Characterization of a New Human Diploid Cell Strain, IMR-90

Nichols, Warren W.; Murphy, Donald G.; Cristofalo, Vincent J.; Toji, Lorraine; Greene, A.E.; Dwight, Selena

doi:10.1126/science.841339

Cited by 354 publications

(140 citation statements)

References 14 publications

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“…IMR-90 human diploid lung ®broblasts (catalog #I90-P04) (Nichols et al, 1977) were obtained from the National Institute on Aging Cell Repository (Camden, NJ). Cells were grown in Dulbecco's modi®ed Eagle medium (Gibco BRL, Gaithersburg, MD) containing 10% iron-supplemented calf serum (Hyclone, Logan, UT) and 3.5 mM glutamine in a humidi®ed 5% CO 2 atmosphere at 378C.…”

Section: Cell Culturementioning

confidence: 99%

Disregulation of mitotic checkpoints and regulatory proteins following acute expression of SV40 large T antigen in diploid human cells

Chang

Ray

et al. 1997

Oncogene

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SV40 large T antigen (T) inactivates the tumor suppressor proteins p53 and pRb, and can induce cells to enter DNA replication at inappropriate times. We show here that T also compromises three cell cycle checkpoints that regulate the entry into and exit from mitosis. Human diploid ®broblasts infected with a retrovirus expressing T displayed an attenuated radiation-induced mitotic delay, were more susceptible to chemical-induced uncoupling of mitosis from the completion of DNA replication, and were more likely to exit mitosis and rereplicate their DNA when mitotic spindle assembly was inhibited. Consistent with altered mitotic checkpoint control, cells expressing T displayed elevated protein levels and/or associated activities of the mitotic regulatory proteins cyclin A, cyclin B, Cdc25C and p34 cdc2 . These changes in mitotic control were evident within 5 ± 10 population doublings after retroviral infection, indicating a direct e ect of T expression. Cells acutely infected with the T-expressing retrovirus su ered numerical and structural chromosome aberrations, including increases in aneuploidy, dicentric chromosomes, chromatid exchanges and chromosome breaks and gaps. These ®ndings indicate that T rapidly disrupts mitotic checkpoints that help maintain genomic stability, and suggest mechanisms by which T induces chromosome aberrations and promotes the immortalization and neoplastic transformation of human cells.

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Section: Cell Culturementioning

confidence: 99%

Disregulation of mitotic checkpoints and regulatory proteins following acute expression of SV40 large T antigen in diploid human cells

Chang

Ray

et al. 1997

Oncogene

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“…The elevated level of actin RNA in this cell line (Fig. 3, lower left panel) as compared with the MNL samples probably relates to its fibroblastic origin (27).…”

Section: Methodsmentioning

confidence: 99%

“…These estimates of myc elevation are in rough agreement with the dot blot data. IMR-90 is a primary cell line (27) that contains nonelevated levels of myc RNA based on dot blot hybridization (data not shown). We used this cell line as a normal standard in Northern blots when normal MNL RNA was in short supply.…”

Section: Methodsmentioning

confidence: 99%

Structure and expression of the oncogene c-myc in fresh tumor material from patients with hematopoietic malignancies.

Rothberg¹,

Erisman²,

Diehl³

et al. 1984

Mol. Cell. Biol.

110

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c-myc is the cellular gene homologous to the transforming sequence of MC29, an acute avian retrovirus. The human c-myc gene was cloned and used to study the structure and expression of c-myc in a variety of human hematopoietic malignancies. In a careful study of 106 patients, c-myc RNA was found to be expressed at elevated levels in tumor cells of 17 leukemia patients and five lymphoma patients. The c-myc gene was found to be rearranged in two lymphomas, an African Burkitt's lymphoma and a non-Hodgkins lymphoma in leukemic phase. The Burkitt's rearrangement involved the insertion of new DNA sequences upstream from the c-myc 5' coding region, presumably replacing the normal c-myc transcriptional promoter. None of the other 104 patients, including 20 with elevated myc expression, exhibited any evidence of a genetic rearrangement involving the c-myc gene. Our results show that there is a subset of hematopoietic malignancies characterized by elevated expression of c-myc. This elevated expression in most cases is not due to obvious genetic changes (rearrangement, amplification) at the c-myc locus nor to chromosomal translocations in the vicinity of this gene.

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“…The identified 743 highconfidence peaks represent putative genomic p53 binding sites in IMR90 fibroblasts 29 treated for 6 h with 5-fluorouracil (5-FU). After comparing these with binding sites previously reported in the cancer cell lines HCT116 23 and U2OS, 24,25 we found that the p53 sites in the normal fibroblasts reside in a distinct genomic landscape significantly different from that previously reported in the cancer cells, pointing at chromatin as a critical factor in the selection of the occupied sites.…”

Section: Distinct P53 Genomic Binding Patterns In Normal and Cancer-dmentioning

confidence: 99%

Distinct p53 genomic binding patterns in normal and cancer-derived human cells

Botcheva¹,

McCorkle²,

McCombie³

et al. 2011

Cell Cycle

118

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Characterization of a New Human Diploid Cell Strain, IMR-90

Cited by 354 publications

References 14 publications

Disregulation of mitotic checkpoints and regulatory proteins following acute expression of SV40 large T antigen in diploid human cells

Disregulation of mitotic checkpoints and regulatory proteins following acute expression of SV40 large T antigen in diploid human cells

Structure and expression of the oncogene c-myc in fresh tumor material from patients with hematopoietic malignancies.

Distinct p53 genomic binding patterns in normal and cancer-derived human cells

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