Example of Therapeutic Advances in Medical Oncology format
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Example of Therapeutic Advances in Medical Oncology format Example of Therapeutic Advances in Medical Oncology format Example of Therapeutic Advances in Medical Oncology format
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Example of Therapeutic Advances in Medical Oncology format Example of Therapeutic Advances in Medical Oncology format Example of Therapeutic Advances in Medical Oncology 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

Therapeutic Advances in Medical Oncology — Template for authors

Publisher: SAGE
Categories Rank Trend in last 3 yrs
Oncology #71 of 340 down down by 28 ranks
journal-quality-icon Journal quality:
High
calendar-icon Last 4 years overview: 463 Published Papers | 3160 Citations
indexed-in-icon Indexed in: Scopus
last-updated-icon Last updated: 15/07/2020
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Related Journals

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SAGE

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High
CiteRatio: 4.0
SJR: 0.73
SNIP: 0.924
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SJR: 1.667
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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.

6.8

11% from 2019

CiteRatio for Therapeutic Advances in Medical Oncology from 2016 - 2020
Year Value
2020 6.8
2019 7.6
2018 8.2
2017 8.6
2016 8.0
graph view Graph view
table view Table view

2.272

1% from 2019

SJR for Therapeutic Advances in Medical Oncology from 2016 - 2020
Year Value
2020 2.272
2019 2.304
2018 2.2
2017 2.238
2016 2.259
graph view Graph view
table view Table view

1.641

8% from 2019

SNIP for Therapeutic Advances in Medical Oncology from 2016 - 2020
Year Value
2020 1.641
2019 1.78
2018 1.702
2017 1.757
2016 1.615
graph view Graph view
table view Table view

insights Insights

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

insights Insights

  • SJR of this journal has decreased by 1% in last years.
  • This journal’s SJR is in the top 10 percentile category.

insights Insights

  • SNIP of this journal has decreased by 8% in last years.
  • This journal’s SNIP is in the top 10 percentile category.

Therapeutic Advances in Medical Oncology

Guideline source: View

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SAGE

Therapeutic Advances in Medical Oncology

Approved by publishing and review experts on SciSpace, this template is built as per for Therapeutic Advances in Medical Oncology formatting guidelines as mentioned in SAGE author instructions. The current version was created on 14 Jul 2020 and has been used by 643 authors to write and format their manuscripts to this journal.

Oncology

Medicine

i
Last updated on
14 Jul 2020
i
ISSN
1758-8340
i
Impact Factor
Medium - 0.955
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
SageV
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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

open accessOpen access Journal Article DOI: 10.1177/1758834011422556
An overview of the c-MET signaling pathway.
Shawna Leslie Organ1, Ming-Sound Tsao

Abstract:

c-MET is a receptor tyrosine kinase that, after binding with its ligand, hepatocyte growth factor, activates a wide range of different cellular signaling pathways, including those involved in proliferation, motility, migration and invasion. Although c-MET is important in the control of tissue homeostasis under normal physiolo... c-MET is a receptor tyrosine kinase that, after binding with its ligand, hepatocyte growth factor, activates a wide range of different cellular signaling pathways, including those involved in proliferation, motility, migration and invasion. Although c-MET is important in the control of tissue homeostasis under normal physiological conditions, it has also been found to be aberrantly activated in human cancers via mutation, amplification or protein overexpression. This paper provides an overview of the c-MET signaling pathway, including its role in the development of cancers, and provides a rationale for targeting the pathway as a possible treatment option. read more read less

Topics:

JAK-STAT signaling pathway (62%)62% related to the paper, Tissue homeostasis (58%)58% related to the paper, Cell signaling (58%)58% related to the paper, Receptor tyrosine kinase (57%)57% related to the paper, Signal transduction (55%)55% related to the paper
View PDF
654 Citations
open accessOpen access Journal Article DOI: 10.1177/1758834015614530
Pharmacologic resistance in colorectal cancer: a review
William A. Hammond1, Abhisek Swaika1, Kabir Mody1

Abstract:

Colorectal cancer (CRC) persists as one of the most prevalent and deadly tumor types in both men and women worldwide. This is in spite of widespread, effective measures of preventive screening, and also major advances in treatment options. Despite advances in cytotoxic and targeted therapy, resistance to chemotherapy remains ... Colorectal cancer (CRC) persists as one of the most prevalent and deadly tumor types in both men and women worldwide. This is in spite of widespread, effective measures of preventive screening, and also major advances in treatment options. Despite advances in cytotoxic and targeted therapy, resistance to chemotherapy remains one of the greatest challenges in long-term management of incurable metastatic disease and eventually contributes to death as tumors accumulate means of evading treatment. We performed a comprehensive literature search on the data available through PubMed, Medline, Scopus, and the ASCO Annual Symposium abstracts through June 2015 for the purpose of this review. We discuss the current state of knowledge of clinically relevant mechanisms of resistance to cytotoxic and targeted therapies now in use for the treatment of CRC. read more read less

Topics:

Targeted therapy (58%)58% related to the paper
View PDF
368 Citations
open accessOpen access Journal Article DOI: 10.1177/1758834014530023
The PI3K/AKT/mTOR pathway in breast cancer: targets, trials and biomarkers.
Elisavet Paplomata1, Ruth O'Regan1

Abstract:

The phosphoinositide 3 kinase (PI3K)/Akt/mammalian (or mechanistic) target of rapamycin (mTOR) pathway is a complicated intracellular pathway, which leads to cell growth and tumor proliferation and plays a significant role in endocrine resistance in breast cancer. Multiple compounds targeting this pathway are being evaluated ... The phosphoinositide 3 kinase (PI3K)/Akt/mammalian (or mechanistic) target of rapamycin (mTOR) pathway is a complicated intracellular pathway, which leads to cell growth and tumor proliferation and plays a significant role in endocrine resistance in breast cancer. Multiple compounds targeting this pathway are being evaluated in clinical trials. These agents are generally well tolerated and can be used in combination with targeted therapies, endocrine therapy or cytotoxic agents. The identification of subtypes of tumors more likely to respond to these therapeutics cannot be overemphasized, since breast cancer is a very heterogeneous malignancy. Activation of pathways such as KRAS and MEK can act as escape mechanisms that lead to resistance, thus a combination of agents targeting multiple steps of the intracellular machinery is promising. There is evidence that tumors with PIK3CA mutations are more sensitive to inhibitors of the PI3K pathway but this has yet to be validated. Large clinical trials with correlative studies are necessary to identify reliable biomarkers of efficacy. read more read less

Topics:

PI3K/AKT/mTOR pathway (63%)63% related to the paper, Phosphoinositide 3-kinase (58%)58% related to the paper, Protein kinase B (53%)53% related to the paper, Breast cancer (51%)51% related to the paper
View PDF
361 Citations
open accessOpen access Journal Article DOI: 10.1177/1758834011422557
c-MET as a potential therapeutic target and biomarker in cancer.
J Rafael Sierra1, Ming-Sound Tsao1

Abstract:

The receptor tyrosine kinase c-MET and its ligand, hepatocyte growth factor (HGF), regulate multiple cellular processes that stimulate cell proliferation, invasion and angiogenesis. This review provides an overview of the evidence to support c-MET or the HGF/c-MET signaling pathway as relevant targets for personalized cancer ... The receptor tyrosine kinase c-MET and its ligand, hepatocyte growth factor (HGF), regulate multiple cellular processes that stimulate cell proliferation, invasion and angiogenesis. This review provides an overview of the evidence to support c-MET or the HGF/c-MET signaling pathway as relevant targets for personalized cancer treatment based on high frequencies of c-MET and/or HGF overexpression, activation, amplification in non-small cell lung carcinoma (NSCLC), gastric, ovarian, pancreatic, thyroid, breast, head and neck, colon and kidney carcinomas. Additionally, the current knowledge of small molecule inhibitors (tivantinib [ARQ 197]), c-MET/HGF antibodies (rilotumumab and MetMAb) and mechanisms of resistance to c-MET-targeted therapies are discussed. read more read less

Topics:

C-Met (58%)58% related to the paper, Tivantinib (57%)57% related to the paper, Rilotumumab (55%)55% related to the paper, Cancer (54%)54% related to the paper, Hepatocyte growth factor (53%)53% related to the paper
View PDF
319 Citations
open accessOpen access Journal Article DOI: 10.1177/1758834009355164
Chemotherapy-induced diarrhea: pathophysiology, frequency and guideline-based management
Alexander Stein1, Wieland Voigt1, Karin Jordan1

Abstract:

Diarrhea is one of the main drawbacks for cancer patients. Possible etiologies could be radiotherapy, chemotherapeutic agents, decreased physical performance, graft versus host disease and infections. Chemotherapy-induced diarrhea (CID) is a common problem, especially in patients with advanced cancer. The incidence of CID has... Diarrhea is one of the main drawbacks for cancer patients. Possible etiologies could be radiotherapy, chemotherapeutic agents, decreased physical performance, graft versus host disease and infections. Chemotherapy-induced diarrhea (CID) is a common problem, especially in patients with advanced cancer. The incidence of CID has been reported to be as high as 50-80% of treated patients (≥30% CTC grade 3-5), especially with 5-fluorouracil bolus or some combination therapies of irinotecan and fluoropyrimidines (IFL, XELIRI). Regardless of the molecular targeted approach of tyrosine kinase inhibitors and antibodies, diarrhea is a common side effect in up to 60% of patients with up to 10% having severe diarrhea. Furthermore, the underlying pathophysiology is still under investigation. Despite the number of clinical trials evaluating therapeutic or prophylactic measures in CID, there are just three drugs recommended in current guidelines: loperamide, deodorized tincture of opium and octreotide. Newer strategies and more effective agents are being developed to reduce the morbidity and mortality associated with CID. Recent research focusing on the prophylactic use of antibiotics, budesonide, probiotics or activated charcoal still have to define the role of these drugs in the routine clinical setting. Whereas therapeutic management and clinical work-up of patients presenting with diarrhea after chemotherapy are rather well defined, prediction and prevention of CID is an evolving field. Current research focuses on establishing predictive factors for CID like uridine diphosphate glucuronosyltransferase-1A1 polymorphisms for irinotecan or dihydropyrimidine-dehydrogenase insufficiency for fluoropyrimidines. read more read less

Topics:

Irinotecan (51%)51% related to the paper, XELIRI (51%)51% related to the paper, Diarrhea (50%)50% related to the paper
View PDF
303 Citations
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Frequently asked questions

1. Can I write Therapeutic Advances in Medical 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 Therapeutic Advances in Medical Oncology guidelines and auto format it.

2. Do you follow the Therapeutic Advances in Medical Oncology guidelines?

Yes, the template is compliant with the Therapeutic Advances in Medical 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 Therapeutic Advances in Medical 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 Therapeutic Advances in Medical Oncology citation style.

4. Can I use the Therapeutic Advances in Medical 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 Therapeutic Advances in Medical Oncology.

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

6. How long does it usually take you to format my papers in Therapeutic Advances in Medical 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 Therapeutic Advances in Medical Oncology.

7. Where can I find the template for the Therapeutic Advances in Medical 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 Therapeutic Advances in Medical Oncology's guidelines and download the same in Word, PDF and LaTeX formats? Give us a try!.

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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. Therapeutic Advances in Medical Oncology an online tool or is there a desktop version?

SciSpace's Therapeutic Advances in Medical 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.

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

12. Is Therapeutic Advances in Medical 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 Therapeutic Advances in Medical 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 Therapeutic Advances in Medical 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 Therapeutic Advances in Medical Oncology?

The 5 most common citation types in order of usage for Therapeutic Advances in Medical 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 Therapeutic Advances in Medical 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 Therapeutic Advances in Medical Oncology's guidelines and download the same in Word, PDF and LaTeX formats? Give us a try!.

16. Can I download Therapeutic Advances in Medical 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 Therapeutic Advances in Medical Oncology Endnote style according to Elsevier guidelines.

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