Possibilities and potential roles of estrogen in the pathogenesis of proliferation hemangiomas formation

Sun, Zhuo; Yi, Chenggang; Zhao, Huan; Han, Dali; Wang, Lu; Nie, Chunlei; Zhang, Guoyou; Yin, Guowen; Wang, Gang; Teng, Xiao-Pin; Fei, Dong-Mei; Wang, Jin; Zhou, Wenkai; Yang, Li; Liu, Bin; Liu, Yin; Zhang, Manjing; Wu, Shang-Min; Zhang, Xi; Pan, Hua; Bo, Xiaochen; Zhao, Kai; Liu, Dan; Guo, Shuzhong

doi:10.1016/j.mehy.2008.02.015

Cited by 30 publications

(22 citation statements)

References 29 publications

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“…Juvenile hemangiomas are characterized by rapid development and involution [2]. Female hormones, in particular estradiol, have been proposed to be associated with their development [21, 22]. These hormones might affect expression of angiopoietin-2, jagged-1, notch-4, neuropilin-2, plexindomain containing receptor 1 and ephrin receptor B3 that are overexpressed in the proliferating phase of growth of juvenile hemangiomas [23].…”

Section: Skin As An Environmentally Regulated Organ - Implicationsmentioning

confidence: 99%

Cytochromes P450 and Skin Cancer: Role of Local Endocrine Pathways

Slominski¹,

Żmijewski²,

Semak³

et al. 2014

ACAMC

103

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Skin is the largest body organ forming a metabolically active barrier between external and internal environments. The metabolic barrier is composed of cytochromes P450 (CYPs) that regulate its homeostasis through activation or inactivation of biologically relevant molecules. In this review we focus our attention on local steroidogenic and secosteroidogenic systems in relation to skin cancer, e.g., prevention, attenuation of tumor progression and therapy. The local steroidogenic system is composed of locally expressed CYPs involved in local production of androgens, estrogens, gluco- and mineralo-corticosteroids from cholesterol (initiated by CYP11A1) or from steroid precursors delivered to the skin, and of their metabolism and/or inactivation. Cutaneous 7-hydroxylases (CYP7A1, CYP7B1 and CYP39) potentially can produce 7-hydroxy/oxy-steroids/sterols with modifying effects on local tumorigenesis. CYP11A1 also transforms 7-dehydrocholesterol (7DHC)→22(OH)7DHC→20,22(OH)2-7DHC→7-dehydropregnenolone, which can be further metabolized to other 5,7-steroidal dienes. These 5,7-dienal intermediates are converted by ultraviolet radiation B (UVB) into secosteroids which show pro-differentiation and anti-cancer properties. Finally, the skin is the site of activation of vitamin D3 through two alternative pathways. The classical one involves sequential hydroxylation at positions 25 and 1 to produce active 1,25(OH)2D3, which is further inactivated through hydroxylation at C24. The novel pathway is initiated by CYP11A1 with predominant production of 20(OH)D3 which is further metabolized to biologically active but non-calcemic D3-hydroxyderivatives. Classical and non-classical (novel) vitamin D analogs show pro-differentiation, anti-proliferative and anticancer properties. In addition, melatonin is metabolized by local CYPs. In conclusion cutaneously expressed CYPs have significant effects on skin physiology and pathology trough regulation of its chemical milieu.

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Section: Skin As An Environmentally Regulated Organ - Implicationsmentioning

confidence: 99%

Cytochromes P450 and Skin Cancer: Role of Local Endocrine Pathways

Slominski¹,

Żmijewski²,

Semak³

et al. 2014

ACAMC

103

View full text Add to dashboard Cite

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“…Other variations include the injection of estrogen into the mice to delay involution, 40 yet the role and contribution of estrogen to hemangiomas is poorly understood. 41,42 The most promising hemangioma has been reported from the laboratory of Dr Joyce Bischoff. These models use stem cells isolated from hemangiomas, which are then suspended in Matrigel and implanted into nude mice, and their subsequent growth is monitored.…”

Section: Lack Of An Animal Model To Study Hemangiomamentioning

confidence: 99%

A Potential Role for Notch Signaling in the Pathogenesis and Regulation of Hemangiomas

Wu¹,

Kitajewski²

2009

Journal of Craniofacial Surgery

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Hemangiomas are the most common benign tumor of infancy, yet its pathogenesis and the mechanisms governing proliferation and involution are not well understood. It is believed that hemangiomas arise out of clonal, abnormal hemangioma endothelial cells (HemECs). The underlying anomaly of the HemEC is not known, although studies have shown that vascular endothelial growth factor (VEGF) and VEGF signaling may influence HemECs. Moreover, there are numerous subtypes of hemangiomas, with differences in natural history, potential for morbidity, and prognosis, and little is known how this relates to HemEC. The Notch signaling pathway is a highly conserved pathway across species from worms to mammals. Notch signaling has been shown to play a role during embryogenesis in directing vascular patterning and development and arterial and venous cell fate determination. Postnatally, it has been implicated in tumor angiogenesis in multiple malignancies. Notch signaling triggers tumor angiogenesis at least in part to stimulation by VEGF, thus establishing that there is a cross talk between the VEGF and Notch pathways. Given the presence of VEGF and its receptors in hemangiomas and known VEGF-Notch cross talk in tumor angiogenesis, the authors hypothesize that Notch signaling may contribute to hemangioma proliferation and involution. Preliminary studies of resected hemangioma specimens by reverse transcription polymerase chain reaction (RT-PCR) show that all 4 Notch receptors and 2 Notch ligands, Jagged1 and Delta-like ligand 4, are expressed by hemangiomas. These findings support a role for Notch in hemangiomas, meriting further analysis of the functional relevance of Notch signaling in hemangiomas.

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“…Subsequently, increased levels of common molecular contributions to endothelial cell migration and new vessel development have been discovered during the proliferative phase of hemangioma growth such as vascular endothelial growth factor (VEGF), basic fibroblast growth factor (b‐FGF), insulin‐like growth factor (IGF), and matrix metalloprotease‐9 (MMP‐9) (Chang et al , 1999; Kleinman et al , 2007). Estrogen and hypoxia‐inducible factor also seem to play a critical role in regulating endothelial cell recruitment and proliferation in these lesions (Chang et al , 2007; Kleinman et al , 2007; Sun et al , 2008). Links to genetic errors in growth factor receptors such as FGFR4, PDGFRB, VEGFR2, and Flt‐4 are also evident in cases of familial hemangiomas (Chiller et al , 2003).…”

mentioning

confidence: 99%

Diagnosis and management of hemangiomas and vascular malformations of the head and neck

2010

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Vascular anomalies are congenital errors in vascular development. They frequently involve the head, neck, and oral cavity. Subdivided into vascular tumors (hemangiomas) and vascular malformations, vascular anomalies remain poorly understood. However, growing interest and recent advances in the diagnosis, management, and molecular characterization of these lesions are improving treatment strategies. The role of the multidisciplinary team cannot be overstated. This review provides both basic and up-to-date knowledge on the most common vascular anomalies encountered by physicians and practitioners. Because treatment options for vascular anomalies are widely variable and often debated, this report aims to provide a comprehensive approach to these lesions based upon current concepts and practical clinical experience.

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Possibilities and potential roles of estrogen in the pathogenesis of proliferation hemangiomas formation

Cited by 30 publications

References 29 publications

Cytochromes P450 and Skin Cancer: Role of Local Endocrine Pathways

Cytochromes P450 and Skin Cancer: Role of Local Endocrine Pathways

A Potential Role for Notch Signaling in the Pathogenesis and Regulation of Hemangiomas

Diagnosis and management of hemangiomas and vascular malformations of the head and neck

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