Minimum regions of genomic imbalance in stage I testicular embryonal carcinoma and association of 22q loss with relapse

Gilbert, Duncan C.; McIntyre, Alan; Summersgill, Brenda; Missiaglia, Edoardo; Goddard, N. C.; Chandler, Ian; Huddart, Robert; Shipley, Janet

doi:10.1002/gcc.20843

Cited by 22 publications

(31 citation statements)

References 43 publications

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“…KRAS activates both the MAP kinase pathway as well as the PI3K/AKT pathway to control cell proliferation and survival [72]. The PI3K/AKT is a key signalling pathway promoting cell proliferation, survival and migration which is subject to modulation by several negative regulators such as PTEN and PI3kip1 [73], [74]. Importantly, the ablation of PTEN is associated with the transformation of CIS cells, the precursor lesion for seminoma and nonseminoma into invasive cancer [73].…”

Section: Discussionmentioning

confidence: 99%

A Unique Combination of Male Germ Cell miRNAs Coordinates Gonocyte Differentiation

McIver¹,

Stanger²,

Santarelli

et al. 2012

PLoS ONE

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The last 100 years have seen a concerning decline in male reproductive health associated with decreased sperm production, sperm function and male fertility. Concomitantly, the incidence of defects in reproductive development, such as undescended testes, hypospadias and testicular cancer has increased. Indeed testicular cancer is now recognised as the most common malignancy in young men. Such cancers develop from the pre-invasive lesion Carcinoma in Situ (CIS), a dysfunctional precursor germ cell or gonocyte which has failed to successfully differentiate into a spermatogonium. It is therefore essential to understand the cellular transition from gonocytes to spermatogonia, in order to gain a better understanding of the aetiology of testicular germ cell tumours. MicroRNA (miRNA) are important regulators of gene expression in differentiation and development and thus highly likely to play a role in the differentiation of gonocytes. In this study we have examined the miRNA profiles of highly enriched populations of gonocytes and spermatogonia, using microarray technology. We identified seven differentially expressed miRNAs between gonocytes and spermatogonia (down-regulated: miR-293, 291a-5p, 290-5p and 294*, up-regulated: miR-136, 743a and 463*). Target prediction software identified many potential targets of several differentially expressed miRNA implicated in germ cell development, including members of the PTEN, and Wnt signalling pathways. These targets converge on the key downstream cell cycle regulator Cyclin D1, indicating that a unique combination of male germ cell miRNAs coordinate the differentiation and maintenance of pluripotency in germ cells.

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Section: Discussionmentioning

confidence: 99%

A Unique Combination of Male Germ Cell miRNAs Coordinates Gonocyte Differentiation

McIver¹,

Stanger²,

Santarelli

et al. 2012

PLoS ONE

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“…During progression, TGCCs are thought to acquire heterogeneous chromosomal gains and losses ending up in a near triploid state. A consistent causative relation of these copy number variations to disease (progression) has not been determined so far [107][108][109][110][111][112][113][114][115][116]. Most markedly, gain of predominantly the whole short arm of chromosome 12 (12p) is specific to invasive GCCs.…”

Section: Malignant Transformation Of Pgcs/gonocytesmentioning

confidence: 99%

An oncofetal and developmental perspective on testicular germ cell cancer

Rijlaarsdam

Looijenga

2014

Seminars in Cancer Biology

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“…For example, the tumor initiating cells of myelodysplastic syndrome (MDS), which can develop into acute myeloid leukemia (AML), are cancer stem cells, at least those with genetic deletion of chromosome 5q [4] . Cancer stem and progenitor cells have been suggested to involve with relapse in many types of cancers [5][6][7][8][9][10][11][12][13] . This tumorigenic recurrence of cancer stem and progenitor cells, which often associates with more aggressive phenotypes compared with differentiated cancer cells, can occur via accumulation of genetic mutations and/or epigenetic defects leading to selective advantage and hence the oncogenic evolution of cancer stem and progenitor cells.…”

Section: Introductionmentioning

confidence: 99%

Epigenetic therapy of cancer stem and progenitor cells by targeting DNA methylation machineries

Wongtrakoongate

2015

WJSC

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Recent advances in stem cell biology have shed light on how normal stem and progenitor cells can evolve to acquire malignant characteristics during tumorigenesis. The cancer counterparts of normal stem and progenitor cells might be occurred through alterations of stem cell fates including an increase in self-renewal capability and a decrease in differentiation and/or apoptosis. This oncogenic evolution of cancer stem and progenitor cells, which often associates with aggressive phenotypes of the tumorigenic cells, is controlled in part by dysregulated epigenetic mechanisms including aberrant DNA methylation leading to abnormal epigenetic memory. Epigenetic therapy by targeting DNA methyltransferases (DNMT) 1, DNMT3Aand DNMT3B via 5-Azacytidine (Aza) and 5-Aza-2'-deoxycytidine (Aza-dC) has proved to be successful toward treatment of hematologic neoplasms especially for patients with myelodysplastic syndrome. In this review, I summarize the current knowledge of mechanisms underlying the inhibition of DNA methylation by Aza and Aza-dC, and of their apoptotic-and differentiation-inducing effects on cancer stem and progenitor cells in leukemia, medulloblastoma, glioblastoma, neuroblastoma, prostate cancer, pancreatic cancer and testicular germ cell tumors. Since cancer stem and progenitor cells are implicated in cancer aggressiveness such as tumor formation, progression, metastasis and recurrence, I propose that effective therapeutic strategies might be achieved through eradication of cancer stem and progenitor cells by targeting the DNA methylation machineries to interfere their "malignant memory". Core tip: Several types of cancers can be developed from genetic and/or epigenetic instabilities of stem and progenitor cells. Epigenetic abnormality involving dysregulation of DNA methylation has been reported to implicate in cancer aggressiveness. Inhibition of DNA methyltransferase activity by DNA methylation inhibitors has shown promising results toward treatment of myelodysplastic syndrome, a disease associated with leukemic stem cells. This review summarizes evidences which are pertinent to the antitumorigenic potential of DNA methylation inhibitors 5-Azacytidine and 5-Aza-2'-deoxycytidine on cancer stem and progenitor cells including those of leukemia and other solid tumors.Wongtrakoongate P. Epigenetic therapy of cancer stem and REVIEWSubmit a

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Minimum regions of genomic imbalance in stage I testicular embryonal carcinoma and association of 22q loss with relapse

Cited by 22 publications

References 43 publications

A Unique Combination of Male Germ Cell miRNAs Coordinates Gonocyte Differentiation

A Unique Combination of Male Germ Cell miRNAs Coordinates Gonocyte Differentiation

An oncofetal and developmental perspective on testicular germ cell cancer

Epigenetic therapy of cancer stem and progenitor cells by targeting DNA methylation machineries

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