Example of Cancer Immunology, Immunotherapy format
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Example of Cancer Immunology, Immunotherapy format Example of Cancer Immunology, Immunotherapy format Example of Cancer Immunology, Immunotherapy format Example of Cancer Immunology, Immunotherapy format Example of Cancer Immunology, Immunotherapy format Example of Cancer Immunology, Immunotherapy format Example of Cancer Immunology, Immunotherapy format Example of Cancer Immunology, Immunotherapy format Example of Cancer Immunology, Immunotherapy format Example of Cancer Immunology, Immunotherapy format Example of Cancer Immunology, Immunotherapy format Example of Cancer Immunology, Immunotherapy format Example of Cancer Immunology, Immunotherapy format Example of Cancer Immunology, Immunotherapy format Example of Cancer Immunology, Immunotherapy format Example of Cancer Immunology, Immunotherapy format Example of Cancer Immunology, Immunotherapy format Example of Cancer Immunology, Immunotherapy format
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Example of Cancer Immunology, Immunotherapy format Example of Cancer Immunology, Immunotherapy format Example of Cancer Immunology, Immunotherapy format Example of Cancer Immunology, Immunotherapy format Example of Cancer Immunology, Immunotherapy format Example of Cancer Immunology, Immunotherapy format Example of Cancer Immunology, Immunotherapy format Example of Cancer Immunology, Immunotherapy format Example of Cancer Immunology, Immunotherapy format Example of Cancer Immunology, Immunotherapy format Example of Cancer Immunology, Immunotherapy format Example of Cancer Immunology, Immunotherapy format Example of Cancer Immunology, Immunotherapy format Example of Cancer Immunology, Immunotherapy format Example of Cancer Immunology, Immunotherapy format Example of Cancer Immunology, Immunotherapy format Example of Cancer Immunology, Immunotherapy format Example of Cancer Immunology, Immunotherapy format
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open access Open Access

Cancer Immunology, Immunotherapy — Template for authors

Publisher: Springer
Categories Rank Trend in last 3 yrs
Oncology #45 of 340 up up by 3 ranks
Immunology and Allergy #29 of 182 up up by 1 rank
Immunology #35 of 202 up up by 2 ranks
Cancer Research #40 of 207 up up by 4 ranks
journal-quality-icon Journal quality:
High
calendar-icon Last 4 years overview: 695 Published Papers | 6522 Citations
indexed-in-icon Indexed in: Scopus
last-updated-icon Last updated: 01/06/2020
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Related Journals

open access Open Access
recommended Recommended

Springer

Quality:  
High
CiteRatio: 10.4
SJR: 5.06
SNIP: 2.281
open access Open Access

Taylor and Francis

Quality:  
High
CiteRatio: 8.4
SJR: 2.078
SNIP: 1.475
open access Open Access
recommended Recommended

Nature

Quality:  
High
CiteRatio: 16.0
SJR: 4.539
SNIP: 2.28
open access Open Access
recommended Recommended

Nature

Quality:  
High
CiteRatio: 53.9
SJR: 20.529
SNIP: 8.97

Journal Performance & Insights

Impact Factor

CiteRatio

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.

A measure of average citations received per peer-reviewed paper published in the journal.

5.442

11% from 2018

Impact factor for Cancer Immunology, Immunotherapy from 2016 - 2019
Year Value
2019 5.442
2018 4.9
2017 4.225
2016 4.711
graph view Graph view
table view Table view

9.4

18% from 2019

CiteRatio for Cancer Immunology, Immunotherapy from 2016 - 2020
Year Value
2020 9.4
2019 8.0
2018 7.3
2017 8.3
2016 9.0
graph view Graph view
table view Table view

insights Insights

  • Impact factor of this journal has increased by 11% in last year.
  • This journal’s impact factor is in the top 10 percentile category.

insights Insights

  • CiteRatio of this journal has increased by 18% in last years.
  • This journal’s CiteRatio is in the top 10 percentile category.

SCImago Journal Rank (SJR)

Source Normalized Impact per Paper (SNIP)

Measures weighted citations received by the journal. Citation weighting depends on the categories and prestige of the citing journal.

Measures actual citations received relative to citations expected for the journal's category.

2.389

22% from 2019

SJR for Cancer Immunology, Immunotherapy from 2016 - 2020
Year Value
2020 2.389
2019 1.957
2018 2.085
2017 1.899
2016 2.113
graph view Graph view
table view Table view

1.226

16% from 2019

SNIP for Cancer Immunology, Immunotherapy from 2016 - 2020
Year Value
2020 1.226
2019 1.058
2018 0.995
2017 1.014
2016 1.14
graph view Graph view
table view Table view

insights Insights

  • SJR of this journal has increased by 22% in last years.
  • This journal’s SJR is in the top 10 percentile category.

insights Insights

  • SNIP of this journal has increased by 16% in last years.
  • This journal’s SNIP is in the top 10 percentile category.

Cancer Immunology, Immunotherapy

Guideline source: View

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Springer

Cancer Immunology, Immunotherapy

Keeping readers informed of the latest research results in the fields of oncology and immunology has always been one of the main services provided by Cancer Immunology, Immunotherapy. To make this service even more comprehensive, the scope of the journal was expanded some year...... Read More

i
Last updated on
01 Jun 2020
i
ISSN
1606-8610
i
Impact Factor
Medium - 0.984
i
Acceptance Rate
42%
i
Open Access
Yes
i
Sherpa RoMEO Archiving Policy
White faq
i
Plagiarism Check
Available via Turnitin
i
Endnote Style
Download Available
i
Bibliography Name
SPBASIC
i
Citation Type
Author Year
(Blonder et al, 1982)
i
Bibliography Example
Beenakker CWJ (2006) Specular andreev reflection in graphene. Phys Rev Lett 97(6):067,007, URL 10.1103/PhysRevLett.97.067007

Top papers written in this journal

Journal Article DOI: 10.1007/S00262-006-0225-8
Metronomic cyclophosphamide regimen selectively depletes CD4+CD25+ regulatory T cells and restores T and NK effector functions in end stage cancer patients

Abstract:

CD4+CD25+ regulatory T cells are involved in the prevention of autoimmune diseases and in tumor-induced tolerance. We previously demonstrated in tumor-bearing rodents that one injection of cyclophosphamide could significantly decrease both numbers and suppressive functions of regulatory T cells, facilitating vaccine-induced t... CD4+CD25+ regulatory T cells are involved in the prevention of autoimmune diseases and in tumor-induced tolerance. We previously demonstrated in tumor-bearing rodents that one injection of cyclophosphamide could significantly decrease both numbers and suppressive functions of regulatory T cells, facilitating vaccine-induced tumor rejection. In humans, iterative low dosing of cyclophosphamide, referred to as "metronomic" therapy, has recently been used in patients with advanced chemotherapy resistant cancers with the aim of reducing tumor angiogenesis. Here we show that oral administration of metronomic cyclophosphamide in advanced cancer patients induces a profound and selective reduction of circulating regulatory T cells, associated with a suppression of their inhibitory functions on conventional T cells and NK cells leading to a restoration of peripheral T cell proliferation and innate killing activities. Therefore, metronomic regimen of cyclophosphamide does not only affect tumor angiogenesis but also strongly curtails immunosuppressive regulatory T cells, favoring a better control of tumor progression. Altogether these data support cyclophosphamide regimen as a valuable treatment for reducing tumor-induced immune tolerance before setting to work anticancer immunotherapy. read more read less

Topics:

T cell (63%)63% related to the paper, Regulatory T cell (63%)63% related to the paper, Metronomic Chemotherapy (63%)63% related to the paper, Interleukin 21 (61%)61% related to the paper, IL-2 receptor (61%)61% related to the paper
1,161 Citations
open accessOpen access Journal Article DOI: 10.1007/S00262-008-0523-4
Increased circulating myeloid-derived suppressor cells correlate with clinical cancer stage, metastatic tumor burden, and doxorubicin–cyclophosphamide chemotherapy

Abstract:

Abnormal accumulation of myeloid-derived suppressor cells (MDSC) is an important mechanism of tumor immune evasion Cyclophosphamide (CTX) has also been shown in non-tumor bearing animals to cause transient surges in MDSC Knowledge of MDSC is primarily based on preclinical work, and to date only few published studies have invo... Abnormal accumulation of myeloid-derived suppressor cells (MDSC) is an important mechanism of tumor immune evasion Cyclophosphamide (CTX) has also been shown in non-tumor bearing animals to cause transient surges in MDSC Knowledge of MDSC is primarily based on preclinical work, and to date only few published studies have involved cancer patients The goal of this study was to test the hypothesis that circulating MDSC levels correlate with clinical cancer stage, CTX-based chemotherapy, and metastatic tumor burden Whole blood was collected from 106 newly diagnosed solid tumor patients (stages I–IV) Percentages of circulating MDSC (Lin−/Lo, HLA DR−, CD33+CD11b+) were determined prior to initiation of systemic therapy In 17 early stage breast cancer patients receiving doxorubicin–cyclophosphamide chemotherapy every 14 days (ddAC) blood was collected on day 1 of each cycle Circulating MDSC were significantly increased in cancer patients of all stages relative to healthy volunteers A significant correlation between circulating MDSC and clinical cancer stage was also observed Moreover, among stage IV patients, those with extensive metastatic tumor burden had the highest percent and absolute number of MDSC Significant increases in circulating MDSC were observed with ddAC when compared with pretreatment levels Circulating MDSC levels correlate with clinical cancer stage, ddAC, and metastatic tumor burden This information must be incorporated into the design of future trials exploring immune-based therapeutic strategies Pharmacologic modulation of MDSC should also be tested in future clinical trials read more read less

Topics:

Cancer (53%)53% related to the paper, Cyclophosphamide (50%)50% related to the paper, Breast cancer (50%)50% related to the paper
View PDF
1,160 Citations
Journal Article DOI: 10.1007/S002620000169
A listing of human tumor antigens recognized by T cells.

Abstract:

Complete list of abbreviations of tumor antigens 707-AP 707 alanine proline-AFP alpha (α)-fetoprotein-ART-4 adenocarcinoma antigen recognized by T cells 4 BAGE B antigen-β-catenin/m β-catenin/mutated-Bcr-abl breakpoint cluster region-Abelson - CAMEL CTL-recognized antigen on melanoma CAP-1 carcinoembryonic antigen peptide-1-C... Complete list of abbreviations of tumor antigens 707-AP 707 alanine proline-AFP alpha (α)-fetoprotein-ART-4 adenocarcinoma antigen recognized by T cells 4 BAGE B antigen-β-catenin/m β-catenin/mutated-Bcr-abl breakpoint cluster region-Abelson - CAMEL CTL-recognized antigen on melanoma CAP-1 carcinoembryonic antigen peptide-1-CASP-8 caspase-8 CDC27m cell-division-cycle 27 mutated-CDK4/m cycline-dependent kinase 4 mutated-CEA carcino-embryonic antigen-CT cancer/testis (antigen)-Cyp-B cyclophilin B DAM differentiation antigen melanoma (the epitopes of DAM-6 and DAM-10 are equivalent, but the gene sequences are different; DAM-6 is also called MAGE-B2. and DAM-10 is also called MAGE-B1) ELF2M elongation factor 2 mutated ETV6-AML1 Ets variant gene 6/acute myeloid leukemia 1 gene ETS G250 glycoprotein 250 - GAGE G antigen GnT-V N-acetylglucosaminyltransferase V -Gp100 glycoprotein 100 kDa-HAGE helicose antigen-HER-2/neu human epidermal receptor-2/ neurological - HLA-A * 0201-R1701 arginine (R) to isoleucine (I) exchange at residue 170 of the α-helix of the α2-domain in the HLA-A2 gene HPV-E7 human papilloma virus E7 HSP70-2M heat shock protein 70-2 mutated HST-2 human signet ring tumor-2 hTERT or hTRT human telomerase reverse transcriptase-iCE intestinal carboxyl esterase KIAA0205 name of the gene as it appears in databases-LAGE L antigen LDLR/FUT low-density lipid receptor/GDP-L-fucose: β-D-galactosidase 2-α-L-fucosyltransferase MAGE melanoma antigen MART-1/Melan-A melanoma antigen recognized by T cells-1/melanoma antigen A MC1R melanocortin 1 receptor Myosin/m myosin mutated-MUC1 mucin 1-MUM-1, -2, -3 melanoma ubiquitous mutated 1, 2, 3 NA88-A NA cDNA clone of patient M88-NY-ESO-1 New York-esophagus 1 - P15 protein 15 p190 minor bcr-abl protein of 190 kDa ber-abl Pml/RARα promyelocytic leukaemia/retinoic acid receptor α-PRAME preferentially expressed antigen of melanoma PSA prostate-specific antigen-PSM prostate-specific membrane antigen-RAGE renal antigen RU1 or RU2 renal ubiquitous 1 or 2 SAGE sarcoma antigen SART-1 or SART-3 squamous antigen rejecting tumor 1 or 3-TEL/ AML1 translocation Ets-family leukemia/acute myeloid leukemia 1 TPI/m triosephosphate isomerase mutated TRP-1 tyrosinase related protein 1, or gp75 TRP-2 tyrosinase related protein 2 TRP-2/ INT2 TRP-2/intron 2 WT1 Wilms' tumor gene Abbreviations used ALL acute lymphoblastic leukemia AML acute myeloid leukemia-APL acute promyelocytic leukemia-CML chronic myelogenous leuke mia-CTL cytotoxic T lymphocytes-Ets E-26 transforming specific (family of transcription factors) H/N head and neck-MHC major histocompatibility complex-NSCLC non-small cell lung carcinoma-ORF open reading frame RCC renal cell carcinoma-SCC squamous cell carcinoma-TSTA tumor-specific transplantation antigens. read more read less

Topics:

Antigen (61%)61% related to the paper, Tyrosinase-related protein-2 (60%)60% related to the paper, Cytotoxic T cell (58%)58% related to the paper, Epitope (57%)57% related to the paper, Myeloid leukemia (56%)56% related to the paper
View PDF
914 Citations
Journal Article DOI: 10.1007/S00262-011-1172-6
An immune-active tumor microenvironment favors clinical response to ipilimumab

Abstract:

Ipilimumab, a fully human monoclonal antibody specific to CTLA-4, has been shown to improve overall survival in metastatic melanoma patients As a consequence of CTLA-4 blockade, ipilimumab treatment is associated with proliferation and activation of peripheral T cells To better understand various tumor-associated components t... Ipilimumab, a fully human monoclonal antibody specific to CTLA-4, has been shown to improve overall survival in metastatic melanoma patients As a consequence of CTLA-4 blockade, ipilimumab treatment is associated with proliferation and activation of peripheral T cells To better understand various tumor-associated components that may influence the clinical outcome of ipilimumab treatment, gene expression profiles of tumors from patients treated with ipilimumab were characterized Gene expression profiling was performed on tumor biopsies collected from 45 melanoma patients before and 3 weeks after the start of treatment in a phase II clinical trial Analysis of pre-treatment tumors indicated that patients with high baseline expression levels of immune-related genes were more likely to respond favorably to ipilimumab Furthermore, ipilimumab appeared to induce two major changes in tumors from patients who exhibited clinical activity: genes involved in immune response showed increased expression, whereas expression of genes for melanoma-specific antigens and genes involved in cell proliferation decreased These changes were associated with the total lymphocyte infiltrate in tumors, and there was a suggestion of association with prolonged overall survival in these patients Many IFN-γ-inducible genes and Th1-associated markers showed increased expression after ipilimumab treatment, suggesting an accumulation of this particular type of T cell at the tumor sites, which might play an important role in mediating the antitumor activity of ipilimumab These results support the proposed mechanism of action of ipilimumab, suggesting that cell-mediated immune responses play an important role in the antitumor activity of ipilimumab read more read less

Topics:

Ipilimumab (67%)67% related to the paper, Melanoma (55%)55% related to the paper, Tumor microenvironment (51%)51% related to the paper, Immunotherapy (51%)51% related to the paper
691 Citations
Journal Article DOI: 10.1007/S00262-004-0653-2
Tumor antigen-specific T helper cells in cancer immunity and immunotherapy.
Keith L. Knutson1, Mary L. Disis2

Abstract:

Historically, cancer-directed immune-based therapies have focused on eliciting a cytotoxic T cell (CTL) response, primarily due to the fact that CTL can directly kill tumors. In addition, many putative tumor antigens are intracellular proteins, and CTL respond to peptides presented in the context of MHC class I which are most... Historically, cancer-directed immune-based therapies have focused on eliciting a cytotoxic T cell (CTL) response, primarily due to the fact that CTL can directly kill tumors. In addition, many putative tumor antigens are intracellular proteins, and CTL respond to peptides presented in the context of MHC class I which are most often derived from intracellular proteins. Recently, increasing importance is being given to the stimulation of a CD4+ T helper cell (Th) response in cancer immunotherapy. Th cells are central to the development of an immune response by activating antigen-specific effector cells and recruiting cells of the innate immune system such as macrophages and mast cells. Two predominant Th cell subtypes exist, Th1 and Th2. Th1 cells, characterized by secretion of IFN-γ and TNF-α, are primarily responsible for activating and regulating the development and persistence of CTL. In addition, Th1 cells activate antigen-presenting cells (APC) and induce limited production of the type of antibodies that can enhance the uptake of infected cells or tumor cells into APC. Th2 cells favor a predominantly humoral response. Particularly important during Th differentiation is the cytokine environment at the site of antigen deposition or in the local lymph node. Th1 commitment relies on the local production of IL-12, and Th2 development is promoted by IL-4 in the absence of IL-12. Specifically modulating the Th1 cell response against a tumor antigen may lead to effective immune-based therapies. Th1 cells are already widely implicated in the tissue-specific destruction that occurs during the pathogenesis of autoimmune diseases, such as diabetes mellitus and multiple sclerosis. Th1 cells directly kill tumor cells via release of cytokines that activate death receptors on the tumor cell surface. We now know that cross-priming of the tumor-specific response by potent APC is a major mechanism of the developing endogenous immune response; therefore, even intracellular proteins can be presented in the context of MHC class II. Indeed, recent studies demonstrate the importance of cross-priming in eliciting CTL. Many vaccine strategies aim to stimulate the Th response specific for a tumor antigen. Early clinical trials have shown that focus on the Th effector arm of the immune system can result in significant levels of both antigen-specific Th cells and CTL, the generation of long lasting immunity, and a Th1 phenotype resulting in the development of epitope spreading. read more read less

Topics:

T helper cell (68%)68% related to the paper, Acquired immune system (67%)67% related to the paper, Antigen presentation (67%)67% related to the paper, Antigen-presenting cell (66%)66% related to the paper, Antigen (65%)65% related to the paper
624 Citations
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Cancer Immunology, Immunotherapy format uses SPBASIC citation style.

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Frequently asked questions

1. Can I write Cancer Immunology, Immunotherapy in LaTeX?

Absolutely not! Our tool has been designed to help you focus on writing. You can write your entire paper as per the Cancer Immunology, Immunotherapy guidelines and auto format it.

2. Do you follow the Cancer Immunology, Immunotherapy guidelines?

Yes, the template is compliant with the Cancer Immunology, Immunotherapy guidelines. Our experts at SciSpace ensure that. If there are any changes to the journal's guidelines, we'll change our algorithm accordingly.

3. Can I cite my article in multiple styles in Cancer Immunology, Immunotherapy?

Of course! We support all the top citation styles, such as APA style, MLA style, Vancouver style, Harvard style, and Chicago style. For example, when you write your paper and hit autoformat, our system will automatically update your article as per the Cancer Immunology, Immunotherapy citation style.

4. Can I use the Cancer Immunology, Immunotherapy templates for free?

Sign up for our free trial, and you'll be able to use all our features for seven days. You'll see how helpful they are and how inexpensive they are compared to other options, Especially for Cancer Immunology, Immunotherapy.

5. Can I use a manuscript in Cancer Immunology, Immunotherapy that I have written in MS Word?

Yes. You can choose the right template, copy-paste the contents from the word document, and click on auto-format. Once you're done, you'll have a publish-ready paper Cancer Immunology, Immunotherapy that you can download at the end.

6. How long does it usually take you to format my papers in Cancer Immunology, Immunotherapy?

It only takes a matter of seconds to edit your manuscript. Besides that, our intuitive editor saves you from writing and formatting it in Cancer Immunology, Immunotherapy.

7. Where can I find the template for the Cancer Immunology, Immunotherapy?

It is possible to find the Word template for any journal on Google. However, why use a template when you can write your entire manuscript on SciSpace , auto format it as per Cancer Immunology, Immunotherapy's guidelines and download the same in Word, PDF and LaTeX formats? Give us a try!.

8. Can I reformat my paper to fit the Cancer Immunology, Immunotherapy's guidelines?

Of course! You can do this using our intuitive editor. It's very easy. If you need help, our support team is always ready to assist you.

9. Cancer Immunology, Immunotherapy an online tool or is there a desktop version?

SciSpace's Cancer Immunology, Immunotherapy is currently available as an online tool. We're developing a desktop version, too. You can request (or upvote) any features that you think would be helpful for you and other researchers in the "feature request" section of your account once you've signed up with us.

10. I cannot find my template in your gallery. Can you create it for me like Cancer Immunology, Immunotherapy?

Sure. You can request any template and we'll have it setup within a few days. You can find the request box in Journal Gallery on the right side bar under the heading, "Couldn't find the format you were looking for like Cancer Immunology, Immunotherapy?”

11. What is the output that I would get after using Cancer Immunology, Immunotherapy?

After writing your paper autoformatting in Cancer Immunology, Immunotherapy, you can download it in multiple formats, viz., PDF, Docx, and LaTeX.

12. Is Cancer Immunology, Immunotherapy's impact factor high enough that I should try publishing my article there?

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 these factors include review board, rejection rates, frequency of inclusion in indexes, and Eigenfactor. You need to assess all these factors before you make your final call.

13. What is Sherpa RoMEO Archiving Policy for Cancer Immunology, Immunotherapy?

SHERPA/RoMEO Database

We extracted this data from Sherpa Romeo to help researchers understand the access level of this journal in accordance with the Sherpa Romeo Archiving Policy for Cancer Immunology, Immunotherapy. The table below indicates the level of access a journal has as per Sherpa Romeo's 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.

14. What are the most common citation types In Cancer Immunology, Immunotherapy?

The 5 most common citation types in order of usage for Cancer Immunology, Immunotherapy are:.

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

15. How do I submit my article to the Cancer Immunology, Immunotherapy?

It is possible to find the Word template for any journal on Google. However, why use a template when you can write your entire manuscript on SciSpace , auto format it as per Cancer Immunology, Immunotherapy's guidelines and download the same in Word, PDF and LaTeX formats? Give us a try!.

16. Can I download Cancer Immunology, Immunotherapy in Endnote format?

Yes, SciSpace provides this functionality. After signing up, you would need to import your existing references from Word or Bib file to SciSpace. Then SciSpace would allow you to download your references in Cancer Immunology, Immunotherapy Endnote style according to Elsevier 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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