Ovarian and endometrial endometrioid carcinomas have distinct CTNNB1 and PTEN mutation profiles

McConechy, Melissa K.; Ding, Jiarui; Senz, Janine; Yang, Winnie; Melnyk, Nataliya; Tone, Alicia A.; Prentice, Leah M; Wiegand, Kimberly C.; McAlpine, Jessica N.; Shah, Sohrab P.; Lee, Cheng‐Han; Goodfellow, Paul J.; Gilks, C Blake; Huntsman, David G.

doi:10.1038/modpathol.2013.107

Cited by 227 publications

(161 citation statements)

References 48 publications

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“…96 In ovarian endometrioid carcinoma, ARID1A was mutated in 80% (4/5) of ovarian endometrioid carcinoma with PTEN mutation but in only 20% (5/25) of samples without PTEN mutation (P = 0.0195). 97 In addition to gynecologic cancers, ARID1A mutations were also significantly associated with PIK3CA-activating mutations in gastric carcinomas. 45 Viewing the totality of the evidence, it is likely that loss of ARID1A function and dysregulation of the PI3K/Akt signaling pathway have a synergistic effect on tumor development.…”

Section: Collaboration Between Arid1a Mutation and Pi3k/akt Pathway Amentioning

confidence: 99%

The emerging roles of ARID1A in tumor suppression

Wang

Shih

2014

Cancer Biology & Therapy

218

187

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Section: Collaboration Between Arid1a Mutation and Pi3k/akt Pathway Amentioning

confidence: 99%

The emerging roles of ARID1A in tumor suppression

Wang

Shih

2014

Cancer Biology & Therapy

218

187

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“…KRAS mutation is 0% to 5% in non-endometrioid endometrial cancers. [46][47][48][49][50][51][52][53][54][55][56] The frequency of KRAS mutations in cervical cancer ranges between 5% and 14%. In the United States, the frequency of KRAS mutation is 8.8% in patients with cervical cancer.…”

Section: Frequency Of Ras Mutation In Genitourinary Cancermentioning

confidence: 99%

Frequency of RAS Mutations (KRAS, NRAS, HRAS) in Human Solid Cancer

Kodaz

2017

EJMO

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T he RAS oncogene affects numerous cellular functions, including growth, proliferation, apoptosis, migration, division, and differentiation of the cells. It has 3 known isoforms: Harvey-RAS (HRAS), Kirsten-RAS (KRAS), and neuroblastoma-RAS (NRAS). RAS has an intrinsic GTPase activity; it encodes proteins binding the guanine nucleotides. KRAS and HRAS were discovered in studies conducted on cancer-causing viruses. Retroviral oncogenes related to murine sarcoma virus genes (Kristen rat sarcoma virus and Harvey rat sarcoma virus) were discovered in 1982. These 2 oncogenes are similar to human KRAS. Approximately 30% of all human cancers have RAS gene involvement. Mutations in KRAS account for about 85% of all RAS mutations in human tumors, NRAS for about 11% to 15%, and HRAS for about 1%. Frequency of RAS mutation in intracranial tumorsGliomas constitute 80% of malignant brain tumors. RAS mutations are very rare in malignant gliomas; no RAS mutation was found in a study in which 30 glioblastoma multiforme (GBM) patients were evaluated. The frequency of NRAS mutation was 2.1% in another study, although KRAS and HRAS mutations were not detected. It was reported that RAS mutation frequency was 12% in a study of isocitrate-dehydrogenase 1-mutant malignant glioma. RAS genes were studied in 21 cases of glioblastoma multiforme, 4 cases of fibrillary astrocytoma, 4 cases of anaplastic astrocytoma, and 15 normal specimens. RAS mutation was de-RAS oncogene affects numerous cellular functions including growth, proliferation, apoptosis, migration, division and differentiation of the cells. It has 3 known isoforms as Harvey-RAS (HRAS), Kirsten -RAS (KRAS) and Neuroblastoma-RAS (NRAS). RAS has an intrinsic GTPase activity. It encodes proteins binding the guanine nucleotides. KRAS and HRAS were discovered in studies carried out on viruses leading to cancer. Retroviral oncogenes related to murine sarcoma virus genes (Kristen Rat Sarcoma Virus and Murine Sarcoma Virus) were discovered in 1982. These two oncogenes are similar to human KRAS. Approximately 30% of all human cancers have ras genes. Mutations in KRAS account for about 85% for all RAS mutations in human tumors, NRAS is about 11-15%, and HRAS is about 1%.

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“…PTEN locates on chromosome 10q23, which is highly susceptible to mutation in human cancers. Mutation or loss of function of PTEN is frequent in a wide range of cancers including glioblastoma multiforme (9), gastric cancer (10), endometrial cancer (11,12), ovarian cancer (12) and lung cancer (13). PTEN can decrease the synthesis of IGF-I, -II and IGF-1R, which in turn generates an autocrine loop to downregulate Akt activation (14,15).…”

Section: Introductionmentioning

confidence: 99%

The phosphatidylinositol 3-kinase/Akt and c-Jun N-terminal kinase signaling in cancer: Alliance or contradiction? (Review)

Zhao

Wang

2015

International Journal of Oncology

102

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Abstract. The phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway and c-Jun N-terminal kinase (JNK) pathway are responsible for regulating a variety of cellular processes including cell growth, migration, invasion and apoptosis. These two pathways are essential to the development and progression of tumors. The dual roles of JNK signaling in apoptosis and tumor development determine the different interactions between the PI3K/Akt and JNK pathways. Activation of PI3K/ Akt signaling can inhibit stress-and cytokine-induced JNK activation through Akt antagonizing and the formation of the JIP1-JNK module, as well as the activities of upstream kinases ASK1, MKK4/7 and MLK. On the other hand, hyperactivation of Akt and JNK is also found in cancers that harbor EGFR overexpression or loss of PTEN. Understanding the activation mechanism of PI3K/Akt and JNK pathways, as well as the interplays between these two pathways in cancer may contribute to the identification of novel therapeutic targets. In the present report, we summarized the current understanding of the PI3K/Akt and JNK signaling networks, as well as their biological roles in cancers. In addition, the interactions and regulatory network between PI3K/Akt and JNK pathways in cancer were discussed.

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Ovarian and endometrial endometrioid carcinomas have distinct CTNNB1 and PTEN mutation profiles

Cited by 227 publications

References 48 publications

The emerging roles of ARID1A in tumor suppression

The emerging roles of ARID1A in tumor suppression

Frequency of RAS Mutations (KRAS, NRAS, HRAS) in Human Solid Cancer

The phosphatidylinositol 3-kinase/Akt and c-Jun N-terminal kinase signaling in cancer: Alliance or contradiction? (Review)

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