Example of Tumor Biology format
Recent searches

Example of Tumor Biology format Example of Tumor Biology format Example of Tumor Biology format Example of Tumor Biology format Example of Tumor Biology format Example of Tumor Biology format Example of Tumor Biology format Example of Tumor Biology format Example of Tumor Biology format Example of Tumor Biology format Example of Tumor Biology format
Sample paper formatted on SciSpace - SciSpace
This content is only for preview purposes. The original open access content can be found here.
Look Inside
Example of Tumor Biology format Example of Tumor Biology format Example of Tumor Biology format Example of Tumor Biology format Example of Tumor Biology format Example of Tumor Biology format Example of Tumor Biology format Example of Tumor Biology format Example of Tumor Biology format Example of Tumor Biology format Example of Tumor Biology 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

Tumor Biology — Template for authors

Publisher: SAGE
Categories Rank Trend in last 3 yrs
Cancer Research #41 of 207 up up by 27 ranks
journal-quality-icon Journal quality:
High
calendar-icon Last 4 years overview: 848 Published Papers | 7923 Citations
indexed-in-icon Indexed in: Scopus
last-updated-icon Last updated: 07/06/2020
Related journals
Insights
General info
Top papers
Popular templates
Get started guide
Why choose from SciSpace
FAQ

Related Journals

open access Open Access
recommended Recommended

PLOS

Quality:  
High
CiteRatio: 9.0
SJR: 3.587
SNIP: 1.457
open access Open Access
recommended Recommended

Nature

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

American Association for Cancer Research

Quality:  
High
CiteRatio: 14.4
SJR: 4.976
SNIP: 1.747
open access Open Access
recommended Recommended

American Association for Cancer Research

Quality:  
High
CiteRatio: 15.8
SJR: 4.103
SNIP: 1.983

Journal Performance & Insights

CiteRatio

SCImago Journal Rank (SJR)

Source Normalized Impact per Paper (SNIP)

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

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.

9.3

7% from 2019

CiteRatio for Tumor Biology from 2016 - 2020
Year Value
2020 9.3
2019 10.0
2018 8.1
2017 6.6
2016 4.8
graph view Graph view
table view Table view

1.055

6% from 2019

SJR for Tumor Biology from 2016 - 2020
Year Value
2020 1.055
2019 1.119
2018 1.057
2017 1.149
2016 1.089
graph view Graph view
table view Table view

0.903

4% from 2019

SNIP for Tumor Biology from 2016 - 2020
Year Value
2020 0.903
2019 0.945
2018 0.853
2017 0.846
2016 0.864
graph view Graph view
table view Table view

insights Insights

  • CiteRatio of this journal has decreased by 7% in last years.
  • This journal’s CiteRatio is in the top 10 percentile category.

insights Insights

  • SJR of this journal has decreased by 6% in last years.
  • This journal’s SJR is in the top 10 percentile category.

insights Insights

  • SNIP of this journal has decreased by 4% in last years.
  • This journal’s SNIP is in the top 10 percentile category.

Tumor Biology

Guideline source: View

All company, product and service names used in this website are for identification purposes only. All product names, trademarks and registered trademarks are property of their respective owners.

Use of these names, trademarks and brands does not imply endorsement or affiliation. Disclaimer Notice

SAGE

Tumor Biology

Tumor Biology is a peer reviewed, open access journal publishing experimental and clinical cancer research. Tumor Biology places special emphasis on articles covering all aspects of tumor markers and tumor targeting, but studies in other areas of clinical and translational can...... Read More

Medicine

i
Last updated on
07 Jun 2020
i
ISSN
1010-4283
i
Impact Factor
Medium - 0.75
i
Open Access
Yes
i
Sherpa RoMEO Archiving Policy
Green faq
i
Plagiarism Check
Available via Turnitin
i
Endnote Style
Download Available
i
Bibliography Name
SageV
i
Citation Type
Numbered (Superscripted)
25
i
Bibliography Example
Blonder GE, Tinkham M and Klapwijk TM. Transition from metallic to tunneling regimes in superconducting microconstrictions: Excess current, charge imbalance, and supercurrent conversion. Phys. Rev. B 1982; 25(7): 4515–4532. URL 10.1103/PhysRevB.25.4515.

Top papers written in this journal

Journal Article DOI: 10.1007/S13277-016-5098-7
Role of interleukin-6 in cancer progression and therapeutic resistance
Neeraj Kumari1, Bilikere S. Dwarakanath2, Asmita Das1, Anant Narayan Bhatt
03 Jun 2016 - Tumor Biology

Abstract:

In the last several decades, the number of people dying from cancer-related deaths has not reduced significantly despite phenomenal advances in the technologies related to diagnosis and therapeutic modalities The principal cause behind limitations in the curability of this disease is the reducing sensitivity of the cancer cel... In the last several decades, the number of people dying from cancer-related deaths has not reduced significantly despite phenomenal advances in the technologies related to diagnosis and therapeutic modalities The principal cause behind limitations in the curability of this disease is the reducing sensitivity of the cancer cells towards conventional anticancer therapeutic modalities, particularly in advance stages of the disease Amongst several reasons, certain secretory factors released by the tumour cells into the microenvironment have been found to confer resistance towards chemo- and radiotherapy, besides promoting growth Interleukin-6 (IL-6), one of the major cytokines in the tumour microenvironment, is an important factor which is found at high concentrations and known to be deregulated in cancer Its overexpression has been reported in almost all types of tumours The strong association between inflammation and cancer is reflected by the high IL-6 levels in the tumour microenvironment, where it promotes tumorigenesis by regulating all hallmarks of cancer and multiple signalling pathways, including apoptosis, survival, proliferation, angiogenesis, invasiveness and metastasis, and, most importantly, the metabolism Moreover, IL-6 protects the cancer cells from therapy-induced DNA damage, oxidative stress and apoptosis by facilitating the repair and induction of countersignalling (antioxidant and anti-apoptotic/pro-survival) pathways Therefore, blocking IL-6 or inhibiting its associated signalling independently or in combination with conventional anticancer therapies could be a potential therapeutic strategy for the treatment of cancers with IL-6-dominated signalling read more read less

Topics:

Cancer (57%)57% related to the paper, Metastasis (55%)55% related to the paper, Cancer cell (54%)54% related to the paper, Carcinogenesis (52%)52% related to the paper, Angiogenesis (50%)50% related to the paper
645 Citations
open accessOpen access Journal Article DOI: 10.1177/1010428317714626
Progress in the treatment of advanced gastric cancer
Zheyu Song1, Yuanyu Wu1, Jiebing Yang1, Dingquan Yang1, Xuedong Fang1
03 Jul 2017 - Tumor Biology

Abstract:

Gastric cancer is one of the most common malignant tumors in the digestive system. Surgery is currently considered to be the only radical treatment. As surgical techniques improve and progress is made in traditional radiotherapy, chemotherapy, and the implementation of neoadjuvant therapy, the 5-year survival rate of early ga... Gastric cancer is one of the most common malignant tumors in the digestive system. Surgery is currently considered to be the only radical treatment. As surgical techniques improve and progress is made in traditional radiotherapy, chemotherapy, and the implementation of neoadjuvant therapy, the 5-year survival rate of early gastric cancer can reach >95%. However, the low rate of early diagnosis means that most patients have advanced-stage disease at diagnosis and so the best surgical window is missed. Therefore, the main treatment for advanced gastric cancer is the combination of neoadjuvant chemoradiotherapy, molecular-targeted therapy, and immunotherapy. In this article, we summarize several common methods used to treat advanced gastric cancer and discuss the progress made in the treatment of gastric cancer in detail. Only clinical practice and clinical research will allow us to prolong the survival time of patients and allow the patients to truly benefit by paying attention to the individual patient cha... read more read less

Topics:

Early Gastric Cancer (60%)60% related to the paper, Neoadjuvant therapy (59%)59% related to the paper, Cancer (57%)57% related to the paper, Survival rate (56%)56% related to the paper, Radiation therapy (55%)55% related to the paper
View PDF
579 Citations
Journal Article DOI: 10.1007/S13277-010-0042-8
Radiation-induced cell death mechanisms.
David Eriksson1, Torgny Stigbrand1
20 May 2010 - Tumor Biology

Abstract:

The main goal when treating malignancies with radiation therapy is to deprive tumor cells of their reproductive potential. One approach to achieve this is by inducing tumor cell apoptosis. Accumulating evidences suggest that induction of apoptosis alone is insufficient to account for the therapeutic effect of radiotherapy. It... The main goal when treating malignancies with radiation therapy is to deprive tumor cells of their reproductive potential. One approach to achieve this is by inducing tumor cell apoptosis. Accumulating evidences suggest that induction of apoptosis alone is insufficient to account for the therapeutic effect of radiotherapy. It has become obvious in the last few years that inhibition of the proliferative capacity of malignant cells following irradiation, especially with solid tumors, can occur via alternative cell death modalities or permanent cell cycle arrests, i.e., senescence. In this review, apoptosis and mitotic catastrophe, the two major cell deaths induced by radiation, are described and dissected in terms of activating mechanisms. Furthermore, treatment-induced senescence and its relevance for the outcome of radiotherapy of cancer will be discussed. The importance of p53 for the induction and execution of these different types of cell deaths is highlighted. The efficiency of radiotherapy and radioimmunotherapy has much to gain by understanding the cell death mechanisms that are induced in tumor cells following irradiation. Strategies to use specific inhibitors that will manipulate key molecules in these pathways in combination with radiation might potentiate therapy and enhance tumor cell kill. read more read less

Topics:

Cell cycle (56%)56% related to the paper, Radiation therapy (54%)54% related to the paper, Mitotic catastrophe (52%)52% related to the paper, Radioimmunotherapy (52%)52% related to the paper, Programmed cell death (51%)51% related to the paper
552 Citations
open accessOpen access Journal Article DOI: 10.1007/S13277-013-1511-7
Collagen as a double-edged sword in tumor progression
Min Fang1, Jingping Yuan1, Chun-Wei Peng1, Yan Li1
01 Apr 2014 - Tumor Biology

Abstract:

It has been recognized that cancer is not merely a disease of tumor cells, but a disease of imbalance, in which stromal cells and tumor microenvironment play crucial roles. Extracellular matrix (ECM) as the most abundant component in tumor microenvironment can regulate tumor cell behaviors and tissue tension homeostasis. Coll... It has been recognized that cancer is not merely a disease of tumor cells, but a disease of imbalance, in which stromal cells and tumor microenvironment play crucial roles. Extracellular matrix (ECM) as the most abundant component in tumor microenvironment can regulate tumor cell behaviors and tissue tension homeostasis. Collagen constitutes the scaffold of tumor microenvironment and affects tumor microenvironment such that it regulates ECM remodeling by collagen degradation and re-deposition, and promotes tumor infiltration, angiogenesis, invasion and migration. While collagen was traditionally regarded as a passive barrier to resist tumor cells, it is now evident that collagen is also actively involved in promoting tumor progression. Collagen changes in tumor microenvironment release biomechanical signals, which are sensed by both tumor cells and stromal cells, trigger a cascade of biological events. In this work, we discuss how collagen can be a double-edged sword in tumor progression, both inhibiting and promoting tumor progression at different stages of cancer development. read more read less

Topics:

Tumor progression (68%)68% related to the paper, Tumor microenvironment (63%)63% related to the paper, Stromal cell (55%)55% related to the paper, Extracellular matrix (54%)54% related to the paper, Angiogenesis (53%)53% related to the paper
View PDF
445 Citations
open accessOpen access Journal Article DOI: 10.1007/S13277-016-5035-9
Major apoptotic mechanisms and genes involved in apoptosis.
Yağmur Kiraz1, Yağmur Kiraz2, Aysun Adan1, Melis Kartal Yandim2, Yusuf Baran2, Yusuf Baran1
09 Apr 2016 - Tumor Biology

Abstract:

As much as the cellular viability is important for the living organisms, the elimination of unnecessary or damaged cells has the opposite necessity for the maintenance of homeostasis in tissues, organs and the whole organism. Apoptosis, a type of cell death mechanism, is controlled by the interactions between several molecule... As much as the cellular viability is important for the living organisms, the elimination of unnecessary or damaged cells has the opposite necessity for the maintenance of homeostasis in tissues, organs and the whole organism. Apoptosis, a type of cell death mechanism, is controlled by the interactions between several molecules and responsible for the elimination of unwanted cells from the body. Apoptosis can be triggered by intrinsically or extrinsically through death signals from the outside of the cell. Any abnormality in apoptosis process can cause various types of diseases from cancer to auto-immune diseases. Different gene families such as caspases, inhibitor of apoptosis proteins, B cell lymphoma (Bcl)-2 family of genes, tumor necrosis factor (TNF) receptor gene superfamily, or p53 gene are involved and/or collaborate in the process of apoptosis. In this review, we discuss the basic features of apoptosis and have focused on the gene families playing critical roles, activation/inactivation mechanisms, upstream/downstream effectors, and signaling pathways in apoptosis on the basis of cancer studies. In addition, novel apoptotic players such as miRNAs and sphingolipid family members in various kind of cancer are discussed. read more read less

Topics:

Inhibitor of apoptosis (68%)68% related to the paper, Intrinsic apoptosis (65%)65% related to the paper, XIAP (61%)61% related to the paper, Programmed cell death (59%)59% related to the paper, Suicide gene (59%)59% related to the paper
View PDF
398 Citations
Author Pic

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.

- Andreas Frutiger, Researcher, ETH Zurich, Institute for Biomedical Engineering

Get MS-Word and LaTeX output to any Journal within seconds
1
Choose a template
Select a template from a library of 40,000+ templates
2
Import a MS-Word file or start fresh
It takes only few seconds to import
3
View and edit your final output
SciSpace will automatically format your output to meet journal guidelines
4
Submit directly or Download
Submit to journal directly or Download in PDF, MS Word or LaTeX

(Before submission check for plagiarism via Turnitin)

clock Less than 3 minutes

What to expect from SciSpace?

Speed and accuracy over MS Word

''

With SciSpace, you do not need a word template for Tumor Biology.

It automatically formats your research paper to SAGE 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

Plagiarism Reports via Turnitin

SciSpace has partnered with Turnitin, the leading provider of Plagiarism Check software.

Using this service, researchers can compare submissions against more than 170 million scholarly articles, a database of 70+ billion current and archived web pages. How Turnitin Integration works?

Turnitin Stats
Publisher Logos

Freedom from formatting guidelines

One editor, 100K journal formats – world's largest collection of journal templates

With such a huge verified library, what you need is already there.

publisher-logos

Easy support from all your favorite tools

Tumor Biology format uses SageV 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

1. Can I write Tumor Biology in LaTeX?

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

2. Do you follow the Tumor Biology guidelines?

Yes, the template is compliant with the Tumor Biology 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 Tumor Biology?

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 Tumor Biology citation style.

4. Can I use the Tumor Biology 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 Tumor Biology.

5. Can I use a manuscript in Tumor Biology 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 Tumor Biology that you can download at the end.

6. How long does it usually take you to format my papers in Tumor Biology?

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

7. Where can I find the template for the Tumor Biology?

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 Tumor Biology'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 Tumor Biology'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. Tumor Biology an online tool or is there a desktop version?

SciSpace's Tumor Biology 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 Tumor Biology?

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 Tumor Biology?”

11. What is the output that I would get after using Tumor Biology?

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

12. Is Tumor Biology'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 Tumor Biology?

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 Tumor Biology. 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 Tumor Biology?

The 5 most common citation types in order of usage for Tumor Biology 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 Tumor Biology?

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

16. Can I download Tumor Biology 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 Tumor Biology Endnote style according to Elsevier guidelines.

Fast and reliable,
built for complaince.

Instant formatting to 100% publisher guidelines on - SciSpace.

Available only on desktops 🖥

No word template required

Typset automatically formats your research paper to Tumor Biology formatting guidelines and citation style.

Verifed journal formats

One editor, 100K journal formats.
With the largest collection of verified journal formats, what you need is already there.

Trusted by academicians

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.

Andreas Frutiger
Researcher & Ex MS Word user
Use this template