Activation of the c-K-ras oncogene in a human pancreas carcinoma

Hirai, Hisamaru; Okabe, Tetsuro; Anraku, Yumi; Fujisawa, Michio; Urabe, Akio; Takaku, Fumimaro

doi:10.1016/s0006-291x(85)80140-6

Cited by 45 publications

(18 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The origin, histological type, grade of differentiation and mutational status of the most frequent genetic changes (p53, K-ras, DPC4/smad4, p16) of PDCL investigated are reported in Table 1 [11,12,16,17,18,19,20,21,22,23,24,25,26,27,28,29,30,31,32,33,34,35,36,37,38]. All the cell lines were cultured as monolayers in RPMI 1640 (Biochrom, Berlin, Germany) supplemented with 10% heat-inactivated fetal calf serum (FCS) (Hyclone, Logan, UT), penicillin and streptomycin (100 mg/ml) under standard culture conditions (5% CO 2 , 95% air in humidified chamber at 37C).…”

Section: Cell Linesmentioning

confidence: 99%

See 1 more Smart Citation

A comprehensive in vitro characterization of pancreatic ductal carcinoma cell line biological behavior and its correlation with the structural and genetic profile

et al. 2004

View full text Add to dashboard Cite

There are a large number of stable pancreatic ductal carcinoma cell lines (PDCL) that are used by researchers worldwide. Detailed data about their differentiation status and genetic alterations are present in the literature, but a systematic correlation with cell biological behavior is often lacking. PDCL ( n=12) were clustered by source of tumor cell (ascites, primary tumor, metastasis), and the data of functional cell biology were correlated with the reported structural and genetic profiles. Major histocompatibility complex expression, chemosensitivity and aneuploidia appeared to be related to the source of PDCL, and proliferative capacity appeared to be related to the grade of differentiation. No correlation between genetic/structural features of PDCL and biological behavior was found. All the cell lines appeared generally insensitive to in vitro treatment with 5-fluorouracil and showed variable degrees of susceptibility to gemcitabine, raltitrexed and oxaliplatin. All the PDCL showed resistance to Fas-mediated apoptosis but were significantly sensitive to the pro-apoptotic effect of inflammatory cytokines [interleukin (IL)-1beta, tumor necrosis factor (TNF)alpha and interferon gamma]. PDCL were characterized for the secretion of several factors relevant to the tumor-immune cross talk. Vascular endothelial growth factor, CCL2, CCL5 and transforming growth factor beta were the factors most frequently released; less frequent was the secretion of CXCL8, CCL22, IL-6 and sporadically CXCL12, IL-10 and hepatocyte growth factor. The cytokines IL-1beta and TNFalpha were always undetectable. In conclusion, a clear correlation between structural/genetic features and function could not be detected, suggesting the weakness of a "morphological" classification for the in vitro studies of pancreatic cancer.

show abstract

Section: Cell Linesmentioning

confidence: 99%

“…Mut [23,30] ? Mut [31] T3M-4 T. Okabe (Japan) [32,33] Male, 64 PDAC G2 [11,12,24,34] Mut (p.m) [11,12] Mut (meth) [11,12] W.t. [11,12] AsPC-1 Ascites M.H Tan (USA) [35,36] Female, 62 PDAC G2 G2 10 26 Yes G1/G2/G3 [35,36] ATCC Mut (p.m.) [11,12] Mut (f.s.)…”

Section: Pdac G1mentioning

confidence: 99%

A comprehensive in vitro characterization of pancreatic ductal carcinoma cell line biological behavior and its correlation with the structural and genetic profile

et al. 2004

View full text Add to dashboard Cite

show abstract

“…Four of the six transforming genes were alleles ofRAS genes (HRAS or NRAS), with mutations affecting codon 12-one from chronic-phase disease and three from blast crisis. Hirai and colleagues (13) reported a mutant allele of NRAS in one of eight patients with chronicphase CML. In combination, the available data suggest that mutations of RAS genes may be more common in blast crisis than in chronic-phase CML, but larger studies will be necessary to test this impression properly.…”

Section: Resultsmentioning

confidence: 99%

Transforming genes in chronic myelogenous leukemia.

Liu

Hjelle

Bishop

1988

Proc. Natl. Acad. Sci. U.S.A.

134

View full text Add to dashboard Cite

Chronic myelogenous leukemia (CML) is a hematopoietic malignancy characterized by an indolent chronic phase that invariably leads to a "blast crisis" indistinguishable from acute leukemia. Using a sensitive assay based on gene transfer and tumorigenesis, we sought evidence that damage to protooncogenes might figure in the progression from the chronic to the blast phase of CML. Seven of the 12 patients with CML examined in this manner harbored transforming genes. Mutations in RAS protooncogenes were detected in the leukemic cells from 1 of 6 chronic-phase patients, and 3 of 6 blast-crisis patients. In addition, a presently unidentified transforming gene (neither RAS nor RAF) was detected in 1 patient with chronic phase and 1 with blast crisis. Our data indicate that mutations in RAS genes may play diverse roles in the pathogenesis of CML.

show abstract

“…Genomic amplification [29,30] as well as enhanced expression of Ki-ras [301 has been observed in human pancreatic tumors. However, so far, we have not detected amplification of c-Ki-rasin the rat adenoma and tumor samples reported in this paper (unpublished observations).…”

Section: Dna Was Transferred T O Genescreen Plus and Hybridized T O 3mentioning

confidence: 99%

Activation of c‐Ki‐ras not detectable in adenomas or adenocarcinomas arising in rat pancreas

Schaeffer

Zurlo

Longnecker

1990

Molecular Carcinogenesis

View full text Add to dashboard Cite

The objective of this study was to determine whether activation of c-Ki-ras occurs in carcinogen-induced rat pancreatic tumors. DNAs from 27 samples, which included adenomas, carcinomas in situ, and adenocarcinomas arising in azaserine-treated rats and corn oil-gavaged rats along with a nafenopin-induced rat pancreatic adenocarcinoma were examined for mutation of c-Ki-ras at codons 12, 13, and 61 by using the polymerase chain reaction. Our results indicate that activation of c-Ki-ras is not a common event during pancreatic carcinogenesis in the rat.

show abstract

Activation of the c-K-ras oncogene in a human pancreas carcinoma

Cited by 45 publications

References 24 publications

A comprehensive in vitro characterization of pancreatic ductal carcinoma cell line biological behavior and its correlation with the structural and genetic profile

A comprehensive in vitro characterization of pancreatic ductal carcinoma cell line biological behavior and its correlation with the structural and genetic profile

Transforming genes in chronic myelogenous leukemia.

Activation of c‐Ki‐ras not detectable in adenomas or adenocarcinomas arising in rat pancreas

Contact Info

Product

Resources

About