Example of Cancer Discovery format
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Example of Cancer Discovery format Example of Cancer Discovery format Example of Cancer Discovery format Example of Cancer Discovery format Example of Cancer Discovery format Example of Cancer Discovery format Example of Cancer Discovery format Example of Cancer Discovery format Example of Cancer Discovery format Example of Cancer Discovery format Example of Cancer Discovery format Example of Cancer Discovery format Example of Cancer Discovery format
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Example of Cancer Discovery format Example of Cancer Discovery format Example of Cancer Discovery format Example of Cancer Discovery format Example of Cancer Discovery format Example of Cancer Discovery format Example of Cancer Discovery format Example of Cancer Discovery format Example of Cancer Discovery format Example of Cancer Discovery format Example of Cancer Discovery format Example of Cancer Discovery format Example of Cancer Discovery format
Sample paper formatted on SciSpace - SciSpace
This content is only for preview purposes. The original open access content can be found here.
open access Open Access ISSN: 21598274 e-ISSN: 21598290
recommended Recommended

Cancer Discovery — Template for authors

Categories Rank Trend in last 3 yrs
Oncology #16 of 340 down down by 1 rank
journal-quality-icon Journal quality:
High
calendar-icon Last 4 years overview: 1071 Published Papers | 18687 Citations
indexed-in-icon Indexed in: Scopus
last-updated-icon Last updated: 15/06/2020
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FAQ

Journal Performance & Insights

  • Impact Factor
  • CiteRatio
  • SJR
  • SNIP

Impact factor determines the importance of a journal by taking a measure of frequency with which the average article in a journal has been cited in a particular year.

29.497

12% from 2018

Impact factor for Cancer Discovery from 2016 - 2019
Year Value
2019 29.497
2018 26.37
2017 24.373
2016 20.011
graph view Graph view
table view Table view

insights Insights

  • Impact factor of this journal has increased by 12% in last year.
  • This journal’s impact factor is in the top 10 percentile category.

CiteRatio is a measure of average citations received per peer-reviewed paper published in the journal.

17.4

14% from 2019

CiteRatio for Cancer Discovery from 2016 - 2020
Year Value
2020 17.4
2019 15.2
2018 16.3
2017 16.3
2016 17.4
graph view Graph view
table view Table view

insights Insights

  • CiteRatio of this journal has increased by 14% in last years.
  • This journal’s CiteRatio is in the top 10 percentile category.

SCImago Journal Rank (SJR) measures weighted citations received by the journal. Citation weighting depends on the categories and prestige of the citing journal.

6.795

10% from 2019

SJR for Cancer Discovery from 2016 - 2020
Year Value
2020 6.795
2019 7.513
2018 7.751
2017 6.996
2016 5.174
graph view Graph view
table view Table view

insights Insights

  • SJR of this journal has decreased by 10% in last years.
  • This journal’s SJR is in the top 10 percentile category.

Source Normalized Impact per Paper (SNIP) measures actual citations received relative to citations expected for the journal's category.

4.069

12% from 2019

SNIP for Cancer Discovery from 2016 - 2020
Year Value
2020 4.069
2019 3.618
2018 3.099
2017 2.436
2016 2.134
graph view Graph view
table view Table view

insights Insights

  • SNIP of this journal has increased by 12% in last years.
  • This journal’s SNIP is in the top 10 percentile category.

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CiteRatio: 6.2 | SJR: 1.667 | SNIP: 1.516
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Cancer Discovery

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American Association for Cancer Research

Cancer Discovery

Cancer Discovery publishes high-impact, peer-reviewed articles describing major advances in research and clinical trials. Cancer Discovery is the essential cancer information resource and also publishes review articles, perspectives and commentaries, news, and Research Watch s...... Read More

Oncology

Medicine

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Last updated on
15 Jun 2020
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ISSN
2159-8274
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Impact Factor
High - 1.13
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Open Access
No
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Sherpa RoMEO Archiving Policy
Yellow faq
i
Plagiarism Check
Available via Turnitin
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Endnote Style
Download Available
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Bibliography Name
Vancouver
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Citation Type
Numbered
[25]
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Bibliography Example
Blonder GE, Tinkham M, Klapwijk TM. Transition from metallic to tunneling regimes in superconducting microconstrictions: Excess current, charge imbalance, and supercurrent con-version. Phys Rev B. 1982;25(7):4515–4532. Available from: 10.1103/PhysRevB.25.4515.

Top papers written in this journal

open accessOpen access Journal Article DOI: 10.1158/2159-8290.CD-12-0095
The cBio Cancer Genomics Portal: An Open Platform for Exploring Multidimensional Cancer Genomics Data
01 May 2012 - Cancer Discovery

Abstract:

The cBio Cancer Genomics Portal (http://cbioportal.org) is an open-access resource for interactive exploration of multidimensional cancer genomics data sets, currently providing access to data from more than 5,000 tumor samples from 20 cancer studies. The cBio Cancer Genomics Portal significantly lowers the barriers between c... The cBio Cancer Genomics Portal (http://cbioportal.org) is an open-access resource for interactive exploration of multidimensional cancer genomics data sets, currently providing access to data from more than 5,000 tumor samples from 20 cancer studies. The cBio Cancer Genomics Portal significantly lowers the barriers between complex genomic data and cancer researchers who want rapid, intuitive, and high-quality access to molecular profiles and clinical attributes from large-scale cancer genomics projects and empowers researchers to translate these rich data sets into biologic insights and clinical applications. read more read less
View PDF
8,873 Citations
open accessOpen access Journal Article DOI: 10.1158/2159-8290.CD-11-0209
The emergence of lncRNAs in cancer biology.
John R. Prensner1, Arul M. Chinnaiyan
01 Oct 2011 - Cancer Discovery

Abstract:

The discovery of numerous non-coding RNA (ncRNA) transcripts in species from yeast to mammals has dramatically altered our understanding of cell biology, especially disease biology such as cancer. In humans, the identification of abundant long ncRNA (lncRNAs) >200 bp in length has catalyzed their characterization as critical ... The discovery of numerous non-coding RNA (ncRNA) transcripts in species from yeast to mammals has dramatically altered our understanding of cell biology, especially disease biology such as cancer. In humans, the identification of abundant long ncRNA (lncRNAs) >200 bp in length has catalyzed their characterization as critical components of cancer biology. Recently, roles for lncRNAs as drivers of tumor suppressive and oncogenic functions have appeared in prevalent cancer types, such as breast and prostate cancer. In this review, we will highlight the emerging impact of ncRNAs in cancer research, with a particular focus on the mechanisms and functions of lncRNAs. read more read less

Topics:

Cancer (52%)52% related to the paper
1,403 Citations
open accessOpen access Journal Article DOI: 10.1158/2159-8274.CD-10-0028
Leukocyte Complexity Predicts Breast Cancer Survival and Functionally Regulates Response to Chemotherapy
01 Jun 2011 - Cancer Discovery

Abstract:

Immune-regulated pathways influence multiple aspects of cancer development. In this article we demonstrate that both macrophage abundance and T-cell abundance in breast cancer represent prognostic indicators for recurrence-free and overall survival. We provide evidence that response to chemotherapy is in part regulated by the... Immune-regulated pathways influence multiple aspects of cancer development. In this article we demonstrate that both macrophage abundance and T-cell abundance in breast cancer represent prognostic indicators for recurrence-free and overall survival. We provide evidence that response to chemotherapy is in part regulated by these leukocytes; cytotoxic therapies induce mammary epithelial cells to produce monocyte/macrophage recruitment factors, including colony stimulating factor 1 (CSF1) and interleukin-34, which together enhance CSF1 receptor (CSF1R)–dependent macrophage infiltration. Blockade of macrophage recruitment with CSF1R-signaling antagonists, in combination with paclitaxel, improved survival of mammary tumor–bearing mice by slowing primary tumor development and reducing pulmonary metastasis. These improved aspects of mammary carcinogenesis were accompanied by decreased vessel density and appearance of antitumor immune programs fostering tumor suppression in a CD8 + T-cell–dependent manner. These data provide a rationale for targeting macrophage recruitment/response pathways, notably CSF1R, in combination with cytotoxic therapy, and identification of a breast cancer population likely to benefit from this novel therapeutic approach. Significance: These findings reveal that response to chemotherapy is in part regulated by the tumor immune microenvironment and that common cytotoxic drugs induce neoplastic cells to produce monocyte/macrophage recruitment factors, which in turn enhance macrophage infiltration into mammary adenocarcinomas. Blockade of pathways mediating macrophage recruitment, in combination with chemotherapy, significantly decreases primary tumor progression, reduces metastasis, and improves survival by CD8 + T-cell–dependent mechanisms, thus indicating that the immune microenvironment of tumors can be reprogrammed to instead foster antitumor immunity and improve response to cytotoxic therapy. Cancer Discovery; 1(1); 54–67. ©2011 AACR . This article is highlighted in the In This Issue feature, p. 4 read more read less

Topics:

Tumor microenvironment (58%)58% related to the paper, Macrophage colony-stimulating factor (56%)56% related to the paper, Metastasis (55%)55% related to the paper, Cancer (54%)54% related to the paper, Primary tumor (53%)53% related to the paper
View PDF
1,312 Citations
open accessOpen access Journal Article DOI: 10.1158/2159-8290.CD-14-0337
AZD9291, an irreversible EGFR TKI, overcomes T790M-mediated resistance to EGFR inhibitors in lung cancer
03 Jun 2014 - Cancer Discovery

Abstract:

First-generation EGFR tyrosine kinase inhibitors (EGFR TKI) provide significant clinical benefit in patients with advanced EGFR-mutant (EGFRm+) non–small cell lung cancer (NSCLC). Patients ultimately develop disease progression, often driven by acquisition of a second T790M EGFR TKI resistance mutation. AZD9291 is a novel ora... First-generation EGFR tyrosine kinase inhibitors (EGFR TKI) provide significant clinical benefit in patients with advanced EGFR-mutant (EGFRm+) non–small cell lung cancer (NSCLC). Patients ultimately develop disease progression, often driven by acquisition of a second T790M EGFR TKI resistance mutation. AZD9291 is a novel oral, potent, and selective third-generation irreversible inhibitor of both EGFRm+ sensitizing and T790M resistance mutants that spares wild-type EGFR. This mono-anilino–pyrimidine compound is structurally distinct from other third-generation EGFR TKIs and offers a pharmacologically differentiated profile from earlier generation EGFR TKIs. Preclinically, the drug potently inhibits signaling pathways and cellular growth in both EGFRm+ and EGFRm+/T790M+ mutant cell lines in vitro, with lower activity against wild-type EGFR lines, translating into profound and sustained tumor regression in EGFR-mutant tumor xenograft and transgenic models. The treatment of 2 patients with advanced EGFRm+ T790M+ NSCLC is described as proof of principle. Significance: We report the development of a novel structurally distinct third-generation EGFR TKI, AZD9291, that irreversibly and selectively targets both sensitizing and resistant T790M+ mutant EGFR while harboring less activity toward wild-type EGFR. AZD9291 is showing promising responses in a phase I trial even at the first-dose level, with first published clinical proof-of-principle validation being presented. Cancer Discov; 4(9); 1046–61. ©2014 AACR. This article is highlighted in the In This Issue feature, p. 973 read more read less

Topics:

EGFR Activating Mutation (63%)63% related to the paper, EGFR inhibitors (58%)58% related to the paper, T790M (56%)56% related to the paper, Osimertinib (55%)55% related to the paper, Rociletinib (52%)52% related to the paper
View PDF
1,263 Citations
open accessOpen access Journal Article DOI: 10.1158/2159-8290.CD-18-0367
Fundamental Mechanisms of Immune Checkpoint Blockade Therapy
Spencer C. Wei1, Colm R. Duffy1, James P. Allison1
01 Sep 2018 - Cancer Discovery

Abstract:

Immune checkpoint blockade is able to induce durable responses across multiple types of cancer, which has enabled the oncology community to begin to envision potentially curative therapeutic approaches. However, the remarkable responses to immunotherapies are currently limited to a minority of patients and indications, highli... Immune checkpoint blockade is able to induce durable responses across multiple types of cancer, which has enabled the oncology community to begin to envision potentially curative therapeutic approaches. However, the remarkable responses to immunotherapies are currently limited to a minority of patients and indications, highlighting the need for more effective and novel approaches. Indeed, an extraordinary amount of preclinical and clinical investigation is exploring the therapeutic potential of negative and positive costimulatory molecules. Insights into the underlying biological mechanisms and functions of these molecules have, however, lagged significantly behind. Such understanding will be essential for the rational design of next-generation immunotherapies. Here, we review the current state of our understanding of T-cell costimulatory mechanisms and checkpoint blockade, primarily of CTLA4 and PD-1, and highlight conceptual gaps in knowledge. Significance: This review provides an overview of immune checkpoint blockade therapy from a basic biology and immunologic perspective for the cancer research community. Cancer Discov; 8(9); 1069–86. ©2018 AACR. read more read less

Topics:

Immune checkpoint (57%)57% related to the paper
1,153 Citations
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SciSpace is a very innovative solution to the formatting problem and existing providers, such as Mendeley or Word did not really evolve in recent years.

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With SciSpace, you do not need a word template for Cancer Discovery.

It automatically formats your research paper to American Association for Cancer Research formatting guidelines and citation style.

You can download a submission ready research paper in pdf, LaTeX and docx formats.

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Cancer Discovery format uses Vancouver citation style.

Automatically format and order your citations and bibliography in a click.

SciSpace allows imports from all reference managers like Mendeley, Zotero, Endnote, Google Scholar etc.

Frequently asked questions

Absolutely not! With our tool, you can freely write without having to focus on LaTeX. You can write your entire paper as per the Cancer Discovery guidelines and autoformat it.

Yes. The template is fully compliant as per the guidelines of this journal. Our experts at SciSpace ensure that. Also, if there's any update in the journal format guidelines, we take care of it and include that in our algorithm.

Sure. We support all the top citation styles like APA style, MLA style, Vancouver style, Harvard style, Chicago style, etc. For example, in case of this journal, when you write your paper and hit autoformat, it will automatically update your article as per the Cancer Discovery citation style.

You can avail our Free Trial for 7 days. I'm sure you'll find our features very helpful. Plus, it's quite inexpensive.

Yup. You can choose the right template, copy-paste the contents from the word doc and click on auto-format. You'll have a publish-ready paper that you can download at the end.

A matter of seconds. Besides that, our intuitive editor saves a load of your time in writing and formating your manuscript.

One little Google search can get you the Word template for any journal. However, why do you need a Word template when you can write your entire manuscript on SciSpace, autoformat it as per Cancer Discovery's guidelines and download the same in Word, PDF and LaTeX formats? Try us out!.

Absolutely! You can do it using our intuitive editor. It's very easy. If you need help, you can always contact our support team.

SciSpace is an online tool for now. We'll soon release a desktop version. You can also request (or upvote) any feature that you think might be helpful for you and the research community in the feature request section once you sign-up with us.

Sure. You can request any template and we'll have it up and running within a matter of 3 working days. You can find the request box in the Journal Gallery on the right sidebar under the heading, "Couldn't find the format you were looking for?".

After you have written and autoformatted your paper, you can download it in multiple formats, viz., PDF, Docx and LaTeX.

To be honest, the answer is NO. The impact factor is one of the many elements that determine the quality of a journal. Few of those factors the review board, rejection rates, frequency of inclusion in indexes, Eigenfactor, etc. You must assess all the factors and then take the final call.

SHERPA/RoMEO Database

We have extracted this data from Sherpa Romeo to help our researchers understand the access level of this journal. The following table indicates the level of access a journal has as per Sherpa Romeo Archiving Policy.

RoMEO Colour Archiving policy
Green Can archive pre-print and post-print or publisher's version/PDF
Blue Can archive post-print (ie final draft post-refereeing) or publisher's version/PDF
Yellow Can archive pre-print (ie pre-refereeing)
White Archiving not formally supported
FYI:
  1. Pre-prints as being the version of the paper before peer review and
  2. Post-prints as being the version of the paper after peer-review, with revisions having been made.

The 5 most common citation types in order of usage are:.

S. No. Citation Style Type
1. Author Year
2. Numbered
3. Numbered (Superscripted)
4. Author Year (Cited Pages)
5. Footnote

Our journal submission experts are skilled in submitting papers to various international journals.

After uploading your paper on SciSpace, you would see a button to request a journal submission service for Cancer Discovery.

Each submission service is completed within 4 - 5 working days.

Yes. SciSpace provides this functionality.

After signing up, you would need to import your existing references from Word or .bib file.

SciSpace would allow download of your references in Cancer Discovery Endnote style, according to american-association-for-cancer-research guidelines.

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I spent hours with MS word for reformatting. It was frustrating - plain and simple. With SciSpace, I can draft my manuscripts and once it is finished I can just submit. In case, I have to submit to another journal it is really just a button click instead of an afternoon of reformatting.

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