Uncommon Mutation, but Common Amplifications, of the<i>PIK3CA</i>Gene in Thyroid Tumors

Wu, Guojun; Mambo, Elizabeth; Guo, Zhen; Hu, Shuiying; Huang, Xin; Gollin, Susanne M.; Trink, Barry; Ladenson, Paul W.; Sidransky, David; Xing, Mingzhao

doi:10.1210/jc.2004-2281

Cited by 181 publications

(130 citation statements)

References 24 publications

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“…Interestingly, the authors also found one PIK3CA mutation out of 88 acute leukaemias (mutation rate ¼ 1.1%) that were analysed in this study, suggesting that PIK3CA mutations are not limited to solid tumours of epithelial origin. An analysis of PIK3CA somatic mutations and amplifications in thyroid cancers (Wu et al, 2005b) did not reveal any PIK3CA mutations; however, this group did find PIK3CA gene amplification in 12% of thyroid adenomas, 5% of papillary thyroid cancers, 24% of follicular thyroid cancers and 71% of thyroid cancer cell lines. More recently, there has been a report of somatic mutations in genes (i.e.…”

Section: Phosphatidylinositol 3-kinase and Human Cancermentioning

confidence: 78%

Mutation of the PIK3CA oncogene in human cancers

2006

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It is now well established that cancer is a genetic disease and that somatic mutations of oncogenes and tumour suppressor genes are the initiators of the carcinogenic process. The phosphatidylinositol 3-kinase signalling pathway has previously been implicated in tumorigenesis, and evidence over the past year suggests a pivotal role for the phosphatidylinositol 3-kinase catalytic subunit, PIK3CA, in human cancers. In this review, we analyse recent reports describing PIK3CA mutations in a variety of human malignancies, and discuss their possible implications for diagnosis and therapy.

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Section: Phosphatidylinositol 3-kinase and Human Cancermentioning

confidence: 78%

Mutation of the PIK3CA oncogene in human cancers

2006

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“…It was previously determined that mutations, or amplification and genomic copy gain of the PI3KCA gene, encoding the catalytic subunit of PI3K, occur in thyroid tumors [77][78][79]. Decreased expression or inactivation of the tumor suppressor gene product PTEN and activation by RAS oncogenes have also been described to activate the PI3K/Akt signaling pathway and play a role in thyroid tumorigenesis [78][79][80]. Combinations of some of these PI3K/Akt genetic alterations, as well as combinations of these alterations with BRAF mutation, were shown to be present in more aggressive thyroid tumors such as ATC [78].…”

Section: The Pi3k/akt Signaling Pathwaymentioning

confidence: 99%

“…Decreased expression or inactivation of the tumor suppressor gene product PTEN and activation by RAS oncogenes have also been described to activate the PI3K/Akt signaling pathway and play a role in thyroid tumorigenesis [78][79][80]. Combinations of some of these PI3K/Akt genetic alterations, as well as combinations of these alterations with BRAF mutation, were shown to be present in more aggressive thyroid tumors such as ATC [78]. Genetic alterations that activate both MAPK and PI3K/Akt pathways were shown to be present in most (81%) ATC cases.…”

Section: The Pi3k/akt Signaling Pathwaymentioning

confidence: 99%

An update on molecular biology of thyroid cancers

Ömür

Baran

2014

Critical Reviews in Oncology/Hematology

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“…According to the study by Hou et al (10) the PI3K/Akt pathway plays a significant role in thyroid tumorigenesis, particularly in FTC and the progression of PTC and FTC to ATC. However, mutations of the PIK3CA gene are not common, although the activation of the PI3K/Akt pathway may be due to the amplification of the PIK3CA gene in certain thyroid cancer patients (18). The activation of the PI3K̸Akt pathway may also be partially attributed to the promoter hypermethylation of phosphatase and tensin homolog (PTEN), which is a negative regulator of Akt (19).…”

Section: Development and Progression Of Thyroid Cancermentioning

confidence: 99%

Autophagy: A potential target for thyroid cancer therapy (Review)

Lü

et al. 2014

Molecular and Clinical Oncology

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Abstract. The sharply increasing incidence of thyroid cancer has attracted considerable attention over the last few years. The combination of surgery, radioiodine ablation and thyroid-stimulating hormone suppression is usually efficient for the majority of thyroid tumors. However, advanced thyroid cancer that is recurrent, metastatic and 131 I-refractory, or medullary thyroid cancer, pose a therapeutic challenge. Autophagy is a process that metabolizes damaged cytoplasmic organelles and long-lived proteins in order to recycle cellular materials and maintain homeostasis. It has been confirmed that autophagy plays a dual role during cancer development, progression and treatment, mainly depending on the type and stage of the tumor. Autophagy modulation has become a potential therapeutic target for diverse diseases. The mechanism of thyroid tumorigenesis and cancer progression was largely demonstrated to be correlated with the dysregulation of the Ras/Raf/mitogenactivated protein kinase kinase̸extracellular signal-regulated kinase and the phosphoinositide 3-kinase̸Akt̸mammalian target of rapamycin pathways, as well as with abnormal epigenetic modifications. Those mechanisms are associated with autophagy regulation and may be beneficial for the treatment of advanced thyroid cancer. However, the number of available studies on the role of autophagy in thyroid cancer development, progression and treatment outcome, is currently limited. The aim of this review was to elaborate on the relevant knowledge and future prospectives of autophagy in the treatment of thyroid cancer.

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Uncommon Mutation, but Common Amplifications, of thePIK3CAGene in Thyroid Tumors

Abstract: These data suggest that mutation of the PIK3CA gene is not common, but its amplification is relatively common and may be a novel mechanism in activating the PI3K/Akt pathway in some thyroid tumors.

Cited by 181 publications

References 24 publications

Mutation of the PIK3CA oncogene in human cancers

Mutation of the PIK3CA oncogene in human cancers

An update on molecular biology of thyroid cancers

Autophagy: A potential target for thyroid cancer therapy (Review)

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