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Cell (Cell)

Publisher :

Cell Press

Scopus Profile
Peer reviewed only
Scopus Profile
Open Access
  • Biochemistry Genetics
  • Molecular Biology
  • cell biology
e-ISSN :

1097-4172

Issue Frequency :

Bi-Weekly

Impact Factor :

66.85

p-ISSN :

0092-8674

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 - 0092-8674, E-ISSN - 1097-4172, Established in - 1974, Impact Factor - 66.85

Not Provide Crossref DOI

Indexed in Scopus, WoS

Not indexed in DOAJ, PubMed, UGC CARE

Indexing

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Scopus
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WoS
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Elsevier

+8 More

Publications of Cell

Research Article
  • dott image Eric Fearon
  • dott image June, 1990

A genetic model for colorectal tumorigenesis

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...

Research Article
  • dott image November, 1993

WAF1, a potential mediator of p53 tumor suppression

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...

Research Article
  • dott image October, 1996

Lessons from Hereditary Colorectal Cancer

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...

Research Article
  • dott image Wafik S. El-Deiry
  • dott image November, 1992

A mammalian cell cycle checkpoint pathway utilizing p53 and GADD45 is defective in ataxia-telangiectasia

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...

Research Article
  • dott image December, 1993

Mutations of a mutS homolog in hereditary nonpolyposis colorectal cancer

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 ...

Research Article
  • dott image August, 1992

p53 function and dysfunction

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...

Research Article
  • dott image January, 1997

Characterization of the Yeast Transcriptome

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...

Research Article
  • dott image Timothy Rittman
  • dott image October, 1999

PPARδ Is an APC-Regulated Target of Nonsteroidal Anti-Inflammatory Drugs

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 ...

Research Article
  • dott image December, 1993

Hypermutability and mismatch repair deficiency in RER+ tumor cells

A subset of sporadic colorectal tumors and most tumors developing in hereditary nonpolyposis colorectal cancer patients display frequent alterations in microsatellite sequences. Such tumors ...

Research Article
  • dott image Eric Fearon
  • dott image February, 1990

Interleukin-2 production by tumor cells bypasses T helper function in the generation of an antitumor response

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 ...

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