Vincristine as a treatment for a large haemangioma threatening vital functions

Fawcett, S.; Grant, Iain; Hall, Per; Kelsall, AW; Nicholson, James C.

doi:10.1016/j.bjps.2003.11.003

Cited by 82 publications

(49 citation statements)

References 12 publications

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“…Surgical intervention is reserved for specific indications and, at this point, is largely up to the discretion of the treating physician. Other therapies, not discussed in detail, such as interferon-a, 91-95 vincristine, [96][97][98][99] cyclophosphamide, 100-103 topical imiquimod, [104][105][106][107][108] and the 1064-nm Nd:YAG laser, 109-111 among others, are currently reserved for life-threatening lesions or those unresponsive to conventional therapy ( Table 3). These therapies are mainly supported by case series and small reviews, and, until physicians see higher levels of evidence proving their efficacy and safety profiles, it will remain unclear whether or not they could serve additional roles in the treatment of IHs.…”

Section: Discussionmentioning

confidence: 99%

Evidence-Based Medicine in the Treatment of Infantile Hemangiomas

Keller

Patel

2015

Facial Plastic Surgery Clinics of North America

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Section: Discussionmentioning

confidence: 99%

Evidence-Based Medicine in the Treatment of Infantile Hemangiomas

Keller

Patel

2015

Facial Plastic Surgery Clinics of North America

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“…Almost 80% of hemangiomas are cutaneous lesions in the neck and head region and some can interfere with feeding, respiration, or vision and require therapeutic intervention. Current treatment options include corticosteroids (Boon et al 1999), a chemotherapeutic agent, vincristine (Enjolras et al 2004;Fawcett et al 2004), interferon α (Ezekowitz et al 1992), and propranolol (Ezekowitz et al 1992;Leaute-Labreze et al 2008), but these therapies are of variable success and are not based on a clear understanding of the mechanism of action.…”

Section: Introductionmentioning

confidence: 98%

Unexpected matrix diseases and novel therapeutic strategies

Nicolae

Olsen

2009

Cell Tissue Res

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Within the framework of a broad definition of the extracellular matrix (ECM), this review discusses three genetic disorders in which major pathogenetic features have been traced back to alterations in the levels/activities of matrix components. In each case, disease-associated alterations are found both intra- and extracellularly. The nature of the ECM involvement is surprising, offers an exciting therapeutic opportunity, and deepens our understanding of ECM-cell interactions. The first of these disorders, cherubism, is a case of inflammatory bone loss in the jaws of children for reasons that are surprisingly systemic in nature, considering the local nature of the disease. The primary defect involves an intracellular signaling molecule, but a major pathogenetic component and therapeutic target of the disease is the extracellular cytokine tumor necrosis factor alpha. The second disorder, Knobloch syndrome, is caused by recessive mutations in collagen XVIII. Although this protein has been classified as belonging to a group of structural macromolecules, the consequence of the mutations is impairment of cellular metabolism. The third disorder, infantile hemangioma, is a common tumor of capillary endothelial cells in infancy. The tumor appears within a few days/weeks after birth, grows rapidly over several months, and regresses over several years. The proliferative phase is the result of constitutively high levels of vascular endothelial cell growth factor (VEGF)-dependent signaling through VEGF receptor 2 (VEGFR2), but recent studies have led to the surprising conclusion that abnormalities in a cell-surface receptor complex controlling expression of the VEGF decoy receptor VEGFR1 is the underlying cause.

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“…Large hemangiomas can cause distortion or obstruction of vital structures and threaten life when located in the viscera. Therapy includes corticosteroid, interferon (7), vincristine (8), and, sometimes, surgical resection. However, these pharmacological treatments are not without side effects and complications (9)(10)(11).…”

Section: Introductionmentioning

confidence: 99%

Genomic Imprinting of IGF2 Is Maintained in Infantile Hemangioma despite its High Level of Expression

Yu¹,

Wylie-Sears²,

Boscolo³

et al. 2004

Mol Med

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Hemangioma, the most common tumor of infancy, is characterized by rapid growth and slow regression. Increased mRNA expression of insulin-like growth factor 2 (IGF2) has been detected in the proliferating phase by cDNA microarray analysis, but the underlying mechanism causing the increase remains unknown. Here, using quantitative real-time polymerase chain reaction (PCR) and immunohistochemistry, we show that IGF2 is highly expressed in both proliferating and involuting phase hemangioma, but is not detectable in other vascular lesions such as pyogenic granuloma, venous malformation, lymphatic malformation, or in normal infant skin. Loss of imprinting of the Igf2 gene has been associated with IGF2 overexpression in a variety of childhood tumors. To determine if loss of imprinting and consequent bi-allelic expression might contribute to the increased expression of IGF2, we examined the genomic imprinting status of Igf2 in 48 individual hemangiomas. We determined allele-specific Igf2 expression using reverse transcriptase-PCR combined with analysis of an Apa I-sensitive restriction fragment length polymorphism. Similar to heterozygous normal skin controls, all 15 informative hemangiomas showed uniform mono-allelic expression of Igf2. Therefore, loss of imprinting is not involved in the increased expression of IGF2 in infantile hemangioma.

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Vincristine as a treatment for a large haemangioma threatening vital functions

Cited by 82 publications

References 12 publications

Evidence-Based Medicine in the Treatment of Infantile Hemangiomas

Evidence-Based Medicine in the Treatment of Infantile Hemangiomas

Unexpected matrix diseases and novel therapeutic strategies

Genomic Imprinting of IGF2 Is Maintained in Infantile Hemangioma despite its High Level of Expression

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