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Efficient immortalization of normal human mammary epithelial cells using two pathologically relevant agents does not require gross genomic alterations

ABSTRACT: Efficient immortalization of normal human mammary epithelial cells using two pathologically relevant agents does not require gross genomic alterations

PROVIDER: PRJNA210349 | ENA |

REPOSITORIES: ENA

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Efficient immortalization of normal human mammary epithelial cells using two pathologically relevant agents does not require gross genomic alterations

Project description:This SuperSeries is composed of the SubSeries listed below.

2013-07-03 | GSE48504 | GEO

Efficient immortalization of normal human mammary epithelial cells using two pathologically relevant agents does not require gross genomic alterations

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-07-03 | E-GEOD-48504 | biostudies-arrayexpress

MDAH-041 Spontaneous Immortalization

Project description:Gene expression at various stages of immortalization

2016-05-12 | GSE46931 | GEO

Immortalization capacity of HPV types is inversely related to chromosomal instability in immortal descendants.

Project description:Human papillomavirus (HPV) induced immortalization of human foreskin keratinocytes (HFK) is a two-step process, including 1) the bypass of replicative senescence and acquisition of an extended lifespan, and 2) the outgrowth of immortal cells. Our previous study showed that the immortalization capacity of HPV is type dependent, as reflected by the presence or absence of a crisis period before reaching immortality. In the present study we determined how the HPV-type specific immortalization capacity relates to DNA damage induction and overall genomic instability. Early passage HFKs transduced with HPV types 16, 18, 31, 33, 35, 45, 51, 59, 66 and 70 showed an increased number of double strand DNA breaks compared to controls, without significant differences between the various HPV-types. However, immortal descendants of HPV-transduced HFKs that underwent a crisis period (HPV45-, 51-, 59-, 66- and 70-transduced HFKs) showed significantly more chromosomal aberrations compared to those without a crisis period (HPV16-, 18-, 31-, and 35-transduced HFKs) (p<0.01). In particular, regions on chromosome 5p, 8, and 9q were significantly more frequently altered in cells with crisis. Interestingly, the hTERT locus at 5p was exclusively gained in cell lines with crisis. Chromothripsis was detected in one of the HPV16-immortalized cell lines in which multiple rearrangements within chromosome 8 resulted in a gain of c-MYC. In conclusion, the present study shows that upon HPV-induced immortalization, the number of chromosomal aberrations is inversely related to the immortalization capacity of the virus type. This suggests that hrHPV types with reduced immortalization capacity in vitro, as reflected by a crisis period, require more genetic host cell aberrations to trigger immortalization. DNA copy number analysis of human keratinocytes transformed by high-risk HPV

2016-08-01 | E-GEOD-72063 | biostudies-arrayexpress

Immortalization capacity of HPV types is inversely related to chromosomal instability in immortal descendants.

2016-08-01 | GSE72063 | GEO

Solanum lycopersicum strain:Gross lisse

Project description:Solanum lycopersicum strain:Gross lisse Genome sequencing

| PRJNA240261 | ENA

Immortalization of normal human mammary epithelial cells in two steps by direct targeting of senescence barriers does not require gross genomic alterations.

Project description:Telomerase reactivation and immortalization are critical for human carcinoma progression. However, little is known about the mechanisms controlling this crucial step, due in part to the paucity of experimentally tractable model systems that can examine human epithelial cell immortalization as it might occur in vivo. We achieved efficient non-clonal immortalization of normal human mammary epithelial cells (HMEC) by directly targeting the 2 main senescence barriers encountered by cultured HMEC. The stress-associated stasis barrier was bypassed using shRNA to p16(INK4); replicative senescence due to critically shortened telomeres was bypassed in post-stasis HMEC by c-MYC transduction. Thus, 2 pathologically relevant oncogenic agents are sufficient to immortally transform normal HMEC. The resultant non-clonal immortalized lines exhibited normal karyotypes. Most human carcinomas contain genomically unstable cells, with widespread instability first observed in vivo in pre-malignant stages; in vitro, instability is seen as finite cells with critically shortened telomeres approach replicative senescence. Our results support our hypotheses that: (1) telomere-dysfunction induced genomic instability in pre-malignant finite cells may generate the errors required for telomerase reactivation and immortalization, as well as many additional "passenger" errors carried forward into resulting carcinomas; (2) genomic instability during cancer progression is needed to generate errors that overcome tumor suppressive barriers, but not required per se; bypassing the senescence barriers by direct targeting eliminated a need for genomic errors to generate immortalization. Achieving efficient HMEC immortalization, in the absence of "passenger" genomic errors, should facilitate examination of telomerase regulation during human carcinoma progression, and exploration of agents that could prevent immortalization.

| S-EPMC4613853 | biostudies-literature

Analysis of Gross Chromosomal Rearrangements in Budding Yeast

Project description:Determine changes in genomic copy across the entire genome for isolated strains with selected gross chromosomal rearrangements relative to the wild-type strain.

2014-03-15 | E-MTAB-2377 | biostudies-arrayexpress

Ploidy influences the cellular responses of gross chromosomal rearrangements in Saccharomyces cerevisiae

Project description:We investigated the effects of the ploidy on cellular response in strains carrying various types of gross chromosomal rearrangements.

2011-06-17 | GSE28285 | GEO

Matrix reverses immortalization-mediated stem cell fate determination

Project description:Matrix reverses immortalization-mediated stem cell fate determination

| PRJNA625241 | ENA