Yazar "Grossman, Ashley B." seçeneğine göre listele

Listeleniyor 1 - 2 / 2
  • Küçük Resim Yok
    Öğe
    Medullary Thyroid Cancer: Molecular Biology and Novel Molecular Therapies
    (KARGER, 2009) Cakir, Mehtap; Grossman, Ashley B.
    Medullary thyroid cancer (MTC) arises from neural-crest-derived parafollicular C cells of the thyroid gland and accounts for approximately 4% of all thyroid cancers. Up to 25-30% of MTC cases occur as inherited disorders while the remaining cases represent the sporadic form of the disease. In this review, the structure and signalling properties of the RET protooncogene in its wild-type and mutant forms, and its role in hereditary and sporadic MTC, are discussed. A full data search was performed through PubMed over the years 2000-2008 with the key words 'medullary thyroid cancer, treatment, molecular biology, RET, molecular mechanism', and all relevant publications have been included, together with selected publications prior to that date. We also review novel therapies for metastatic MTC, especially the tyrosine kinase inhibitors which have activity at multiple receptor subtypes, and summarize the current ongoing trials in this area. While such tyrosine kinase inhibitors, particularly those affecting RET activity such as vandetanib, sorafenib and sunitinib, are promising, the low rate of partial responses and absence of complete responses in all of the various trials of monotherapy emphasize the need for new and more effective single agents or combinations of therapeutic agents with acceptable toxicity. Copyright (C) 2009 S. Karger AG, Basel
  • Küçük Resim Yok
    Öğe
    Targeting MAPK (Ras/ERK) and PI3K/Akt pathways in pituitary tumorigenesis
    (TAYLOR & FRANCIS LTD, 2009) Cakir, Mehtap; Grossman, Ashley B.
    Background: Pituitary adenomas are common intracranial neoplasms, comprising 10 - 15% of all brain tumors. Data from autopsy studies suggest that pituitary adenomas develop in 17 - 25% of the population. Nevertheless, the pathogenesis of sporadic pituitary tumors still remains obscure. Objective: In this review, the roles of MAPK (mainly Ras/extracellular signal-regulated protein kinase (ERK)) and PI3K/Akt signaling pathways in pituitary tumorigenesis are summarised. Methods: A full data search was performed through PubMed over the years 2000 - 2009 with key words I pituitary, pituitary tumor, molecular biology, Akt, MAPK, PI3K, ERK', and all relevant publications have been included, together with selected publications prior to that date. Growth factor receptor mutations and overexpression, G protein mutations, other signaling pathway abnormalities or genetic syndromes associated with pituitary tumors are not discussed as these topics are behind the scope of this review. Conclusions: There are preclinical data and human pituitary tumor studies that are compatible with increased Ras/ERK and/or PI3K/Akt pathway activity in pituitary tumors. Future research focusing on scaffold proteins and signaling modulators regulating these pathways may help identify the initiating transforming events and accordingly new strategies may be developed targeting these pathways in pituitary tumors.