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Journal Photo for Cell
Peer reviewed only Open Access

Cell (Cell)

Publisher : Cell Press
Biochemistry Genetics Molecular Biology cell biology
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e-ISSN 1097-4172
p-ISSN 0092-8674
Issue Frequency Bi-Weekly
Impact Factor 66.85
Est. Year 1974
Mobile 8663142355
Country United States
Language English
APC YES
Impact Factor Assignee Google Scholar
Email jpham@cell.com

Journal Descriptions

Cell was launched in 1974 as the "journal of exciting biology." Now a part of Cell Press, a family of scientific journals, Cell is committed to building on the journal's legacy and reputation for publishing need-to-know conceptual advances in biomedical science and to providing authors with a fast, fair, informed, and responsive review process. Cell maintains editorial independence from its sister journals. Our Ph.D.-trained scientific editors work with authors, reviewers, and editorial board members with the goal of publishing the most interesting discoveries in biology every year, including an annual review issue. Every paper published in Cell is freely available starting 12 months after publication.

Cell (Cell) is :-

  • International, Peer-Reviewed, Open Access, Refereed, Biochemistry Genetics, Molecular Biology, cell biology , Online or Print , Bi-Weekly Journal

  • UGC Approved, ISSN Approved: P-ISSN P-ISSN: 0092-8674, E-ISSN: 1097-4172, Established: 1974, Impact Factor: 66.85
  • Does Not Provide Crossref DOI

  • Indexed in: Scopus, WoS

  • Not indexed in DOAJ, PubMed, UGC CARE

Indexing

Publications of Cell

A genetic model for colorectal tumorigenesis
Bert Vogelstein June, 1990
Tumorigenesis has long been thought to be a multistep process (Foulds, 1958); however, only recently has it become possible to identify the molecular events that underlie the initiation and...
WAF1, a potential mediator of p53 tumor suppression
Daniel B. Levy November, 1993
The ability of p53 to activate transcription from specific sequences suggests that genes induced by p53 may mediate its biological role as a tumor suppressor. Using a subtractive hybridizati...
Lessons from Hereditary Colorectal Cancer
Bert Vogelstein October, 1996
A large body of evidence supports the idea that accumulated genetic changes underlie the development of neoplasia. This multistep process is well illustrated by colorectal cancers, which typ...
A mammalian cell cycle checkpoint pathway utilizing p53 and GADD45 is defective in ataxia-telangiectasia
Bert Vogelstein November, 1992
Cell cycle checkpoints can enhance cell survival and limit mutagenic events following DNA damage. Primary murine fibroblasts became deficient in a G1 checkpoint activated by ionizing radiati...
Mutations of a mutS homolog in hereditary nonpolyposis colorectal cancer
Bert Vogelstein December, 1993
Recent studies have shown that a locus responsible for hereditary nonpolyposis colorectal cancer (HNPCC) is on chromosome 2p and that tumors developing in these patients contain alterations ...
p53 function and dysfunction
Bert Vogelstein August, 1992
The word “cancer” is used to describe a group of heterogeneous pathologic states in which cells multiply abnormally and invade surrounding tissues. There are hundreds of different kind...
Characterization of the Yeast Transcriptome
Bert Vogelstein January, 1997
We have analyzed the set of genes expressed from the yeast genome, herein called the transcriptome, using serial analysis of gene expression. Analysis of 60,633 transcripts revealed 4,665 ge...
PPARδ Is an APC-Regulated Target of Nonsteroidal Anti-Inflammatory Drugs
Timothy Rittman October, 1999
PPARδ was identified as a target of APC through the analysis of global gene expression profiles in human colorectal cancer (CRC) cells. PPARδ expression was elevated in CRCs and repressed ...
Hypermutability and mismatch repair deficiency in RER+ tumor cells
Bert Vogelstein December, 1993
A subset of sporadic colorectal tumors and most tumors developing in hereditary nonpolyposis colorectal cancer patients display frequent alterations in microsatellite sequences. Such tumors ...
Interleukin-2 production by tumor cells bypasses T helper function in the generation of an antitumor response
Bert Vogelstein February, 1990
A poorly immunogenic murine colon cancer was used to investigate mechanisms of antitumor immunity. Injection of tumor cells engineered by gene transfection to secrete IL-2 stimulated an MHC ...