Studies on four cellular proto-oncogenes and their expression in PCC4 embryonal carcinoma cells: Amplification of c-Ki-ras oncogene

Vilette, Didier; Emanoil-Ravier, Rodica; Tobaly, J.; Périès, J.

doi:10.1016/0006-291x(85)90076-2

Cited by 9 publications

(5 citation statements)

References 32 publications

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“…In contrast, the pKBE-2 probe, containing the v-Ki-ras gene [24], detected EcoRI fragments of 6.7, 3.0-3.1 and 2.5 kbp, in addition to the endogenous mouse c-Ki-ra.s fragments, in the DNA of two primary transformants ( fig.lB, lanes 1 and 4,5, [27]. Fig.2 (lanes b,c) shows that both transformants expressed clearly detectable amounts of p21 protein, although at a slightly lower level than that expressed by the PCC4 mouse teratocarcinoma cell line used as a positive control (lane a) and in which the c-Ki-ras gene is amplified at least IO-fold [18]. Comparatively, the p21 ras protein band was barely detectable in lysates from untransformed NIH 3T3 cells (not shown).…”

Section: Resultsmentioning

confidence: 99%

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Activation of c‐Ki‐ras coexists with c‐myc amplification in cells from a nude mouse tumor induced by the human breast carcinoma cell line SW 613‐S

Carloni

Champ²,

Vilarem

et al. 1988

FEBS Letters

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In vitro transfection experiments have shown that cooperation between two different oncogenes can confer a fully malignant phenotype to primary rodent cells. We have previously reported that SW 613-Tul cells, derived from a tumor induced in a nude mouse by the human breast carcinoma cell line SW 613-S showed a 30-fold amplification of the c-m_rc gene. In the present work, we show that these cells also harbor an activated c-Ki-ras gene capable of inducing the formation of foci upon transfection of NIH 3T3 cells with SW 613-Tul genomic DNA. Our results suggest that both the c-myc and c-Ki-ras oncogenes, activated by two different mechanisms, may cooperate in the full expression of the tumorigenic phenotype of SW 613-Tul cells.

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Section: Resultsmentioning

confidence: 99%

“…PCC-4 is a mouse teratocarcinema cell line, in which the c-Ki-rus gene is amplified lo-20-fold [18].…”

Section: Cell Linesmentioning

confidence: 99%

Activation of c‐Ki‐ras coexists with c‐myc amplification in cells from a nude mouse tumor induced by the human breast carcinoma cell line SW 613‐S

Carloni

Champ²,

Vilarem

et al. 1988

FEBS Letters

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“…Differences in nomenclature between the clinical and fundamental research settings may be confusing. A human testicular or ovarian tumor associating mixed embryonal carcinoma and teratoma would be considered a mixed germ cell tumor, whereas a similar tumor would be called teratocarcinoma in a murine setting [ 25 ]. In an attempt to clarify the confusion in terminology, the position by Nature Biotechnology was to consider “teratocarcinoma” as a malignant tumor composed of both somatic tissues and undifferentiated embryonal carcinoma cells [ 26 ].…”

Section: Discussionmentioning

confidence: 99%

“…The tumors produced from hepatocyte-derived iPSC reprogrammed without myc showed a minor embryonal carcinoma component (~10%), with only mild MYC immunohistochemical expression. The latter finding might be indicative of a more advanced stage of differentiation, since terminal differentiation results in decreased MYC expression [ 25 ]. Of note, small foci of fetal hepatocytes were part of the teratoma elements.…”

Section: Discussionmentioning

confidence: 99%

Human Hepatocyte‐Derived Induced Pluripotent Stem Cells: MYC Expression, Similarities to Human Germ Cell Tumors, and Safety Issues

Unzu

Friedli

Bosman

et al. 2016

Stem Cells International

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Induced pluripotent stem cells (iPSC) are a most promising approach to the development of a hepatocyte transplantable mass sufficient to induce long-term correction of inherited liver metabolic diseases, thus avoiding liver transplantation. Their intrinsic self-renewal ability and potential to differentiate into any of the three germ layers identify iPSC as the most promising cell-based therapeutics, but also as drivers of tumor development. Teratoma development currently represents the gold standard to assess iPSC pluripotency. We analyzed the tumorigenic potential of iPSC generated from human hepatocytes (HEP-iPSC) and compared their immunohistochemical profiles to that of tumors developed from fibroblast and hematopoietic stem cell-derived iPSC. HEP-iPSC generated tumors significantly presented more malignant morphological features than reprogrammed fibroblasts or CD34+ iPSC. Moreover, the protooncogene myc showed the strongest expression in HEP-iPSC, compared to only faint expression in the other cell subsets. Random integration of transgenes and the use of potent protooncogenes such as myc might be a risk factor for malignant tumor development if hepatocytes are used for reprogramming. Nonviral vector delivery systems or reprogramming of cells obtained from less invasive harvesting methods would represent interesting options for future developments in stem cell-based approaches for liver metabolic diseases.

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“…Genetic abnormalities of proto.oncogenes have been described in murine and human ECC lines by us [5][6][7] and by others [8,9] and these always involve rag protooncogenes. We have described a c-Ki-ras amplification in 2 independently passaged murine PCC4 sublines, PCC4(DB) and PCC4(DV), and have shown that this amplification was not found in the original PCC4 cell line, PCC4(HJ).…”

Section: Introductionmentioning

confidence: 99%

In vitro growth properties and PCR ras gene analysis of a murine embryonal carcinoma cell line harboring an amplified C‐Ki‐ras gene

Vilette¹,

d'Auriol

Galibert

et al. 1989

Biology of the Cell

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Ras proto-oncogenes are thought to be involved in both proliferation and malignant processes. We examined some growth properties of a murine embryonal carcinoma cell line (ECC), PCC4, that have been shown previously to be amplified for the c-KI-ras gene. Our results show that doubling time and plating efficiency are not significantly affected by such amplification. To examine the possible link between malignant behavior and c-Ki-ras alteration, we investigated activating mutations in this PCC4 cell line as well as in other ECC. Analysis of the in vitro amplified Ki-ras gene by PCR technology has not revealed point mutations in any of the ECC examined.

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Studies on four cellular proto-oncogenes and their expression in PCC4 embryonal carcinoma cells: Amplification of c-Ki-ras oncogene

Cited by 9 publications

References 32 publications

Activation of c‐Ki‐ras coexists with c‐myc amplification in cells from a nude mouse tumor induced by the human breast carcinoma cell line SW 613‐S

Activation of c‐Ki‐ras coexists with c‐myc amplification in cells from a nude mouse tumor induced by the human breast carcinoma cell line SW 613‐S

Human Hepatocyte‐Derived Induced Pluripotent Stem Cells: MYC Expression, Similarities to Human Germ Cell Tumors, and Safety Issues

In vitro growth properties and PCR ras gene analysis of a murine embryonal carcinoma cell line harboring an amplified C‐Ki‐ras gene

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