Example of Molecular Cancer Therapeutics format
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Example of Molecular Cancer Therapeutics format Example of Molecular Cancer Therapeutics format Example of Molecular Cancer Therapeutics format Example of Molecular Cancer Therapeutics format Example of Molecular Cancer Therapeutics format Example of Molecular Cancer Therapeutics format Example of Molecular Cancer Therapeutics format Example of Molecular Cancer Therapeutics format Example of Molecular Cancer Therapeutics format Example of Molecular Cancer Therapeutics format Example of Molecular Cancer Therapeutics format Example of Molecular Cancer Therapeutics format Example of Molecular Cancer Therapeutics format
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Example of Molecular Cancer Therapeutics format Example of Molecular Cancer Therapeutics format Example of Molecular Cancer Therapeutics format Example of Molecular Cancer Therapeutics format Example of Molecular Cancer Therapeutics format Example of Molecular Cancer Therapeutics format Example of Molecular Cancer Therapeutics format Example of Molecular Cancer Therapeutics format Example of Molecular Cancer Therapeutics format Example of Molecular Cancer Therapeutics format Example of Molecular Cancer Therapeutics format Example of Molecular Cancer Therapeutics format Example of Molecular Cancer Therapeutics format
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open access Open Access ISSN: 15357163 e-ISSN: 15388514

Molecular Cancer Therapeutics — Template for authors

Categories Rank Trend in last 3 yrs
Oncology #38 of 340 down down by 6 ranks
Cancer Research #34 of 207 down down by 6 ranks
journal-quality-icon Journal quality:
High
calendar-icon Last 4 years overview: 959 Published Papers | 9873 Citations
indexed-in-icon Indexed in: Scopus
last-updated-icon Last updated: 03/06/2020
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FAQ

Journal Performance & Insights

  • Impact Factor
  • CiteRatio
  • SJR
  • SNIP

Impact factor 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.

5.615

16% from 2018

Impact factor for Molecular Cancer Therapeutics from 2016 - 2019
Year Value
2019 5.615
2018 4.856
2017 5.365
2016 5.764
graph view Graph view
table view Table view

insights Insights

  • Impact factor of this journal has increased by 16% in last year.
  • This journal’s impact factor is in the top 10 percentile category.

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

10.3

10% from 2019

CiteRatio for Molecular Cancer Therapeutics from 2016 - 2020
Year Value
2020 10.3
2019 9.4
2018 9.4
2017 10.0
2016 9.6
graph view Graph view
table view Table view

insights Insights

  • CiteRatio of this journal has increased by 10% 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.

2.717

10% from 2019

SJR for Molecular Cancer Therapeutics from 2016 - 2020
Year Value
2020 2.717
2019 2.463
2018 2.536
2017 2.755
2016 2.737
graph view Graph view
table view Table view

insights Insights

  • SJR of this journal has increased by 10% 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.

1.313

6% from 2019

SNIP for Molecular Cancer Therapeutics from 2016 - 2020
Year Value
2020 1.313
2019 1.24
2018 1.223
2017 1.248
2016 1.32
graph view Graph view
table view Table view

insights Insights

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

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American Association for Cancer Research

CiteRatio: 15.8 | SJR: 4.103 | SNIP: 1.983
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American Association for Cancer Research

CiteRatio: 18.2 | SJR: 5.427 | SNIP: 2.243
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CiteRatio: 8.7 | SJR: 2.273 | SNIP: 1.157
Molecular Cancer Therapeutics

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American Association for Cancer Research

Molecular Cancer Therapeutics

Molecular Cancer Therapeutics will focus on basic research that has implications for cancer therapeutics in the following areas: Experimental Cancer Therapeutics, Identification of Molecular Targets, Targets for Chemoprevention, New Models, Cancer Chemistry and Drug Discovery,...... Read More

Oncology

Cancer Research

Medicine

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Last updated on
03 Jun 2020
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ISSN
1535-7163
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Impact Factor
High - 1.441
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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: 10.1158/1535-7163.MCT-14-0983
PD-L1 Expression as a Predictive Biomarker in Cancer Immunotherapy
Sandip Pravin Patel1, Razelle Kurzrock1

Abstract:

The resurgence of cancer immunotherapy stems from an improved understanding of the tumor microenvironment. The PD-1/PD-L1 axis is of particular interest, in light of promising data demonstrating a restoration of host immunity against tumors, with the prospect of durable remissions. Indeed, remarkable clinical responses have b... The resurgence of cancer immunotherapy stems from an improved understanding of the tumor microenvironment. The PD-1/PD-L1 axis is of particular interest, in light of promising data demonstrating a restoration of host immunity against tumors, with the prospect of durable remissions. Indeed, remarkable clinical responses have been seen in several different malignancies including, but not limited to, melanoma, lung, kidney, and bladder cancers. Even so, determining which patients derive benefit from PD-1/PD-L1-directed immunotherapy remains an important clinical question, particularly in light of the autoimmune toxicity of these agents. The use of PD-L1 (B7-H1) immunohistochemistry (IHC) as a predictive biomarker is confounded by multiple unresolved issues: variable detection antibodies, differing IHC cutoffs, tissue preparation, processing variability, primary versus metastatic biopsies, oncogenic versus induced PD-L1 expression, and staining of tumor versus immune cells. Emerging data suggest that patients whose tumors overexpress PD-L1 by IHC have improved clinical outcomes with anti-PD-1-directed therapy, but the presence of robust responses in some patients with low levels of expression of these markers complicates the issue of PD-L1 as an exclusionary predictive biomarker. An improved understanding of the host immune system and tumor microenvironment will better elucidate which patients derive benefit from these promising agents. read more read less

Topics:

Cancer immunotherapy (53%)53% related to the paper, Immunotherapy (52%)52% related to the paper, Tumor microenvironment (52%)52% related to the paper
View PDF
1,197 Citations
open accessOpen access Journal Article DOI: 10.1158/1535-7163.MCT-08-0013
Preclinical overview of sorafenib, a multikinase inhibitor that targets both Raf and VEGF and PDGF receptor tyrosine kinase signaling
Scott Wilhelm1, Lila Adnane, Philippa Newell, Augusto Villanueva, Josep M. Llovet, Mark Lynch

Abstract:

Although patients with advanced refractory solid tumors have poor prognosis, the clinical development of targeted protein kinase inhibitors offers hope for the future treatment of many cancers. In vivo and in vitro studies have shown that the oral multikinase inhibitor, sorafenib, inhibits tumor growth and disrupts tumor micr... Although patients with advanced refractory solid tumors have poor prognosis, the clinical development of targeted protein kinase inhibitors offers hope for the future treatment of many cancers. In vivo and in vitro studies have shown that the oral multikinase inhibitor, sorafenib, inhibits tumor growth and disrupts tumor microvasculature through antiproliferative, antiangiogenic, and/or proapoptotic effects. Sorafenib has shown antitumor activity in phase II/III trials involving patients with advanced renal cell carcinoma and hepatocellular carcinoma. The multiple molecular targets of sorafenib (the serine/threonine kinase Raf and receptor tyrosine kinases) may explain its broad preclinical and clinical activity. This review highlights the antitumor activity of sorafenib across a variety of tumor types, including renal cell, hepatocellular, breast, and colorectal carcinomas in the preclinical setting. In particular, preclinical evidence that supports the different mechanisms of action of sorafenib is discussed. read more read less

Topics:

Sorafenib (66%)66% related to the paper, Receptor tyrosine kinase (55%)55% related to the paper
View PDF
1,154 Citations
open accessOpen access Journal Article DOI: 10.1158/1535-7163.MCT-17-0386
Tumor Mutational Burden as an Independent Predictor of Response to Immunotherapy in Diverse Cancers.

Abstract:

Immunotherapy induces durable responses in a subset of patients with cancer. High tumor mutational burden (TMB) may be a response biomarker for PD-1/PD-L1 blockade in tumors such as melanoma and non-small cell lung cancer (NSCLC). Our aim was to examine the relationship between TMB and outcome in diverse cancers treated with ... Immunotherapy induces durable responses in a subset of patients with cancer. High tumor mutational burden (TMB) may be a response biomarker for PD-1/PD-L1 blockade in tumors such as melanoma and non-small cell lung cancer (NSCLC). Our aim was to examine the relationship between TMB and outcome in diverse cancers treated with various immunotherapies. We reviewed data on 1,638 patients who had undergone comprehensive genomic profiling and had TMB assessment. Immunotherapy-treated patients (N = 151) were analyzed for response rate (RR), progression-free survival (PFS), and overall survival (OS). Higher TMB was independently associated with better outcome parameters (multivariable analysis). The RR for patients with high (≥20 mutations/mb) versus low to intermediate TMB was 22/38 (58%) versus 23/113 (20%; P = 0.0001); median PFS, 12.8 months vs. 3.3 months (P ≤ 0.0001); median OS, not reached versus 16.3 months (P = 0.0036). Results were similar when anti-PD-1/PD-L1 monotherapy was analyzed (N = 102 patients), with a linear correlation between higher TMB and favorable outcome parameters; the median TMB for responders versus nonresponders treated with anti-PD-1/PD-L1 monotherapy was 18.0 versus 5.0 mutations/mb (P < 0.0001). Interestingly, anti-CTLA4/anti-PD-1/PD-L1 combinations versus anti-PD-1/PD-L1 monotherapy was selected as a factor independent of TMB for predicting better RR (77% vs. 21%; P = 0.004) and PFS (P = 0.024). Higher TMB predicts favorable outcome to PD-1/PD-L1 blockade across diverse tumors. Benefit from dual checkpoint blockade did not show a similarly strong dependence on TMB. Mol Cancer Ther; 16(11); 2598-608. ©2017 AACR. read more read less
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1,104 Citations
open accessOpen access Journal Article DOI: 10.1158/1535-7163.MCT-08-0017
Identification and characterization of NVP-BEZ235, a new orally available dual phosphatidylinositol 3-kinase/mammalian target of rapamycin inhibitor with potent in vivo antitumor activity

Abstract:

The phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin inhibitor (mTOR) pathway is often constitutively activated in human tumor cells, providing unique opportunities for anticancer therapeutic intervention. NVP-BEZ235 is an imidazo[4,5-c]quinoline derivative that inhibits PI3K and mTOR kinase activity by ... The phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin inhibitor (mTOR) pathway is often constitutively activated in human tumor cells, providing unique opportunities for anticancer therapeutic intervention. NVP-BEZ235 is an imidazo[4,5-c]quinoline derivative that inhibits PI3K and mTOR kinase activity by binding to the ATP-binding cleft of these enzymes. In cellular settings using human tumor cell lines, this molecule is able to effectively and specifically block the dysfunctional activation of the PI3K pathway, inducing G(1) arrest. The cellular activity of NVP-BEZ235 translates well in in vivo models of human cancer. Thus, the compound was well tolerated, displayed disease stasis when administered orally, and enhanced the efficacy of other anticancer agents when used in in vivo combination studies. Ex vivo pharmacokinetic/pharmacodynamic analyses of tumor tissues showed a time-dependent correlation between compound concentration and PI3K/Akt pathway inhibition. Collectively, the preclinical data show that NVP-BEZ235 is a potent dual PI3K/mTOR modulator with favorable pharmaceutical properties. NVP-BEZ235 is currently in phase I clinical trials. read more read less

Topics:

PI3K/AKT/mTOR pathway (61%)61% related to the paper, Kinase activity (58%)58% related to the paper, Protein kinase B (57%)57% related to the paper, RPTOR (56%)56% related to the paper, In vivo (54%)54% related to the paper
View PDF
1,079 Citations
open accessOpen access Journal Article
Specific inhibition of cyclin-dependent kinase 4/6 by PD 0332991 and associated antitumor activity in human tumor xenografts

Abstract:

PD 0332991 is a highly specific inhibitor of cyclin-dependent kinase 4 (Cdk4) (IC50, 0.011 micromol/L) and Cdk6 (IC50, 0.016 micromol/L), having no activity against a panel of 36 additional protein kinases. It is a potent antiproliferative agent against retinoblastoma (Rb)-positive tumor cells in vitro, inducing an exclusive ... PD 0332991 is a highly specific inhibitor of cyclin-dependent kinase 4 (Cdk4) (IC50, 0.011 micromol/L) and Cdk6 (IC50, 0.016 micromol/L), having no activity against a panel of 36 additional protein kinases. It is a potent antiproliferative agent against retinoblastoma (Rb)-positive tumor cells in vitro, inducing an exclusive G1 arrest, with a concomitant reduction of phospho-Ser780/Ser795 on the Rb protein. Oral administration of PD 0332991 to mice bearing the Colo-205 human colon carcinoma produces marked tumor regression. Therapeutic doses of PD 0332991 cause elimination of phospho-Rb and the proliferative marker Ki-67 in tumor tissue and down-regulation of genes under the transcriptional control of E2F. The results indicate that inhibition of Cdk4/6 alone is sufficient to cause tumor regression and a net reduction in tumor burden in some tumors. read more read less

Topics:

CDK4/6 Inhibition (60%)60% related to the paper, Tumor M2-PK (59%)59% related to the paper, Cyclin-dependent kinase 4 (57%)57% related to the paper, Cyclin-dependent kinase 6 (55%)55% related to the paper, Kinase (53%)53% related to the paper
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998 Citations
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Molecular Cancer Therapeutics 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 Molecular Cancer Therapeutics 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 Molecular Cancer Therapeutics 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 Molecular Cancer Therapeutics'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

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After uploading your paper on SciSpace, you would see a button to request a journal submission service for Molecular Cancer Therapeutics.

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 Molecular Cancer Therapeutics Endnote style, according to american-association-for-cancer-research guidelines.

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