The stem cell markers Oct4A, Nanog and c-Myc are expressed in ascites cells and tumor tissue of ovarian cancer patients

Di, Jiabo; Boer, Tjitske Duiveman-de; Zusterzeel, Petra L.M.; Figdor, Carl G.; Massuger, Leon F.A.G.; Torensma, Ruurd

doi:10.1007/s13402-013-0142-8

Cited by 53 publications

(38 citation statements)

References 58 publications

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“…This leads to the unregulated increased expression of various genes promoting cancer formation. Furthermore, Myc has been identified as an essential factor driving the production of pluripotent stem cells and has been linked with putative ovarian CSC factors including Oct4 and Nanog 71, 72 . Recently, the microRNA let-7a was demonstrated to negatively regulate Myc resulting in cell growth/ proliferation inhibition in lymphoma cells 73 .…”

Section: Cancer Stem Cells and Micrornasmentioning

confidence: 99%

Epithelial-to-mesenchymal transition and the cancer stem cell phenotype: insights from cancer biology with therapeutic implications for colorectal cancer

et al. 2014

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Although mortality from colorectal cancer (CRC) is decreasing, colorectal cancer is still the second highest cause of cancer related deaths in America. Chemotherapy and radiation therapy now play central roles in our strategies to fight cancer, although we continue to lack novel strategies overcoming therapeutic resistance. Molecular mechanisms of therapeutic resistance in CRC continue to be under intense investigation. In this review, we highlight the recent evidence linking epithelial-to-mesenchymal transition (EMT) with aggressive tumor biology as well as with the cancer stem cells (CSC) across multiple organ systems including colon cancer. Furthermore, in the era of neo-adjuvant treatment, the clinical implications are concerning that our treatments may have the potential to induce more aggressive cancer cells through EMT, perhaps even generating CSCs more capable of metastasis and further resistant to treatment. This concern and potential reality highlights the critical need for further understanding the impact of clinical therapy on the pathobiology of cancer and further supports the need to therapeutically target the CSC. Besides serving as potential biomarkers for aggressive tumor biology and therapeutic resistance, EMT and CSC molecular pathways may highlight novel therapeutic targets as strategies for improving the response to conventional anti-neoplastic agents translating into improved oncologic outcomes.

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Section: Cancer Stem Cells and Micrornasmentioning

confidence: 99%

Epithelial-to-mesenchymal transition and the cancer stem cell phenotype: insights from cancer biology with therapeutic implications for colorectal cancer

et al. 2014

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“…Recently, the c-myc gene was reported to be amplified in patients with early-stage ovarian cancer, which was associated with prognosis (Di et al, 2013). In this study, c-myc was highly expressed in ovarian borderline mucinous cystadenoma and ovarian mucinous cystadenoma, and the positive expression rates increased in the order of ovarian mucinous cystadenoma, borderline mucinous cystadenoma, and mucinous cystadenoma; the values showed statistically significant differences (P < 0.05).…”

Section: Discussionmentioning

confidence: 55%

Expression of c-myc and mutation of the KRAS gene in patients with ovarian mucinous tumors

Li¹,

Sun²,

He³

2015

Genet. Mol. Res.

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ABSTRACT. We examined the expression of c-myc and mutations in the KRAS gene in ovarian mucinous tumors to explore the pathogenesis of these tumors and the feasibility of targeted gene therapy. Expression of c-myc protein and mutations in the KRAS gene in 24 cases of ovarian mucinous cystadenoma, 46 cases of ovarian borderline mucinous cystadenoma, and 46 cases of ovarian mucinous cystadenocarcinoma were detected using the immunohistochemistry PV-9000 2-step method and polymerase chain reaction-restriction fragment length polymorphism. The positive expression rates of c-myc in ovarian mucinous cystadenoma, borderline mucinous cystadenoma, and cystadenocarcinoma were 0, 39.1, and 65.2%, respectively (P < 0.01), while the mutation rates in KRAS were 0, 39.1 and 13.0%, respectively. The mutation rate of the borderline group was significantly higher, while rates in the other 2 groups were similar (P > 0.05). c-myc was not correlated with clinical stage, pathological grade, or age of patients with ovarian mucinous cystadenocarcinoma or borderline mucinous cystadenoma (P > 0.05), but was correlated with tumor size (P < 0.05). Mutations in KRAS were not correlated with clinical stage or tumor size in patients with borderline mucinous cystadenoma (P > 0.05), whereas it 10753 c-myc expression and KRAS mutation ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (3): 10752-10759 (2015) was correlated with age (P < 0.05). In borderline mucinous cystadenoma, c-myc expression and KRAS mutations were not correlated (P > 0.05). c-myc is involved in the formation of ovarian borderline mucinous cystadenoma and mucinous cystadenocarcinoma, and the KRAS gene may contribute to the formation of borderline mucinous cystadenoma.

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“…Disialogangliosidase GD2 is expressed by Rb cells that metastasize to the BM and the expression level of GD2 synthase, the essential enzyme for its synthesis, has been found to be increased in Rb cells [59]. CD44 is the main receptor of hyaluronan (HA), a component of the extracellular matrix that is frequently over-expressed in cancer stem cells (CSCs) [60]. It is involved in the metastatic spread of several cancers including carcinomas, myelomas and sarcomas [61].…”

Section: Retinoblastoma Cell Homing In the Bone Marrowmentioning

confidence: 99%

The bone marrow metastasis niche in retinoblastoma

et al. 2015

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The stem cell markers Oct4A, Nanog and c-Myc are expressed in ascites cells and tumor tissue of ovarian cancer patients

Abstract: The expression of stem cell genes was detected in a small proportion of tumor cells present in ascites as well as in tumor tissue. IL-6 plays an important role in the induction of c-Myc.

Cited by 53 publications

References 58 publications

Epithelial-to-mesenchymal transition and the cancer stem cell phenotype: insights from cancer biology with therapeutic implications for colorectal cancer

Epithelial-to-mesenchymal transition and the cancer stem cell phenotype: insights from cancer biology with therapeutic implications for colorectal cancer

Expression of c-myc and mutation of the KRAS gene in patients with ovarian mucinous tumors

The bone marrow metastasis niche in retinoblastoma

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