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Example of Pharmacogenomics and Personalized Medicine format Example of Pharmacogenomics and Personalized Medicine format Example of Pharmacogenomics and Personalized Medicine format Example of Pharmacogenomics and Personalized Medicine format Example of Pharmacogenomics and Personalized Medicine format Example of Pharmacogenomics and Personalized Medicine format Example of Pharmacogenomics and Personalized Medicine format Example of Pharmacogenomics and Personalized Medicine format Example of Pharmacogenomics and Personalized Medicine format Example of Pharmacogenomics and Personalized Medicine format Example of Pharmacogenomics and Personalized Medicine format Example of Pharmacogenomics and Personalized Medicine format Example of Pharmacogenomics and Personalized Medicine format Example of Pharmacogenomics and Personalized Medicine format Example of Pharmacogenomics and Personalized Medicine format Example of Pharmacogenomics and Personalized Medicine format Example of Pharmacogenomics and Personalized Medicine format Example of Pharmacogenomics and Personalized Medicine format Example of Pharmacogenomics and Personalized Medicine format
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open access Open Access

Pharmacogenomics and Personalized Medicine — Template for authors

Publisher: Dove Medical Press
Categories Rank Trend in last 3 yrs
Pharmacology #132 of 297 down down by 107 ranks
Molecular Medicine #106 of 167 down down by 82 ranks
journal-quality-icon Journal quality:
Good
calendar-icon Last 4 years overview: 157 Published Papers | 663 Citations
indexed-in-icon Indexed in: Scopus
last-updated-icon Last updated: 05/07/2020
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Related Journals

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Taylor and Francis

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CiteRatio: 10.4
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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.

4.2

14% from 2019

CiteRatio for Pharmacogenomics and Personalized Medicine from 2016 - 2020
Year Value
2020 4.2
2019 4.9
2018 5.3
2017 8.4
2016 7.4
graph view Graph view
table view Table view

0.845

13% from 2019

SJR for Pharmacogenomics and Personalized Medicine from 2016 - 2020
Year Value
2020 0.845
2019 0.967
2018 0.965
2017 1.353
2016 1.208
graph view Graph view
table view Table view

1.323

17% from 2019

SNIP for Pharmacogenomics and Personalized Medicine from 2016 - 2020
Year Value
2020 1.323
2019 1.135
2018 0.848
2017 1.555
2016 1.099
graph view Graph view
table view Table view

insights Insights

  • CiteRatio of this journal has decreased by 14% in last years.
  • This journal’s CiteRatio is in the top 10 percentile category.

insights Insights

  • SJR of this journal has decreased by 13% in last years.
  • This journal’s SJR is in the top 10 percentile category.

insights Insights

  • SNIP of this journal has increased by 17% in last years.
  • This journal’s SNIP is in the top 10 percentile category.

Pharmacogenomics and Personalized Medicine

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Dove Medical Press

Pharmacogenomics and Personalized Medicine

Pharmacogenomics and Personalized Medicine is an international, peer-reviewed, open-access journal characterizing the influence of genotype on pharmacology leading to the development of personalized treatment programs and individualized drug selection for improved safety, effi...... Read More

Pharmacology

Molecular Medicine

Pharmacology, Toxicology and Pharmaceutics

i
Last updated on
05 Jul 2020
i
ISSN
1178-7066
i
Open Access
Yes
i
Sherpa RoMEO Archiving Policy
Blue faq
i
Plagiarism Check
Available via Turnitin
i
Endnote Style
Download Available
i
Bibliography Name
unsrt
i
Citation Type
Numbered
[25]
i
Bibliography Example
C. W. J. Beenakker. Specular andreev reflection in graphene. Phys. Rev. Lett., 97(6):067007, 2006.

Top papers written in this journal

open accessOpen access Journal Article DOI: 10.2147/PGPM.S38295
Human ABC transporter ABCG2/BCRP expression in chemoresistance: basic and clinical perspectives for molecular cancer therapeutics
Kohji Noguchi1, Kazuhiro Katayama1, Yoshikazu Sugimoto1

Abstract:

Adenine triphosphate (ATP)-binding cassette (ABC) transporter proteins, such as ABCB1/P-glycoprotein (P-gp) and ABCG2/breast cancer resistance protein (BCRP), transport various structurally unrelated compounds out of cells. ABCG2/BCRP is referred to as a “half-type” ABC transporter, functioning as a homodimer, and transports ... Adenine triphosphate (ATP)-binding cassette (ABC) transporter proteins, such as ABCB1/P-glycoprotein (P-gp) and ABCG2/breast cancer resistance protein (BCRP), transport various structurally unrelated compounds out of cells. ABCG2/BCRP is referred to as a “half-type” ABC transporter, functioning as a homodimer, and transports anticancer agents such as irinotecan, 7-ethyl-10-hydroxycamptothecin (SN-38), gefitinib, imatinib, methotrexate, and mitoxantrone from cells. The expression of ABCG2/BCRP can confer a multidrug-resistant phenotype on cancer cells and affect drug absorption, distribution, metabolism, and excretion in normal tissues, thus modulating the in vivo efficacy of chemotherapeutic agents. Clarification of the substrate preferences and structural relationships of ABCG2/BCRP is essential for our understanding of the molecular mechanisms underlying its effects in vivo during chemotherapy. Its single-nucleotide polymorphisms are also involved in determining the efficacy of chemotherapeutics, and those that reduce the functional activity of ABCG2/BCRP might be associated with unexpected adverse effects from normal doses of anticancer drugs that are ABCG2/BCRP substrates. Importantly, many recently developed molecular-targeted cancer drugs, such as the tyrosine kinase inhisbitors, imatinib mesylate, gefitinib, and others, can also interact with ABCG2/BCRP. Both functional single-nucleotide polymorphisms and inhibitory agents of ABCG2/BCRP modulate the in vivo pharmacokinetics and pharmacodynamics of these molecular cancer treatments, so the pharmacogenetics of ABCG2/BCRP is an important consideration in the application of molecular-targeted chemotherapies. read more read less

Topics:

Imatinib mesylate (58%)58% related to the paper, Abcg2 (51%)51% related to the paper, ATP-binding cassette transporter (50%)50% related to the paper
View PDF
160 Citations
open accessOpen access Journal Article DOI: 10.2147/PGPM.S23462
Association of the 5-HTT gene-linked promoter region (5-HTTLPR) polymorphism with psychiatric disorders: review of psychopathology and pharmacotherapy.

Abstract:

Serotonin (5-HT) regulates important biological and psychological processes including mood, and may be associated with the development of several psychiatric disorders. An association between psychopathology and genes that regulate 5-HT neurotransmission is a robust area of research. Identification of the genes responsible fo... Serotonin (5-HT) regulates important biological and psychological processes including mood, and may be associated with the development of several psychiatric disorders. An association between psychopathology and genes that regulate 5-HT neurotransmission is a robust area of research. Identification of the genes responsible for the predisposition, development, and pharmacological response of various psychiatric disorders is crucial to the advancement of our understanding of their underlying neurobiology. This review highlights research investigating 5-HT transporter (5-HTTLPR) polymorphism, because studies investigating the impact of the 5-HTTLPR polymorphism have demonstrated significant associations with many psychiatric disorders. Decreased transcriptional activity of the S allele ("risk allele") may be associated with a heightened amygdala response leading to anxiety-related personality traits, major depressive disorder, suicide attempts, and bipolar disorder. By contrast, increased transcriptional activity of the L allele is considered protective for depression but is also associated with completed suicide, nicotine dependence, and attention deficit hyperactivity disorder. For some disorders, such as post-traumatic stress disorder and major depressive disorder, the research suggests that treatment response may vary by allele (such as an enhanced response to serotonin specific reuptake inhibitors in patients with major depressive disorder and post-traumatic stress disorder with L alleles), and for alcohol dependence, the association and treatment for S or L alleles may vary with alcoholic subtype. While some studies suggest that 5-HTTLPR polymorphism can moderate the response to pharmacotherapy, the association between 5-HTTLPR alleles and therapeutic outcomes is inconsistent. The discovery of triallelic 5-HTTLPR alleles (L(A)/L(G)/S) may help to explain some of the conflicting results of many past association studies, while concurrently providing more meaningful data in the future. Studies assessing 5-HTTLPR as the solitary genetic factor contributing to the etiology of psychiatric disorders continue to face the challenges of statistically small effect sizes and limited replication. read more read less

Topics:

Major depressive disorder (62%)62% related to the paper, Bipolar disorder (59%)59% related to the paper, Attention deficit hyperactivity disorder (57%)57% related to the paper, 5-HTTLPR (56%)56% related to the paper, Psychopathology (52%)52% related to the paper
View PDF
137 Citations
open accessOpen access Journal Article DOI: 10.2147/PGPM.S52762
Clinical potential of novel therapeutic targets in breast cancer: CDK4/6, Src, JAK/STAT, PARP, HDAC, and PI3K/AKT/mTOR pathways.
Sarah R. Hosford1, Todd W. Miller1

Abstract:

Breast cancers expressing estrogen receptor α, progesterone receptor, or the human epidermal growth factor receptor 2 (HER2) proto-oncogene account for approximately 90% of cases, and treatment with antiestrogens and HER2-targeted agents has resulted in drastically improved survival in many of these patients. However, de novo... Breast cancers expressing estrogen receptor α, progesterone receptor, or the human epidermal growth factor receptor 2 (HER2) proto-oncogene account for approximately 90% of cases, and treatment with antiestrogens and HER2-targeted agents has resulted in drastically improved survival in many of these patients. However, de novo or acquired resistance to antiestrogen and HER2-targeted therapies is common, and many tumors will recur or progress despite these treatments. Additionally, the remaining 10% of breast tumors are negative for estrogen receptor α, progesterone receptor, and HER2 (“triple-negative”), and a clinically proven tumor-specific drug target for this group has not yet been identified. Therefore, the identification of new therapeutic targets in breast cancer is of vital clinical importance. Preclinical studies elucidating the mechanisms driving resistance to standard therapies have identified promising targets including cyclin-dependent kinase 4/6, phosphoinositide 3-kinase, poly adenosine diphosphate–ribose polymerase, Src, and histone deacetylase. Herein, we discuss the clinical potential and status of new therapeutic targets in breast cancer. read more read less

Topics:

Estrogen receptor (59%)59% related to the paper, Antiestrogen (56%)56% related to the paper, Breast cancer (56%)56% related to the paper, Progesterone receptor (55%)55% related to the paper, Palbociclib (53%)53% related to the paper
View PDF
115 Citations
open accessOpen access Journal Article DOI: 10.2147/PGPM.S63715
Pharmacogenomic knowledge gaps and educational resource needs among physicians in selected specialties.

Abstract:

BACKGROUND The use of pharmacogenomic testing in the clinical setting has the potential to improve the safety and effectiveness of drug therapy, yet studies have revealed that physicians lack knowledge about the topic of pharmacogenomics, and are not prepared to implement it in the clinical setting. This study further explore... BACKGROUND The use of pharmacogenomic testing in the clinical setting has the potential to improve the safety and effectiveness of drug therapy, yet studies have revealed that physicians lack knowledge about the topic of pharmacogenomics, and are not prepared to implement it in the clinical setting. This study further explores the pharmacogenomic knowledge deficit and educational resource needs among physicians. MATERIALS AND METHODS Surveys of primary care physicians, cardiologists, and psychiatrists were conducted. RESULTS Few physicians reported familiarity with the topic of pharmacogenomics, but more reported confidence in their knowledge about the influence of genetics on drug therapy. Only a small minority had undergone formal training in pharmacogenomics, and a majority reported being unsure what type of pharmacogenomic tests were appropriate to order for the clinical situation. Respondents indicated that an ideal pharmacogenomic educational resource should be electronic and include such components as how to interpret pharmacogenomic test results, recommendations for prescribing, population subgroups most likely to be affected, and contact information for laboratories offering pharmacogenomic testing. CONCLUSION Physicians continue to demonstrate pharmacogenomic knowledge gaps, and are unsure about how to use pharmacogenomic testing in clinical practice. Educational resources that are clinically oriented and easily accessible are preferred by physicians, and may best support appropriate clinical implementation of pharmacogenomics. read more read less

Topics:

Pharmacogenomic Testing (73%)73% related to the paper, Pharmacogenomic Test (58%)58% related to the paper, Knowledge deficit (56%)56% related to the paper, Population (51%)51% related to the paper
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110 Citations
open accessOpen access Journal Article DOI: 10.2147/PGPM.S115741
Treatment-resistant schizophrenia: current insights on the pharmacogenomics of antipsychotics.
John Lally1, Fiona Gaughran2, Philip Timms3, Sarah R Curran4

Abstract:

Up to 30% of people with schizophrenia do not respond to two (or more) trials of dopaminergic antipsychotics. They are said to have treatment-resistant schizophrenia (TRS). Clozapine is still the only effective treatment for TRS, although it is underused in clinical practice. Initial use is delayed, it can be hard for patient... Up to 30% of people with schizophrenia do not respond to two (or more) trials of dopaminergic antipsychotics. They are said to have treatment-resistant schizophrenia (TRS). Clozapine is still the only effective treatment for TRS, although it is underused in clinical practice. Initial use is delayed, it can be hard for patients to tolerate, and clinicians can be uncertain as to when to use it. What if, at the start of treatment, we could identify those patients likely to respond to clozapine - and those likely to suffer adverse effects? It is likely that clinicians would feel less inhibited about using it, allowing clozapine to be used earlier and more appropriately. Genetic testing holds out the tantalizing possibility of being able to do just this, and hence the vital importance of pharmacogenomic studies. These can potentially identify genetic markers for both tolerance of and vulnerability to clozapine. We aim to summarize progress so far, possible clinical applications, limitations to the evidence, and problems in applying these findings to the management of TRS. Pharmacogenomic studies of clozapine response and tolerability have produced conflicting results. These are due, at least in part, to significant differences in the patient groups studied. The use of clinical pharmacogenomic testing - to personalize clozapine treatment and identify patients at high risk of treatment failure or of adverse events - has moved closer over the last 20 years. However, to develop such testing that could be used clinically will require larger, multicenter, prospective studies. read more read less

Topics:

Pharmacogenomic Testing (60%)60% related to the paper, Clozapine (52%)52% related to the paper, Tolerability (50%)50% related to the paper
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101 Citations
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Frequently asked questions

1. Can I write Pharmacogenomics and Personalized Medicine in LaTeX?

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

2. Do you follow the Pharmacogenomics and Personalized Medicine guidelines?

Yes, the template is compliant with the Pharmacogenomics and Personalized Medicine 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 Pharmacogenomics and Personalized Medicine?

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 Pharmacogenomics and Personalized Medicine citation style.

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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 Pharmacogenomics and Personalized Medicine.

5. Can I use a manuscript in Pharmacogenomics and Personalized Medicine 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 Pharmacogenomics and Personalized Medicine that you can download at the end.

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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 Pharmacogenomics and Personalized Medicine?

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 Pharmacogenomics and Personalized Medicine. 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 Pharmacogenomics and Personalized Medicine?

The 5 most common citation types in order of usage for Pharmacogenomics and Personalized Medicine 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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16. Can I download Pharmacogenomics and Personalized Medicine 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 Pharmacogenomics and Personalized Medicine Endnote style according to Elsevier guidelines.

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