NCI-navy medical oncology branch cell line data base

Phelps, Ruby; Johnson, Bruce E.; Ihde, Daniel C.; Gazdar, Adi F.; Carbone, David P.; McClintock, Patrick R.; Linnoila, R. Ilona; Matthews, Mary J.; Bunn, Paul A.; Carney, Desmond N.; Minna, John D.; Mulshine, James L.

doi:10.1002/jcb.240630505

Cited by 261 publications

(230 citation statements)

References 7 publications

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“…Human DNA Tumor cell lines were established from lung cancer patients according to techniques described previously (Phelps et al, 1996). Tumor and normal tissue were obtained from patients at surgical resection or post-mortem examination (Johnson et al, 1988).…”

Section: Methodsmentioning

confidence: 99%

Hypermethylation of Ron proximal promoter associates with lack of full-length Ron and transcription of oncogenic short-Ron from an internal promoter

Angeloni

Danilkovitch‐Miagkova

Иванова

et al. 2007

Oncogene

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The gene for tyrosine-kinase receptor Ron (MST1R) resides in the chromosome 3p21.3 region, frequently affected in common human malignancies. The gene generates two transcripts, 5 and 2 kb-long, full-length Ron (flRon) and short-form Ron (sfRon), respectively. Here, we show for the first time that the variegated Ron expression is associated with variations in the methylation patterns of two distinct CpG islands in Ron proximal promoter. Widespread hypermethylation associates with lack of flRon whereas hypermethylation of the distal island associates with transcription of sfRon, a constitutively active tyrosine-kinase that drives cell proliferation. sfRon inhibition with kinase-dead transgenes decreases cancer cell growth and induces cellular differentiation. sfRon could be a new drug target in cancer types in which it contributes to tumor progression.

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Section: Methodsmentioning

confidence: 99%

Hypermethylation of Ron proximal promoter associates with lack of full-length Ron and transcription of oncogenic short-Ron from an internal promoter

Angeloni

Danilkovitch‐Miagkova

Иванова

et al. 2007

Oncogene

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“…The 41 lung cancer cell lines described were established at the National Cancer Institute (NCI-H series) and at the Hamon Center for Therapeutic Oncology Research, University of Texas Southwestern Medical Center (HCC series) except for SW-900 and SK-MES-1 (Fogh et al, 1977;Phelps et al, 1996). These cell lines have been deposited for distribution in the American Type Culture Collection (http://www.atcc.org).…”

Section: Dna Samplesmentioning

confidence: 99%

“…Small cell lung cancer exhibits a more aggressive phenotype that inevitably reoccurs after initial response to chemotherapy while the clinical outcome of NSCLC is often hard to determine (Zakowski, 2003;Kurup and Hanna, 2004;Stupp et al, 2004). Much of our current knowledge of these subtypes has been derived from a canonical set of cell lines derived from primary tumours (Phelps et al, 1996). These lines have been particularly crucial in the understanding of SCLC for which surgical resection is rarely performed (Rostad et al, 2004).…”

mentioning

confidence: 99%

Differential disruption of cell cycle pathways in small cell and non-small cell lung cancer

Coe¹,

Lockwood²,

Girard

et al. 2006

Br J Cancer

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Lung cancer is the leading cause of cancer-related mortality in the world, with small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC) comprising the two major cell types. Although these cell types can be distinguished readily at the histological level, knowledge of their underlying molecular differences is very limited. In this study, we compared 14 SCLC cell lines against 27 NSCLC cell lines using an integrated array comparative genomic hybridisation and gene expression profiling approach to identify subtypespecific disruptions. Using stringent criteria, we have identified 159 of the genes that are responsible for the different biology of these cell types. Sorting of these genes by their biological functions revealed the differential disruption of key components involved in cell cycle pathways. Our novel comparative combined genome and transcriptome analysis not only identified differentially altered genes, but also revealed that certain shared pathways are preferentially disrupted at different steps in these cell types. Small cell lung cancer exhibited increased expression of MRP5, activation of Wnt pathway inhibitors, and upregulation of p38 MAPK activating genes, while NSCLC showed downregulation of CDKN2A, and upregulation of MAPK9 and EGFR. This information suggests that cell cycle upregulation in SCLC and NSCLC occurs through drastically different mechanisms, highlighting the need for differential molecular target selection in the treatment of these cancers.

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“…[21][22][23] Twenty-seven lung cancer cell lines and 23 breast cancer cell lines and were grown in RPMI-1640 medium (Life Technologies Inc., Rockville, MD) supplemented with 5% FBS and incubated in 5% CO 2 at 37°C. Four non-malignant mesothelial primary cell cultures (HCC3466, HCC3468, HCC3469, HCC3471) were established by AFG from pleural effusions that were cytologically normal or reactive arising in patients free of cancer.…”

Section: Cell Linesmentioning

confidence: 99%

Aberrant methylation of trail decoy receptor genes is frequent in multiple tumor types

Shivapurkar

Toyooka

et al. 2004

Intl Journal of Cancer

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147

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TNF-related apoptosis-inducing ligand (TRAIL) selectively induces programmed cell death (apoptosis) in various cancer cells but not in normal cells. TRAIL is known to bind to 4 different receptors, 2 proapoptotic (DR4 andDR5Several members of the tumor necrosis factor receptor superfamily, which includes tumor necrosis factor receptor 1, Fas (Apo-1/CD95), and the decoy receptors for TRAIL (Apo-2L), regulate programmed cell death (apoptosis). Upon engagement by their respective ligands, tumor necrosis factor receptor 1 and Fas recruit adaptor molecules and activate a cascade of cysteine proteases (caspases), the proteolytic activity of which results in apoptosis. The TRAIL-activated DR4 (also TNFRSF10A, Apo-2, TRAIL-R1) 1,2 and DR5 (also TNFRSF10B, KILLER/DR5, TRICK2, TRAIL-R3) receptors 2-4 have also been shown to initiate a caspase-mediated apoptotic pathway. 4 Death inducing DR4 and DR5 and the decoy receptors DcR1 (also TNFRSF10C, TRID, TRAIL-R3) and DcR2 (also TNFRSF10D, TRUNDD, TRAIL-R4) are structurally related, especially in their extracellular domains and are all located at 8p 21-22. 5,6 Decoy receptor DcR1 completely lacks the intra-cellular death domain and DcR2 contains a truncated, nonfunctional death domain and appear unable to induce apoptosis. The extracellular domains of DcR1 or DcR2 compete with those of DR4 or DR5 for TRAIL binding. Thus, based on the current knowledge, DcR1 or DcR2 are believed to inhibit apoptosis induction mediated through DR4 and DR5. 5 Inactivation of genes may occur via point mutations, allelic loss (LOH), homozygous deletions or by aberrant methylation. 7-9 Aberrant methylation of 5Ј gene promoter regions associated with gene silencing is an epigenetic phenomenon involving many genes observed in almost all cancer types, including breast cancers, lung cancers and mesotheliomas. 9 -18 We have demonstrated loss of expression (at RNA and protein level) of DR4 and DR5 in lung cancer cell lines, although the mechanism was not via methylation. 19 Recently, 20 it was reported that DcR1 and DcR2 expression are frequently silenced by aberrant methylation of 5Ј regions of these genes in pediatric tumor cell lines and neuroblastomas. In our study, we examined the methylation and expression status of DcR1, DcR2, DR4 and DR5 in breast and lung cancers and malignant mesothelioma (MM). We also examined the methylation status of TRAIL receptor genes in many other types of malignancies. We tried to correlate methylation status with clinical features of patients including survival and histological type in lung breast MM and prostate cancer. MATERIAL AND METHODS Cell linesCell lines were initiated by AFG (breast, lung, some MMs) or HIP (most MMs). [21][22][23] Twenty-seven lung cancer cell lines and 23 breast cancer cell lines and were grown in RPMI-1640 medium (Life Technologies Inc., Rockville, MD) supplemented with 5% FBS and incubated in 5% CO 2 at 37°C. Four non-malignant mesothelial primary cell cultures (HCC3466, HCC3468, HCC3469,

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NCI-navy medical oncology branch cell line data base

Abstract: The cell line data base described in this paper includes both clinical information about the patients from whom the cell lines were derived and information about the in vitro analyses performed of the cell lines.

Cited by 261 publications

References 7 publications

Hypermethylation of Ron proximal promoter associates with lack of full-length Ron and transcription of oncogenic short-Ron from an internal promoter

Hypermethylation of Ron proximal promoter associates with lack of full-length Ron and transcription of oncogenic short-Ron from an internal promoter

Differential disruption of cell cycle pathways in small cell and non-small cell lung cancer

Aberrant methylation of trail decoy receptor genes is frequent in multiple tumor types

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