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Example of BMC Cancer format Example of BMC Cancer format Example of BMC Cancer format Example of BMC Cancer format Example of BMC Cancer format Example of BMC Cancer format Example of BMC Cancer format Example of BMC Cancer format Example of BMC Cancer format Example of BMC Cancer format Example of BMC Cancer format Example of BMC Cancer format Example of BMC Cancer format Example of BMC Cancer format Example of BMC Cancer format Example of BMC Cancer format Example of BMC Cancer format Example of BMC Cancer format
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open access Open Access

BMC Cancer — Template for authors

Publisher: Springer
Categories Rank Trend in last 3 yrs
Oncology #107 of 340 down down by 17 ranks
Genetics #112 of 325 down down by 19 ranks
Cancer Research #96 of 207 down down by 17 ranks
journal-quality-icon Journal quality:
Good
calendar-icon Last 4 years overview: 4614 Published Papers | 25070 Citations
indexed-in-icon Indexed in: Scopus
last-updated-icon Last updated: 19/06/2020
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General info
Top papers
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FAQ

Related Journals

open access Open Access

Springer

Quality:  
Good
CiteRatio: 4.9
SJR: 1.322
SNIP: 1.034
open access Open Access

Springer

Quality:  
Good
CiteRatio: 4.1
SJR: 0.946
SNIP: 0.798
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

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.

3.15

7% from 2018

Impact factor for BMC Cancer from 2016 - 2019
Year Value
2019 3.15
2018 2.933
2017 3.288
2016 3.288
graph view Graph view
table view Table view

5.4

15% from 2019

CiteRatio for BMC Cancer from 2016 - 2020
Year Value
2020 5.4
2019 4.7
2018 5.0
2017 5.9
2016 5.4
graph view Graph view
table view Table view

insights Insights

  • Impact factor of this journal has increased by 7% in last year.
  • This journal’s impact factor is in the top 10 percentile category.

insights Insights

  • CiteRatio of this journal has increased by 15% 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.

1.358

15% from 2019

SJR for BMC Cancer from 2016 - 2020
Year Value
2020 1.358
2019 1.186
2018 1.336
2017 1.464
2016 1.488
graph view Graph view
table view Table view

1.218

19% from 2019

SNIP for BMC Cancer from 2016 - 2020
Year Value
2020 1.218
2019 1.021
2018 1.068
2017 1.103
2016 1.099
graph view Graph view
table view Table view

insights Insights

  • SJR of this journal has increased by 15% in last years.
  • This journal’s SJR is in the top 10 percentile category.

insights Insights

  • SNIP of this journal has increased by 19% in last years.
  • This journal’s SNIP is in the top 10 percentile category.

BMC Cancer

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Springer

BMC Cancer

Approved by publishing and review experts on SciSpace, this template is built as per for BMC Cancer formatting guidelines as mentioned in Springer author instructions. The current version was created on and has been used by 766 authors to write and format their manuscripts to this journal.

i
Last updated on
19 Jun 2020
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ISSN
1606-8610
i
Open Access
Yes
i
Sherpa RoMEO Archiving Policy
White faq
i
Plagiarism Check
Available via Turnitin
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Endnote Style
Download Available
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Citation Type
Numbered
[25]
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Bibliography Example
Blonder, G.E., Tinkham, M., Klapwijk, T.M.: Transition from metallic to tunneling regimes in superconducting microconstrictions: Excess current, charge imbalance, and supercurrent conversion. Phys. Rev. B 25(7), 4515–4532 (1982)

Top papers written in this journal

open accessOpen access Journal Article DOI: 10.1186/1471-2407-12-421
Hypoxic enhancement of exosome release by breast cancer cells
Hamish W King1, Michael Michael1, Jonathan M. Gleadle1
24 Sep 2012 - BMC Cancer

Abstract:

Exosomes are nanovesicles secreted by tumour cells which have roles in paracrine signalling during tumour progression, including tumour-stromal interactions, activation of proliferative pathways and bestowing immunosuppression. Hypoxia is an important feature of solid tumours which promotes tumour progression, angiogenesis an... Exosomes are nanovesicles secreted by tumour cells which have roles in paracrine signalling during tumour progression, including tumour-stromal interactions, activation of proliferative pathways and bestowing immunosuppression. Hypoxia is an important feature of solid tumours which promotes tumour progression, angiogenesis and metastasis, potentially through exosome-mediated signalling. Breast cancer cell lines were cultured under either moderate (1% O2) or severe (0.1% O2) hypoxia. Exosomes were isolated from conditioned media and quantitated by nanoparticle tracking analysis (NTA) and immunoblotting for the exosomal protein CD63 in order to assess the impact of hypoxia on exosome release. Hypoxic exosome fractions were assayed for miR-210 by real-time reverse transcription polymerase chain reaction and normalised to exogenous and endogenous control genes. Statistical significance was determined using the Student T test with a P value of < 0.05 considered significant. Exposure of three different breast cancer cell lines to moderate (1% O2) and severe (0.1% O2) hypoxia resulted in significant increases in the number of exosomes present in the conditioned media as determined by NTA and CD63 immunoblotting. Activation of hypoxic signalling by dimethyloxalylglycine, a hypoxia-inducible factor (HIF) hydroxylase inhibitor, resulted in significant increase in exosome release. Transfection of cells with HIF-1α siRNA prior to hypoxic exposure prevented the enhancement of exosome release by hypoxia. The hypoxically regulated miR-210 was identified to be present at elevated levels in hypoxic exosome fractions. These data provide evidence that hypoxia promotes the release of exosomes by breast cancer cells, and that this hypoxic response may be mediated by HIF-1α. Given an emerging role for tumour cell-derived exosomes in tumour progression, this has significant implications for understanding the hypoxic tumour phenotype, whereby hypoxic cancer cells may release more exosomes into their microenvironment to promote their own survival and invasion. read more read less

Topics:

Exosome (63%)63% related to the paper, Cancer cell (54%)54% related to the paper, Microvesicles (51%)51% related to the paper, Hypoxia (medical) (50%)50% related to the paper, Paracrine signalling (50%)50% related to the paper
View PDF
805 Citations
open accessOpen access Journal Article DOI: 10.1186/1471-2407-14-1
Prolyl-4-hydroxylase α subunit 2 promotes breast cancer progression and metastasis by regulating collagen deposition
Gaofeng Xiong1, Lei Deng1, Jieqing Zhu1, Piotr G. Rychahou1, Ren Xu1
02 Jan 2014 - BMC Cancer

Abstract:

Background Increased collagen deposition provides physical and biochemical signals to support tumor growth and invasion during breast cancer development. Therefore, inhibition of collagen synthesis and deposition has been considered a strategy to suppress breast cancer progression. Collagen prolyl-4-hydroxylase α subunit 2 (... Background Increased collagen deposition provides physical and biochemical signals to support tumor growth and invasion during breast cancer development. Therefore, inhibition of collagen synthesis and deposition has been considered a strategy to suppress breast cancer progression. Collagen prolyl-4-hydroxylase α subunit 2 (P4HA2), an enzyme hydroxylating proline residues in -X-Pro-Gly- sequences, is a potential therapeutic target for the disorders associated with increased collagen deposition. However, expression and function of P4HA2 in breast cancer progression are not well investigated. read more read less

Topics:

Collagen Type III (57%)57% related to the paper, Metastasis (55%)55% related to the paper, Breast cancer (53%)53% related to the paper, Procollagen-proline dioxygenase (51%)51% related to the paper
View PDF
670 Citations
open accessOpen access Journal Article DOI: 10.1186/S12885-015-1546-9
M1 and M2 macrophages derived from THP-1 cells differentially modulate the response of cancer cells to etoposide.
Marie Genin1, Francois Clement1, Antoine Fattaccioli1, Martine Raes1, Carine Michiels1
08 Aug 2015 - BMC Cancer

Abstract:

Background: Tumor associated macrophages (TAMs) are present in high density in solid tumors. TAMs share many characteristics with alternatively activated macrophages, also called M2. They have been shown to favor tumor development and a role in chemoresistance has also been suggested. Here, we investigated the effects of M2 i... Background: Tumor associated macrophages (TAMs) are present in high density in solid tumors. TAMs share many characteristics with alternatively activated macrophages, also called M2. They have been shown to favor tumor development and a role in chemoresistance has also been suggested. Here, we investigated the effects of M2 in comparison to M1 macrophages on cancer cell sensitivity to etoposide. Methods: We set up a model of macrophage polarization, starting from THP-1 monocytes differentiated into macrophages using PMA (Phorbol 12-myristate 13-acetate). Once differentiated (M0 macrophages), they were incubated with IL-4 and IL-13 in order to obtain M2 polarized macrophages or with IFN-gamma and LPS for classical macrophage activation (M1). To mimic the communication between cancer cells and TAMs, M0, M1 or M2 macrophages and HepG2 or A549 cancer cells were co-cultured during respectively 16 (HepG2) or 24 (A549) hours, before etoposide exposure for 24 (HepG2) or 16 (A549) hours. After the incubation, the impact of etoposide on macrophage polarization was studied and cancer cell apoptosis was assessed by western-blot for cleaved caspase-3 and cleaved PARP-1 protein, caspase activity assay and FACS analysis of Annexin V and PI staining. Results: mRNA and protein expression of M1 and M2 markers confirmed the polarization of THP-1-derived macrophages, which provide a new, easy and well-characterized model of polarized human macrophages. Etoposide-induced cancer cell apoptosis was markedly reduced in the presence of THP-1 M2 macrophages, while apoptosis was increased in cells co-cultured with M1 macrophages. On the other hand, etoposide did not influence M1 or M2 polarization. Conclusions: These results evidence for the first time a clear protective effect of M2 on the contrary to M1 macrophages on etoposide-induced cancer cell apoptosis. read more read less

Topics:

Myeloid-derived Suppressor Cell (64%)64% related to the paper, Macrophage polarization (64%)64% related to the paper, Macrophage-activating factor (63%)63% related to the paper, Interleukin 8 (61%)61% related to the paper, Adipose tissue macrophages (61%)61% related to the paper
View PDF
592 Citations
open accessOpen access Journal Article DOI: 10.1186/1471-2407-10-337
Cardiotoxicity of anthracycline agents for the treatment of cancer: systematic review and meta-analysis of randomised controlled trials
Lesley Smith, Victoria Cornelius, Chris Plummer1, Gill Levitt, Mark Verrill1, Peter Canney2, Alison Jones3
29 Jun 2010 - BMC Cancer

Abstract:

Background: We conducted a systematic review and meta-analysis to clarify the risk of early and late cardiotoxicity of anthracycline agents in patients treated for breast or ovarian cancer, lymphoma, myeloma or sarcoma. Methods: Randomized controlled trials were sought using comprehensive searches of electronic databases in J... Background: We conducted a systematic review and meta-analysis to clarify the risk of early and late cardiotoxicity of anthracycline agents in patients treated for breast or ovarian cancer, lymphoma, myeloma or sarcoma. Methods: Randomized controlled trials were sought using comprehensive searches of electronic databases in June 2008. Reference lists of retrieved articles were also scanned for additional articles. Outcomes investigated were early or late clinical and sub-clinical cardiotoxicity. Trial quality was assessed, and data were pooled through meta-analysis where appropriate. Results: Fifty-five published RCTs were included; the majority were on women with advanced breast cancer. A significantly greater risk of clinical cardiotoxicity was found with anthracycline compared with non-anthracycline regimens (OR 5.43 95% confidence interval: 2.34, 12.62), anthracycline versus mitoxantrone (OR 2.88 95% confidence interval: 1.29, 6.44), and bolus versus continuous anthracycline infusions (OR 4.13 95% confidence interval: 1.75, 9.72). Risk of clinical cardiotoxicity was significantly lower with epirubicin versus doxorubicin (OR 0.39 95% confidence interval: 0.20, 0.78), liposomal versus non-liposomal doxorubicin (OR 0.18 95% confidence interval: 0.08, 0.38) and with a concomitant cardioprotective agent (OR 0.21 95% confidence interval: 0.13, 0.33). No statistical heterogeneity was found for these pooled analyses. A similar pattern of results were found for subclinical cardiotoxicity; with risk significantly greater with anthracycline containing regimens and bolus administration; and significantly lower risk with epirubicin, liposomal doxorubicin versus doxorubicin but not epirubicin, and with concomitant use of a cardioprotective agent. Low to moderate statistical heterogeneity was found for two of the five pooled analyses, perhaps due to the different criteria used for reduction in Left Ventricular Ejection Fraction. Meta-analyses of any cardiotoxicity (clinical and subclinical) showed moderate to high statistical heterogeneity for four of five pooled analyses; criteria for any cardiotoxic event differed between studies. Nonetheless the pattern of results was similar to those for clinical or subclinical cardiotoxicity described above. read more read less

Topics:

Cardiotoxicity (60%)60% related to the paper, Epirubicin (60%)60% related to the paper, Anthracycline (59%)59% related to the paper, Confidence interval (55%)55% related to the paper, Lower risk (50%)50% related to the paper
View PDF
575 Citations
open accessOpen access Journal Article DOI: 10.1186/1471-2407-11-108
Interaction and uptake of exosomes by ovarian cancer cells
Cristina Escrevente, Sascha Keller1, Peter Altevogt1, Júlia Costa
27 Mar 2011 - BMC Cancer

Abstract:

Exosomes consist of membrane vesicles that are secreted by several cell types, including tumors and have been found in biological fluids. Exosomes interact with other cells and may serve as vehicles for the transfer of protein and RNA among cells. SKOV3 exosomes were labelled with carboxyfluoresceine diacetate succinimidyl-es... Exosomes consist of membrane vesicles that are secreted by several cell types, including tumors and have been found in biological fluids. Exosomes interact with other cells and may serve as vehicles for the transfer of protein and RNA among cells. SKOV3 exosomes were labelled with carboxyfluoresceine diacetate succinimidyl-ester and collected by ultracentrifugation. Uptake of these vesicles, under different conditions, by the same cells from where they originated was monitored by immunofluorescence microscopy and flow cytometry analysis. Lectin analysis was performed to investigate the glycosylation properties of proteins from exosomes and cellular extracts. In this work, the ovarian carcinoma SKOV3 cell line has been shown to internalize exosomes from the same cells via several endocytic pathways that were strongly inhibited at 4°C, indicating their energy dependence. Partial colocalization with the endosome marker EEA1 and inhibition by chlorpromazine suggested the involvement of clathrin-dependent endocytosis. Furthermore, uptake inhibition in the presence of 5-ethyl-N-isopropyl amiloride, cytochalasin D and methyl-beta-cyclodextrin suggested the involvement of additional endocytic pathways. The uptake required proteins from the exosomes and from the cells since it was inhibited after proteinase K treatments. The exosomes were found to be enriched in specific mannose- and sialic acid-containing glycoproteins. Sialic acid removal caused a small but non-significant increase in uptake. Furthermore, the monosaccharides D-galactose, α-L-fucose, α-D-mannose, D-N-acetylglucosamine and the disaccharide β-lactose reduced exosomes uptake to a comparable extent as the control D-glucose. In conclusion, exosomes are internalized by ovarian tumor cells via various endocytic pathways and proteins from exosomes and cells are required for uptake. On the other hand, exosomes are enriched in specific glycoproteins that may constitute exosome markers. This work contributes to the knowledge about the properties and dynamics of exosomes in cancer. read more read less

Topics:

Exosome (72%)72% related to the paper, Endosome (57%)57% related to the paper, Microvesicles (55%)55% related to the paper, Endocytosis (50%)50% related to the paper, Endocytic cycle (50%)50% related to the paper
View PDF
518 Citations
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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

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With SciSpace, you do not need a word template for BMC Cancer.

It automatically formats your research paper to Springer formatting guidelines and citation style.

You can download a submission ready research paper in pdf, LaTeX and docx formats.

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Time taken to format a paper and Compliance with guidelines

Plagiarism Reports via Turnitin

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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?

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Frequently asked questions

1. Can I write BMC Cancer in LaTeX?

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

2. Do you follow the BMC Cancer guidelines?

Yes, the template is compliant with the BMC Cancer 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 BMC Cancer?

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 BMC Cancer citation style.

4. Can I use the BMC Cancer 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 BMC Cancer.

5. Can I use a manuscript in BMC Cancer 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 BMC Cancer that you can download at the end.

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

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

7. Where can I find the template for the BMC Cancer?

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 BMC Cancer'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 BMC Cancer'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. BMC Cancer an online tool or is there a desktop version?

SciSpace's BMC Cancer 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 BMC Cancer?

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 BMC Cancer?”

11. What is the output that I would get after using BMC Cancer?

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

12. Is BMC Cancer'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 BMC Cancer?

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 BMC Cancer. 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 BMC Cancer?

The 5 most common citation types in order of usage for BMC Cancer 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 BMC Cancer?

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

16. Can I download BMC Cancer 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 BMC Cancer 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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