Example of Frontiers in Oncology format
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Example of Frontiers in Oncology format Example of Frontiers in Oncology format Example of Frontiers in Oncology format Example of Frontiers in Oncology format Example of Frontiers in Oncology format Example of Frontiers in Oncology format Example of Frontiers in Oncology format Example of Frontiers in Oncology format Example of Frontiers in Oncology format Example of Frontiers in Oncology format Example of Frontiers in Oncology format Example of Frontiers in Oncology format Example of Frontiers in Oncology format Example of Frontiers in Oncology format Example of Frontiers in Oncology format Example of Frontiers in Oncology format Example of Frontiers in Oncology format Example of Frontiers in Oncology format Example of Frontiers in Oncology format
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Example of Frontiers in Oncology format Example of Frontiers in Oncology format Example of Frontiers in Oncology format Example of Frontiers in Oncology format Example of Frontiers in Oncology format Example of Frontiers in Oncology format Example of Frontiers in Oncology format Example of Frontiers in Oncology format Example of Frontiers in Oncology format Example of Frontiers in Oncology format Example of Frontiers in Oncology format Example of Frontiers in Oncology format Example of Frontiers in Oncology format Example of Frontiers in Oncology format Example of Frontiers in Oncology format Example of Frontiers in Oncology format Example of Frontiers in Oncology format Example of Frontiers in Oncology format Example of Frontiers in Oncology format
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This content is only for preview purposes. The original open access content can be found here.
open access Open Access

Frontiers in Oncology — Template for authors

Publisher: Frontiers Media
Categories Rank Trend in last 3 yrs
Oncology #174 of 340 down down by 130 ranks
Cancer Research #141 of 207 down down by 101 ranks
journal-quality-icon Journal quality:
Medium
calendar-icon Last 4 years overview: 5051 Published Papers | 19712 Citations
indexed-in-icon Indexed in: Scopus
last-updated-icon Last updated: 19/07/2020
Related journals
Insights
General info
Top papers
Popular templates
Get started guide
Why choose from SciSpace
FAQ

Related Journals

open access Open Access
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Nature

Quality:  
High
CiteRatio: 16.0
SJR: 4.539
SNIP: 2.28
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American Association for Cancer Research

Quality:  
High
CiteRatio: 15.8
SJR: 4.103
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recommended Recommended

American Association for Cancer Research

Quality:  
High
CiteRatio: 18.2
SJR: 5.427
SNIP: 2.243
open access Open Access

American Association for Cancer Research

Quality:  
High
CiteRatio: 8.7
SJR: 2.273
SNIP: 1.157

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.

4.848

17% from 2018

Impact factor for Frontiers in Oncology from 2016 - 2019
Year Value
2019 4.848
2018 4.137
2017 4.416
2016 5.425
graph view Graph view
table view Table view

3.9

11% from 2019

CiteRatio for Frontiers in Oncology from 2016 - 2020
Year Value
2020 3.9
2019 3.5
2018 5.4
2017 8.6
2016 8.4
graph view Graph view
table view Table view

insights Insights

  • Impact factor of this journal has increased by 17% in last year.
  • This journal’s impact factor is in the top 10 percentile category.

insights Insights

  • CiteRatio of this journal has increased by 11% 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.

1.834

11% from 2019

SJR for Frontiers in Oncology from 2016 - 2020
Year Value
2020 1.834
2019 1.654
2018 1.918
2017 2.023
2016 2.042
graph view Graph view
table view Table view

1.251

12% from 2019

SNIP for Frontiers in Oncology from 2016 - 2020
Year Value
2020 1.251
2019 1.117
2018 1.213
2017 1.356
2016 1.213
graph view Graph view
table view Table view

insights Insights

  • SJR of this journal has increased by 11% in last years.
  • This journal’s SJR is in the top 10 percentile category.

insights Insights

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

Frontiers in Oncology

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Frontiers Media

Frontiers in Oncology

Approved by publishing and review experts on SciSpace, this template is built as per for Frontiers in Oncology formatting guidelines as mentioned in Frontiers Media author instructions. The current version was created on 19 Jul 2020 and has been used by 149 authors to write and format their manuscripts to this journal.

Oncology

Cancer Research

Medicine

i
Last updated on
19 Jul 2020
i
ISSN
2234-943X
i
Open Access
No
i
Sherpa RoMEO Archiving Policy
Green faq
i
Plagiarism Check
Available via Turnitin
i
Endnote Style
Download Available
i
Bibliography Name
frontiersinSCNS_ENG_HUMS
i
Citation Type
Numbered
[25]
i
Bibliography Example
Blonder GE, Tinkham M, Klapwijk TM. Transition from metallic to tunneling regimes in superconducting microconstrictions: Excess current, charge imbalance, and supercurrent conversion. Phys. Rev. B 25 (1982) 4515–4532.

Top papers written in this journal

open accessOpen access Journal Article DOI: 10.3389/FONC.2014.00064
Targeting PI3K/Akt/mTOR Signaling in Cancer.
Camillo Porta, Chiara Paglino, Alessandra Mosca1
14 Apr 2014 - Frontiers in Oncology

Abstract:

The phosphatidylinositol-3-kinase (PI3K)/Akt and the mammalian target of rapamycin (mTOR) signaling pathways are two pathways crucial to many aspects of cell growth and survival, in physiological as well as in pathological conditions (e.g., cancer). Indeed, they are so interconnected that, in a certain sense, they could be re... The phosphatidylinositol-3-kinase (PI3K)/Akt and the mammalian target of rapamycin (mTOR) signaling pathways are two pathways crucial to many aspects of cell growth and survival, in physiological as well as in pathological conditions (e.g., cancer). Indeed, they are so interconnected that, in a certain sense, they could be regarded as a single, unique pathway. In this paper, after a general overview of the biological significance and the main components of these pathways, we address the present status of the development of specific PI3K, Akt, and mTOR inhibitors, from already registered medicines to novel compounds that are just leaving the laboratory bench. read more read less

Topics:

PI3K/AKT/mTOR pathway (65%)65% related to the paper, RPTOR (63%)63% related to the paper, Phosphoinositide 3-kinase (59%)59% related to the paper, Ridaforolimus (55%)55% related to the paper, Protein kinase B (55%)55% related to the paper
View PDF
1,075 Citations
open accessOpen access Journal Article DOI: 10.3389/FONC.2018.00086
Anti-PD-1 and Anti-CTLA-4 Therapies in Cancer: Mechanisms of Action, Efficacy, and Limitations.
Judith A. Seidel1, Atsushi Otsuka1, Kenji Kabashima1, Kenji Kabashima2
28 Mar 2018 - Frontiers in Oncology

Abstract:

Melanoma, a skin cancer associated with high mortality rates, is highly radio- and chemotherapy resistant but can also be very immunogenic. These circumstances have led to a recent surge in research into therapies aiming to boost anti-tumor immune responses in cancer patients. Among these immunotherapies, neutralizing antibod... Melanoma, a skin cancer associated with high mortality rates, is highly radio- and chemotherapy resistant but can also be very immunogenic. These circumstances have led to a recent surge in research into therapies aiming to boost anti-tumor immune responses in cancer patients. Among these immunotherapies, neutralizing antibodies targeting the immune checkpoints T-lymphocyte-associated protein 4 (CTLA-4) and programmed cell death protein 1 (PD-1) are being hailed as particularly successful. These antibodies have resulted in dramatic improvements in disease outcome and are now clinically approved in many countries. However, the majority of advanced stage melanoma patients do not respond or will relapse, and the hunt for the "magic bullet" to treat the disease continues. This review examines the mechanisms of action and the limitations of anti-PD-1/PD-L1 and anti-CTLA-4 antibodies which are the two types of checkpoint inhibitors currently available to patients and further explores the future avenues of their use in melanoma and other cancers. read more read less

Topics:

Magic bullet (58%)58% related to the paper, Immunotherapy (53%)53% related to the paper, Skin cancer (53%)53% related to the paper, Cancer (52%)52% related to the paper
View PDF
810 Citations
open accessOpen access Journal Article DOI: 10.3389/FONC.2015.00155
Implications of the Hybrid Epithelial/Mesenchymal Phenotype in Metastasis
20 Jul 2015 - Frontiers in Oncology

Abstract:

Understanding cell-fate decisions during tumorigenesis and metastasis is a major challenge in modern cancer biology. One canonical cell-fate decision that cancer cells undergo is Epithelial-to-Mesenchymal Transition (EMT) and its reverse Mesenchymal-to-Epithelial Transition (MET). While transitioning between these two phenoty... Understanding cell-fate decisions during tumorigenesis and metastasis is a major challenge in modern cancer biology. One canonical cell-fate decision that cancer cells undergo is Epithelial-to-Mesenchymal Transition (EMT) and its reverse Mesenchymal-to-Epithelial Transition (MET). While transitioning between these two phenotypes – epithelial and mesenchymal, cells can also attain a hybrid epithelial/ mesenchymal (i.e. partial or intermediate EMT) phenotype. Cells in this phenotype have mixed epithelial (eg. adhesion) and mesenchymal (eg. migration) properties, thereby allowing them to move collectively as clusters of Circulating Tumor Cells (CTCs). If these clusters enter the circulation, they can be more apoptosis-resistant and more capable of initiating metastatic lesions than cancer cells moving individually with wholly mesenchymal phenotypes, having undergone a complete EMT. Here, we review the operating principles of the core regulatory network for EMT/MET that acts as a ‘three-way’ switch giving rise to three distinct phenotypes – epithelial, mesenchymal and hybrid epithelial/mesenchymal. We further characterize this hybrid E/M phenotype in terms of its capabilities in terms of collective cell migration, tumor-initiation, cell-cell communication, and drug resistance. We elucidate how the highly interconnected coupling between these modules coordinates cell-fate decisions among a population of cancer cells in the dynamic tumor, hence facilitating tumor-stroma interactions, formation of CTC clusters, and consequently cancer metastasis. Finally, we discuss the multiple advantages that the hybrid epithelial/mesenchymal phenotype have as compared to a complete EMT phenotype and argue that these collectively migrating cells are the primary ‘bad actors’ of metastasis. read more read less

Topics:

Cancer stem cell (57%)57% related to the paper, Cancer cell (52%)52% related to the paper, Mesenchymal stem cell (51%)51% related to the paper, Population (51%)51% related to the paper, Metastasis (50%)50% related to the paper
View PDF
554 Citations
open accessOpen access Journal Article DOI: 10.3389/FONC.2012.00073
Radiation-induced brain injury: A review
19 Jul 2012 - Frontiers in Oncology

Abstract:

Approximately 100,000 primary and metastatic brain tumor patients/year in the US survive long enough (>6 months) to experience radiation-induced brain injury. Prior to 1970, the human brain was thought to be highly radioresistant; the acute CNS syndrome occurs after single doses >30 Gy; white matter necrosis occurs at fractio... Approximately 100,000 primary and metastatic brain tumor patients/year in the US survive long enough (>6 months) to experience radiation-induced brain injury. Prior to 1970, the human brain was thought to be highly radioresistant; the acute CNS syndrome occurs after single doses >30 Gy; white matter necrosis occurs at fractionated doses >60 Gy. Although white matter necrosis is uncommon with modern techniques, functional deficits, including progressive impairments in memory, attention, and executive function have become important, because they have profound effects on quality of life. Preclinical studies have provided valuable insights into the pathogenesis of radiation-induced cognitive impairment. Given its central role in memory and neurogenesis, the majority of these studies have focused on the hippocampus. Irradiating pediatric and young adult rodent brains leads to several hippocampal changes including neuroinflammation and a marked reduction in neurogenesis. These data have been interpreted to suggest that shielding the hippocampus will prevent clinical radiation-induced cognitive impairment. However, this interpretation may be overly simplistic. Studies using older rodents, that more closely match the adult human brain tumor population, indicate that, unlike pediatric and young adult rats, older rats fail to show a radiation-induced decrease in neurogenesis or a loss of mature neurons. Nevertheless, older rats still exhibit cognitive impairment. This occurs in the absence of demyelination and/or white matter necrosis similar to what is observed clinically, suggesting that more subtle molecular, cellular and/or microanatomic modifications are involved in this radiation-induced brain injury. Given that radiation-induced cognitive impairment likely reflects damage to both hippocampal- and non-hippocampal-dependent domains, there is a critical need to investigate the microanatomic and functional effects of radiation in various brain regions as well as their integration at clinically relevant doses and schedules. Recently developed techniques in neuroscience and neuroimaging provide not only an opportunity to accomplish this, but they also offer the opportunity to identify new biomarkers and new targets for interventions to prevent or ameliorate these late effects. read more read less

Topics:

Human brain (52%)52% related to the paper, Poison control (52%)52% related to the paper, Population (52%)52% related to the paper, Neurogenesis (51%)51% related to the paper
View PDF
509 Citations
open accessOpen access Journal Article DOI: 10.3389/FONC.2019.01370
Role of Matrix Metalloproteinases in Angiogenesis and Cancer.
06 Dec 2019 - Frontiers in Oncology

Abstract:

During angiogenesis, new vessels emerge from existing endothelial lined vessels to promote the degradation of the vascular basement membrane and remodel the extracellular matrix (ECM), followed by endothelial cell migration, and proliferation and the new generation of matrix components. Matrix metalloproteinases (MMPs) partic... During angiogenesis, new vessels emerge from existing endothelial lined vessels to promote the degradation of the vascular basement membrane and remodel the extracellular matrix (ECM), followed by endothelial cell migration, and proliferation and the new generation of matrix components. Matrix metalloproteinases (MMPs) participate in the disruption, tumor neovascularization, and subsequent metastasis while tissue inhibitors of metalloproteinases (TIMPs) downregulate the activity of these MMPs. Then, the angiogenic response can be directly or indirectly mediated by MMPs through the modulation of the balance between pro- and anti-angiogenic factors. This review analyzes recent knowledge on MMPs and their participation in angiogenesis. read more read less

Topics:

Angiogenesis (60%)60% related to the paper, Matrix metalloproteinase (57%)57% related to the paper, Neovascularization (55%)55% related to the paper, Extracellular matrix (54%)54% related to the paper
View PDF
488 Citations
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Frequently asked questions

1. Can I write Frontiers in Oncology in LaTeX?

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

2. Do you follow the Frontiers in Oncology guidelines?

Yes, the template is compliant with the Frontiers in Oncology 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 Frontiers in Oncology?

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 Frontiers in Oncology citation style.

4. Can I use the Frontiers in Oncology 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 Frontiers in Oncology.

5. Can I use a manuscript in Frontiers in Oncology 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 Frontiers in Oncology that you can download at the end.

6. How long does it usually take you to format my papers in Frontiers in Oncology?

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

7. Where can I find the template for the Frontiers in Oncology?

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 Frontiers in Oncology'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 Frontiers in Oncology'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. Frontiers in Oncology an online tool or is there a desktop version?

SciSpace's Frontiers in Oncology 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 Frontiers in Oncology?

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 Frontiers in Oncology?”

11. What is the output that I would get after using Frontiers in Oncology?

After writing your paper autoformatting in Frontiers in Oncology, you can download it in multiple formats, viz., PDF, Docx, and LaTeX.

12. Is Frontiers in Oncology'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 Frontiers in Oncology?

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 Frontiers in Oncology. 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 Frontiers in Oncology?

The 5 most common citation types in order of usage for Frontiers in Oncology 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 Frontiers in Oncology?

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 Frontiers in Oncology's guidelines and download the same in Word, PDF and LaTeX formats? Give us a try!.

16. Can I download Frontiers in Oncology 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 Frontiers in Oncology Endnote style according to Elsevier guidelines.

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