Example of Cancer Immunology Research format
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Example of Cancer Immunology Research format Example of Cancer Immunology Research format Example of Cancer Immunology Research format Example of Cancer Immunology Research format Example of Cancer Immunology Research format Example of Cancer Immunology Research format Example of Cancer Immunology Research format Example of Cancer Immunology Research format
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Example of Cancer Immunology Research format Example of Cancer Immunology Research format Example of Cancer Immunology Research format Example of Cancer Immunology Research format Example of Cancer Immunology Research format Example of Cancer Immunology Research format Example of Cancer Immunology Research format Example of Cancer Immunology Research 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: 23266066 e-ISSN: 23266074
recommended Recommended

Cancer Immunology Research — Template for authors

Categories Rank Trend in last 3 yrs
Cancer Research #18 of 207 down down by 6 ranks
Immunology #21 of 202 down down by 7 ranks
journal-quality-icon Journal quality:
High
calendar-icon Last 4 years overview: 595 Published Papers | 8568 Citations
indexed-in-icon Indexed in: Scopus
last-updated-icon Last updated: 01/06/2020
Insights & related journals
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Journal Performance & Insights

  • CiteRatio
  • SJR
  • SNIP

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

14.4

22% from 2019

CiteRatio for Cancer Immunology Research from 2016 - 2020
Year Value
2020 14.4
2019 11.8
2018 14.6
2017 15.5
2016 11.4
graph view Graph view
table view Table view

insights Insights

  • CiteRatio of this journal has increased by 22% 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.

4.976

8% from 2019

SJR for Cancer Immunology Research from 2016 - 2020
Year Value
2020 4.976
2019 4.598
2018 4.99
2017 4.956
2016 4.518
graph view Graph view
table view Table view

insights Insights

  • SJR of this journal has increased by 8% 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.

1.747

17% from 2019

SNIP for Cancer Immunology Research from 2016 - 2020
Year Value
2020 1.747
2019 1.497
2018 1.606
2017 1.596
2016 1.489
graph view Graph view
table view Table view

insights Insights

  • SNIP of this journal has increased by 17% in last years.
  • This journal’s SNIP is in the top 10 percentile category.

Related Journals

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CiteRatio: 9.4 | SJR: 2.389 | SNIP: 1.226
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CiteRatio: 10.4 | SJR: 5.06 | SNIP: 2.281
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Taylor and Francis

CiteRatio: 8.4 | SJR: 2.078 | SNIP: 1.475
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Taylor and Francis

CiteRatio: 8.2 | SJR: 1.864 | SNIP: 1.641
Cancer Immunology Research

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American Association for Cancer Research

Cancer Immunology Research

Cancer Immunology Research publishes outstanding original articles reporting major advances in cancer immunology that span the discipline from basic investigations in host-tumor interactions to developmental therapeutics in model systems, early translational studies in patient...... Read More

Cancer Research

Immunology

Biochemistry, Genetics and Molecular Biology

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Last updated on
01 Jun 2020
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ISSN
2326-6066
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Open Access
No
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Sherpa RoMEO Archiving Policy
Yellow faq
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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: 10.1158/2326-6066.CIR-16-0297
Myeloid-Derived Suppressor Cells
Dmitry I. Gabrilovich1

Abstract:

The development of tumor-specific T cell tolerance is largely responsible for tumor escape. Accumulation of myeloid-derived suppressor cells (MDSCs) in animal tumor models as well as in cancer patients is involved in tumor-associated T cell tolerance. In recent years, it has become increasingly evident that MDSCs bring about ... The development of tumor-specific T cell tolerance is largely responsible for tumor escape. Accumulation of myeloid-derived suppressor cells (MDSCs) in animal tumor models as well as in cancer patients is involved in tumor-associated T cell tolerance. In recent years, it has become increasingly evident that MDSCs bring about antigen-specific T cell tolerance by various mechanisms, which is the focus of this chapter. read more read less

Topics:

Myeloid-derived Suppressor Cell (61%)61% related to the paper, T cell (60%)60% related to the paper, Tumor Escape (52%)52% related to the paper, Cellular differentiation (52%)52% related to the paper
View PDF
796 Citations
open accessOpen access Journal Article DOI: 10.1158/2326-6066.CIR-13-0127
PD-L1 Expression in Triple-Negative Breast Cancer

Abstract:

Early-phase trials targeting the T-cell inhibitory molecule programmed cell death ligand 1 (PD-L1) have shown clinical efficacy in cancer. This study was undertaken to determine whether PD-L1 is overexpressed in triple-negative breast cancer (TNBC) and to investigate the loss of PTEN as a mechanism of PD-L1 regulation. The Ca... Early-phase trials targeting the T-cell inhibitory molecule programmed cell death ligand 1 (PD-L1) have shown clinical efficacy in cancer. This study was undertaken to determine whether PD-L1 is overexpressed in triple-negative breast cancer (TNBC) and to investigate the loss of PTEN as a mechanism of PD-L1 regulation. The Cancer Genome Atlas (TCGA) RNA sequencing data showed significantly greater expression of the PD-L1 gene in TNBC ( n = 120) compared with non-TNBC ( n = 716; P + tumors had greater CD8 + T-cell infiltrate than PD-L1 − tumors (688 cells/mm vs. 263 cells/mm; P Cancer Immunol Res; 2(4); 361–70. ©2014 AACR . read more read less

Topics:

Breast cancer (56%)56% related to the paper, Triple-negative breast cancer (56%)56% related to the paper, Triple Negative Breast Neoplasms (53%)53% related to the paper, PTEN (53%)53% related to the paper
View PDF
657 Citations
open accessOpen access Journal Article DOI: 10.1158/2326-6066.CIR-13-0013
Anti-CTLA-4 antibodies of IgG2a isotype enhance antitumor activity through reduction of intratumoral regulatory T cells.

Abstract:

Antitumor activity of CTLA-4 antibody blockade is thought to be mediated by interfering with the negative regulation of T-effector cell (Teff) function resulting from CTLA-4 engagement by B7-ligands. In addition, a role for CTLA-4 on regulatory T cells (Treg), wherein CTLA-4 loss or inhibition results in reduced Treg function... Antitumor activity of CTLA-4 antibody blockade is thought to be mediated by interfering with the negative regulation of T-effector cell (Teff) function resulting from CTLA-4 engagement by B7-ligands. In addition, a role for CTLA-4 on regulatory T cells (Treg), wherein CTLA-4 loss or inhibition results in reduced Treg function, may also contribute to antitumor responses by anti-CTLA-4 treatment. We have examined the role of the immunoglobulin constant region on the antitumor activity of anti-CTLA-4 to analyze in greater detail the mechanism of action of anti-CTLA-4 antibodies. Anti-CTLA-4 antibody containing the murine immunoglobulin G (IgG)2a constant region exhibits enhanced antitumor activity in subcutaneous established MC38 and CT26 colon adenocarcinoma tumor models compared with anti-CTLA-4 containing the IgG2b constant region. Interestingly, anti-CTLA-4 antibodies containing mouse IgG1 or a mutated mouse IgG1-D265A, which eliminates binding to all Fcγ receptors (FcγR), do not show antitumor activity in these models. Assessment of Teff and Treg populations at the tumor and in the periphery showed that anti-CTLA-4-IgG2a mediated a rapid and dramatic reduction of Tregs at the tumor site, whereas treatment with each of the isotypes expanded Tregs in the periphery. Expansion of CD8 + Teffs is observed with both the IgG2a and IgG2b anti-CTLA-4 isotypes, resulting in a superior Teff to Treg ratio for the IgG2a isotype. These data suggest that anti-CTLA-4 promotes antitumor activity by a selective reduction of intratumoral Tregs along with concomitant activation of Teffs. Cancer Immunol Res; 1(1); 32–42. ©2013 AACR . read more read less

Topics:

Isotype (54%)54% related to the paper, Immunoglobulin G (53%)53% related to the paper, CD8 (50%)50% related to the paper, Antibody (50%)50% related to the paper
View PDF
620 Citations
open accessOpen access Journal Article DOI: 10.1158/2326-6066.CIR-14-0112
NF-κB, an Active Player in Human Cancers
Yifeng Xia1, Shen Shen1, Inder M. Verma1

Abstract:

NF-κB comprises a family of five transcription factors that form distinct protein complexes, which bind to consensus DNA sequences at promoter regions of responsive genes regulating cellular processes. The past three decades have witnessed remarkable progress in understanding the NF-κB signaling pathway in physiologic and pat... NF-κB comprises a family of five transcription factors that form distinct protein complexes, which bind to consensus DNA sequences at promoter regions of responsive genes regulating cellular processes. The past three decades have witnessed remarkable progress in understanding the NF-κB signaling pathway in physiologic and pathologic conditions. The role of NF-κB in human cancer initiation, development, metastasis, and resistance to treatment has drawn particular attention. A significant number of human cancers have constitutive NF-κB activity due to the inflammatory microenvironment and various oncogenic mutations. NF-κB activity not only promotes tumor cells' proliferation, suppresses apoptosis, and attracts angiogenesis, but it also induces epithelial-mesenchymal transition, which facilitates distant metastasis. In certain circumstances, NF-κB activation may also remodel local metabolism and anergize the immune system to favor tumor growth. Suppression of NF-κB in myeloid cells or tumor cells usually leads to tumor regression, which makes the NF-κB pathway a promising therapeutic target. However, because of its vital role in various biologic activities, components of the NF-κB pathway need to be carefully selected and evaluated to design targeted therapies. read more read less

Topics:

Carcinogenesis (53%)53% related to the paper, Transcription factor (52%)52% related to the paper, Epithelial–mesenchymal transition (52%)52% related to the paper, Angiogenesis (51%)51% related to the paper
View PDF
613 Citations
open accessOpen access Journal Article DOI: 10.1158/2326-6066.CIR-13-0170
Mesothelin-Specific Chimeric Antigen Receptor mRNA-Engineered T Cells Induce Antitumor Activity in Solid Malignancies

Abstract:

Off-target toxicity due to the expression of target antigens in normal tissue represents a major obstacle to the use of chimeric antigen receptor (CAR)-engineered T cells for treatment of solid malignancies. To circumvent this issue, we established a clinical platform for engineering T cells with transient CAR expression by u... Off-target toxicity due to the expression of target antigens in normal tissue represents a major obstacle to the use of chimeric antigen receptor (CAR)-engineered T cells for treatment of solid malignancies. To circumvent this issue, we established a clinical platform for engineering T cells with transient CAR expression by using in vitro transcribed mRNA encoding a CAR that includes both the CD3-ζ and 4-1BB costimulatory domains. We present two case reports from ongoing trials indicating that adoptive transfer of mRNA CAR T cells that target mesothelin (CARTmeso cells) is feasible and safe without overt evidence of off-tumor on-target toxicity against normal tissues. CARTmeso cells persisted transiently within the peripheral blood after intravenous administration and migrated to primary and metastatic tumor sites. Clinical and laboratory evidence of antitumor activity was shown in both patients, and the CARTmeso cells elicited an antitumor immune response revealed by the development of novel antiself antibodies. These data show the potential of using mRNA-engineered T cells to evaluate, in a controlled manner, potential off-tumor on-target toxicities and show that short-lived CAR T cells can induce epitope spreading and mediate antitumor activity in patients with advanced cancer. Thus, these findings support the development of mRNA CAR-based strategies for carcinoma and other solid tumors. Cancer Immunol Res; 2(2); 112–20. ©2013 AACR . read more read less

Topics:

Cytotoxic T cell (62%)62% related to the paper, Adoptive cell transfer (59%)59% related to the paper, Antigen (59%)59% related to the paper, Chimeric antigen receptor (58%)58% related to the paper, Immunotherapy (57%)57% related to the paper
View PDF
590 Citations
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With SciSpace, you do not need a word template for Cancer Immunology Research.

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.

Time comparison

Time taken to format a paper and Compliance with guidelines

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Cancer Immunology Research 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 Immunology Research 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 Immunology Research 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 Immunology Research'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 Immunology Research.

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 Immunology Research 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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