers identified by North: GLUT1 (14), merosin (12), Lewis Y antigen (12), and Fc␥-RIIb (12), the following three markers have been independently reported in hemangioma and placental vessels: type III iodothyronine deiodinase (15,16), indoleamine 2,3-deoxygenase (17,18), and insulin-like growth factor 2 (IGF2) § § (19,20). No other tissue jointly expresses these markers.…”

mentioning

confidence: 99%

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Evidence by molecular profiling for a placental origin of infantile hemangioma

Barnes

Huang

Kaipainen

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

176

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The origin of the pathogenic endothelial cells in common infantile hemangioma is unknown. We show here that the transcriptomes of human placenta and infantile hemangioma are sufficiently similar to suggest a placental origin for this tumor, expanding on recent immunophenotypical studies that have suggested this possibility [North, P. E., et al. (2001) Arch. Dermatol. 137, 559 -570]. The transcriptomes of placenta, hemangioma, and eight normal and diseased tissues were compared by hierarchical and nonhierarchical clustering analysis of >7,800 genes. We found that the level of transcriptome similarity between placenta and hemangioma exceeded that of any other tissue compared and paralleled that observed between a given tissue and its derived tumor, such as normal and cancerous lung. The degree of similarity was even greater when a subset of endothelial cell-specific genes was analyzed. Genes preferentially expressed in both placenta and hemangiomas were identified, including 17-␤ hydroxysteroid dehydrogenase type 2 and tissue factor pathway inhibitor 2. These data demonstrate the value of global molecular profiling of tissues as a tool for hypothesis-driven research. Furthermore, it suggests that the unique self-limited growth of infantile hemangioma may, in fact, mirror the lifetime of placental endothelium.angiogenesis ͉ endothelium ͉ microarray ͉ gene array

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Section: Discussionmentioning

confidence: 55%

mentioning

confidence: 99%

Evidence by molecular profiling for a placental origin of infantile hemangioma

Barnes

Huang

Kaipainen

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

176

View full text Add to dashboard Cite

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“…Kaposiform hemangioendothelioma, common infantile hemangioma, and rapidly involuting congenital hemangioma frequently have a similar clinical appearance in neonates, and the histopathologic diagnosis can be difficult in small biopsies. It has been previously shown that infantile hemangioma is positive for erythrocyte-type glucose transporter protein (GLUT1), 19 whereas kaposiform hemangioendothelioma does not react with GLUT1. 5,19 D2-40, which also exhibits different reactivity in these two lesions, thus, can be used as an additional or alternative diagnostic marker.…”

Section: D2-40 In Kaposiform Hemangioendotheliomamentioning

confidence: 99%

“…It has been previously shown that infantile hemangioma is positive for erythrocyte-type glucose transporter protein (GLUT1), 19 whereas kaposiform hemangioendothelioma does not react with GLUT1. 5,19 D2-40, which also exhibits different reactivity in these two lesions, thus, can be used as an additional or alternative diagnostic marker. Kaposiform hemangioendothelioma is the fifth known vascular lesion that is reportedly positive for D2-40: previously the immunopositivity was shown in lymphatic malformation (lymphangioma), Kaposi sarcoma, angiosarcoma, 13 and hobnail hemangioma.…”

Section: D2-40 In Kaposiform Hemangioendotheliomamentioning

confidence: 99%

D2-40 immunohistochemical analysis of pediatric vascular tumors reveals positivity in kaposiform hemangioendothelioma

et al. 2005

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“…Twenty-four percent (26%) of the cases examined had ulceration, which is a complication that can lead to hemorrhage and infection, and therefore was noted. The presence of glucose transporter-1 (Glut-1), which is a specific marker of infantile hemangioma, 38 was confirmed in 39% of the cases. Glut-1 staining was not performed or reported in the remaining cases.…”

Section: Clinicopathologic Characteristics Of Infantile Hemangioma Anmentioning

confidence: 99%

Vascular tumors have increased p70 S6-kinase activation and are inhibited by topical rapamycin

Gerald²,

Perruzzi³

et al. 2013

Laboratory Investigation

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Vascular tumors are endothelial cell neoplasms whose cellular and molecular mechanisms, leading to tumor formation, are poorly understood, and current therapies have limited efficacy with significant side effects. We have investigated mechanistic (mammalian) target of rapamycin (mTOR) signaling in benign and malignant vascular tumors, and the effects of mTOR kinase inhibitor as a potential therapy for these lesions. Human vascular tumors (infantile hemangioma and angiosarcoma) were analyzed by immunohistochemical stains and western blot for the phosphorylation of p70 S6-kinase (S6K) and S6 ribosomal protein (S6), which are activated downstream of mTOR complex-1 (mTORC1). To assess the function of S6K, tumor cells with genetic knockdown of S6K were analyzed for cell proliferation and migration. The effects of topical rapamycin, an mTOR inhibitor, on mTORC1 and mTOR complex-2 (mTORC2) activities, as well as on tumor growth and migration, were determined. Vascular tumors showed increased activation of S6K and S6. Genetic knockdown of S6K resulted in reduced tumor cell proliferation and migration. Rapamycin fully inhibited mTORC1 and partially inhibited mTORC2 activities, including the phosphorylation of Akt (serine 473) and PKCa, in vascular tumor cells. Rapamycin significantly reduced vascular tumor growth in vitro and in vivo. As a potential localized therapy for cutaneous vascular tumors, topically applied rapamycin effectively reduced tumor growth with limited systemic drug absorption. These findings reveal the importance of mTOR signaling pathways in benign and malignant vascular tumors. The mTOR pathway is an important therapeutic target in vascular tumors, and topical mTOR inhibitors may provide an alternative and well-tolerated therapy for the treatment of cutaneous vascular lesions.

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GLUT1: A newly discovered immunohistochemical marker for juvenile hemangiomas

Cited by 766 publications

References 41 publications

Evidence by molecular profiling for a placental origin of infantile hemangioma

Evidence by molecular profiling for a placental origin of infantile hemangioma

D2-40 immunohistochemical analysis of pediatric vascular tumors reveals positivity in kaposiform hemangioendothelioma

Vascular tumors have increased p70 S6-kinase activation and are inhibited by topical rapamycin

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