Insulin-like growth factor 2 and its receptors (IGF 1R and IGF 2R/mannose 6-phosphate) in endometrial adenocarcinoma

Pavelić, Jasminka; Radaković, Branko; Pavelić, Krešimir

doi:10.1016/j.ygyno.2007.02.012

Cited by 53 publications

(47 citation statements)

References 41 publications

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“…Overexpression of insulin receptor (IR) or IGF1 receptor (IGF1R) induces endometrial hyperplasia and promotes EEC cell growth through activation of PI3K/Akt/mTOR signaling (McCampbell et al 2006). IGF1R and IGF2 levels were much higher in advanced stage (stages III-IV) malignant tissue as compared to stages I-II or endometrial hyperplasia (Pavelic et al 2007). Elevated levels of circulating insulin and endometrial IGF1 were found to increase the aggressiveness of EC (Gunter et al 2008).…”

Section: Cell Signaling Pathwaysmentioning

confidence: 99%

Tumor progression, metastasis, and modulators of epithelial–mesenchymal transition in endometrioid endometrial carcinoma: an update

Makker

Goel

2015

Endocrine-Related Cancer

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Endometrioid endometrial carcinoma (EEC), also known as type 1 endometrial cancer (EC), accounts for over 70-80% of all cases that are usually associated with estrogen stimulation and often develops in a background of atypical endometrial hyperplasia. The increased incidence of EC is mainly confined to this type of cancer. Most EEC patients present at an early stage and generally have a favorable prognosis; however, up to 30% of EEC present as high risk tumors, which have invaded deep into the myometrium at diagnosis and progressively lead to local or extra pelvic metastasis. The poor survival of advanced EC is related to the lack of effective therapies, which can be attributed to poor understanding of the molecular mechanisms underlying the progression of disease toward invasion and metastasis. Multiple lines of evidence illustrate that epithelial-mesenchymal transition (EMT)-like events are central to tumor progression and malignant transformation, endowing the incipient cancer cell with invasive and metastatic properties. The aim of this review is to summarize the current knowledge on molecular events associated with EMT in progression, invasion, and metastasis of EEC. Further, the role of epigenetic modifications and microRNA regulation, tumor microenvironment, and microcystic elongated and fragmented glands like invasion pattern have been discussed. We believe this article may perhaps stimulate further research in this field that may aid in identifying high risk patients within this clinically challenging patient group and also lead to the recognition of novel targets for the prevention of metastasis -the most fatal consequence of endometrial carcinogenesis.

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Section: Cell Signaling Pathwaysmentioning

confidence: 99%

Tumor progression, metastasis, and modulators of epithelial–mesenchymal transition in endometrioid endometrial carcinoma: an update

Makker

Goel

2015

Endocrine-Related Cancer

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“…Our local data showed low expression of IGF2 in endometrioid endometrial cancer compared with normal endometrium (82). Low expression of IGF2 was corresponds to an early stage of endometrial cancer (83). All reported results from these expression profiling studies have concluded that different histologic types of endometrial cancer displayed different expression profiles.…”

Section: Gene Expression Profiling In Endometrial Cancermentioning

confidence: 49%

Genomic Expression Profiles: From Molecular Signatures to Clinical Oncology Translation

Mokhtar¹,

Murad²,

Then³

et al. 2013

Oncogenomics and Cancer Proteomics - Novel Approaches in Biomarkers Discovery and Therapeutic Targets in Cancer

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“…These authors suggested that estrogen-dependent activation of the IGF-1 autocrine loop may result in tumor growth by stimulating the process of neoangiogenesis [22]. The presence of IGF-1R receptors were demonstrated both, in EC tissues and healthy endometrium (Table 2) [20,23,24]. Regardless, statistically significantly higher receptor binding affinity was found in EC tissues as compared to healthy endometrium.…”

Section: Hypothetical Role Of Igf-1 In the Biology Of Endometrial Cancermentioning

confidence: 97%

“…On further analysis, these authors detected both, overexpression and lowered mRNA IGF-1 expression (39% ing proliferation of tumor cells and stimulating the process of neo-angiogenesis (Table 1) [12][13][14][15]. However, the results of in vivo studies are not as unambiguous (Table 2) [16][17][18][19][20][21].…”

Section: Hypothetical Role Of Igf-1 In the Biology Of Endometrial Cancermentioning

confidence: 99%

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Does IGF-1 play a role in the biology of endometrial cancer?

Majchrzak-Baczmańska

Malinowski

2016

Ginekol Pol

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Insulin-like growth factor 1 (IGF-1) is a mitogen which plays a key role in regulating cell proliferation, differentiation, and apoptosis. It belongs to the family of proteins also composed of insulin-like growth factor 2 (IGF-2), two types of membrane receptors (IGF-1R and IGF-2R), 6 binding proteins (IGFBP 1-6), hydrolyzing proteases, and reactive molecules binding proteins, which regulate the activity of growth factors. Disturbances in the functioning of IGFBP/IGF/1GF1R can lead to induction of carcinogenesis, which has been demonstrated in breast, prostate or colon cancers. Findings evaluating the role of IGF-1 in endometrial cancer biology are ambiguous and contradictory. Therefore, in the present study, we analyzed the role of IGF-1 in the process of carcinogenesis of endometrial cancer, based on the available literature.

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Insulin-like growth factor 2 and its receptors (IGF 1R and IGF 2R/mannose 6-phosphate) in endometrial adenocarcinoma

Cited by 53 publications

References 41 publications

Tumor progression, metastasis, and modulators of epithelial–mesenchymal transition in endometrioid endometrial carcinoma: an update

Tumor progression, metastasis, and modulators of epithelial–mesenchymal transition in endometrioid endometrial carcinoma: an update

Genomic Expression Profiles: From Molecular Signatures to Clinical Oncology Translation

Does IGF-1 play a role in the biology of endometrial cancer?

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