Oncotarget, exhibited by its publisher Impact Journals, will be participating virtually at the AACR Annual Meeting this year, from April 10-15 and May 17-21, 2021.
Oncotarget participating in the Annual AACR Meeting 2021 #AACR
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The American Association for Cancer Research (AACR) organizes an annual meeting program covering some of the most recent discoveries in cancer research. The conference aims to highlight work from the best minds in research and medicine from institutions all over the world. Oncotarget, exhibited by its publisher Impact Journals, will be participating virtually at the AACR Annual Meeting this year.
As of June 2020, Scopus released their latest 2019 Journal Rankings on Oncology. Oncotarget is among their highest rated (Q1) journals and ranked number one in total citations in oncology. The journal has published outstanding papers and reviews by authors including Bert Vogelstein, Peter K. Vogt, Pier Paolo Pandolfi, Arnold J. Levine, Brian Druker, and Carol Prives. Founding Oncotarget Editorial Board members include Nobel Laureates Andrew V. Schally and Gregg L. Semenza; Lasker Award recipients Alexander Varshavsky, Brian J. Druker, and Gregg L. Semenza; and 16 members of the US National Academy of Sciences. Oncotarget is indexed and archived in PubMed, PubMed Central, Scopus, EMBASE, and META (Chan Zuckerberg Initiative) .
The 2021 AACR conference, a two-week online event, will take place from April 10-15 and May 17-21, 2021. Topics include population science and prevention, cancer biology, translational and clinical studies, survivorship, and advocacy.
In 2019, Oncotarget participated in the AACR Annual Meeting at the Georgia World Congress Center in Atlanta, Georgia, USA, and “AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics,” at the Hynes Convention Center in Boston, Massachusetts, USA. The total registration count from the 2019 AACR Annual Meeting was over 21,000—nearly 16,000 of which were scientific attendees from all over the world. Click here to view photos from Oncotarget’s participation in the 2019 AACR Annual Meeting.
Follow the Oncotarget Twitter account (@Oncotarget) for live updates about the conference using the #AACR21 hashtag.
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Young people living in the Andes Mountains are disproportionately affected by hepatocellular carcinoma compared to other youth around the world. Researchers conducted a study to better understand the cause.
Peru. View of the Urubamba River through the Aguascalientes Village.
The Trending with Impact series highlights Oncotarget publications attracting higher visibility among readers around the world online, in the news, and on social media—beyond normal readership levels. Look for future science news and articles about the latest trending publications here, and atOncotarget.com.
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Andean people live in sparsely populated regions in the Andes Mountains of South America. It is the longest mountain range in the world; spanning seven countries from southern Peru to southern Argentina. Due to the high elevations (averaging 13,000 feet; peaking at 22,834 feet), these areas are known for such low oxygen levels that Andean people have adapted physiologically to the extreme conditions.
Around the world, hepatocellular carcinoma (HCC) is the main form of primary liver cancer and commonly affects older patients after they have had prolonged liver disease. However, among Andean people, half of the total patients who develop HCC are adolescents and young adults. Researchers—from Sorbonne Université, Institut Pasteur, Université de Rennes, and Université de Toulouse in France, and the Instituto Nacional de Enfermedades Neoplásicas in Peru—conducted a study to better understand HCC in Andean people.
“To deepen our understanding of the molecular determinants of the disease in this population, we conducted an integrative analysis of gene expression and DNA methylation in HCC developed by 74 Peruvian patients, including 39 adolescents and young adults.”
The Study
“The 74 Peruvian patients with HCC included in the present study carried mitochondrial DNA (mtDNA) haplotypes of the four ancestral lineages (A–D) shared by Indigenous American populations (Figure 1A and Table 1) [23].”
The researchers retrospectively conducted transcriptome profiling of patient samples from 74 Peruvian patients with HCC. They compared gene expression data (after batch-effect removal) and found that Peruvian HCC is characterized as a distinct molecular subtype. This, now referred to as the “Amerind signature,” identifies Peruvian HCC as a distinct phenotypic cluster.
“A 961 gene signature was defined (hereinafter referred to as “Amerind signature”), of which 806 were upregulated and 155 downregulated in Peruvian HCC (Figure 3A and Supplementary Table 4).”
Methylome profiling was also conducted by the researchers to show the dynamics of DNA methylation marks, which revealed that Peruvian HCC is associated with a genome-wide hypermethylation pattern. They explain that DNA hydroxymethylation also represents a relevant epigenetic mark in Peruvian HCC. In addition, the researchers found evidence that Peruvian HCC tumor cells have a weaker retinoid signaling signature, which opens the door to potential therapeutic targets.
“The genomic analysis of Peruvian HCC evidenced a weaker retinoid signaling signature in tumor cells, which could pinpoint novel targets and drugs for anticancer targeted therapy (Figure 1C and Supplementary Table 1) [45]. We hypothesized that this weaker retinoid signaling could be responsible for the increased proliferation; hence, the pharmacological response to RA should antagonize this process.”
Conclusion
After comparing this sample of patients with Peruvian HCC with other HCC tumors from other countries around the world, molecular divergence in Peruvian HCC was demonstrated by showing “hierarchical clustering relying on a large and meaningful gene expression signature.” The researchers do not yet know if these differences are due to external/geographic or genomic factors.
“Whether this molecular phenotype is due to anthropological specificities embedded in genome architecture, to extrinsic etiological cues, or to subtle interplays between both components remains to be ascertained.”
With this being said, the researchers believe that this study stresses the need to carefully consider the potentially prominent roles of human genomic architecture and biogeography when it comes to cancer and underreported minorities and Indigenous patients, especially in low- and middle-income countries. They are forthcoming about limitations in their study and mention having analyzed a fairly small sized cohort. Importantly, the findings from this study create a case for developing therapeutics that are tailored to this new molecular subtype of HCC.
“The present study establishes a foundation for the dissection of the functional importance of RA-mediated epigenetic control in HCC and therapeutics tailored to patients with Indigenous American ancestry.”
Click here to read the full scientific study, published in Oncotarget.
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Oncotarget is a unique platform designed to house scientific studies in a journal format that is available for anyone to read—without a paywall making access more difficult. This means information that has the potential to benefit our societies from the inside out can be shared with friends, neighbors, colleagues and other researchers, far and wide.
Researchers in this study employed one of the few available murine cachexia models and validated its ability to be used in future studies of cancer-derived myocardial damage.
Part of Figure 2: Alterations in the myocardium of CT26-inoculated BALB/c mice.
The Trending with Impact series highlights Oncotarget publications attracting higher visibility among readers around the world online, in the news, and on social media—beyond normal readership levels. Look for future science news and articles about the latest trending publications here, and at Oncotarget.com.
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Cachexia, a complex metabolic syndrome characterized in part by the loss of muscle mass, can account for up to 30% of all cancer-related deaths. Myocardial atrophy, or cardiac remodeling/degradation, is a phenotype of cachexia and a common cause of death.
“The causes of cancer-derived myocardial impairment might be the effects of cancer itself, background heart disease, and influence of cancer treatments; however, they have not been given much clinical importance, and specific treatment efforts are delayed [8].”
Researchers from Nara Medical University, Hanna Central Hospital, and Hoshida Minami Hospital in Nara and Osaka, Japan, and Nantong University in Jiangsu Province, China, note that while myocardial damage in cancer patients is known to be a cause of death, there are few murine cachexia models available to evaluate cancer-derived heart disorders. Thus, there is a need for further studies that may allow researchers to establish an intervention to prevent myocardial damage in cancer patients.
“In this study, we used the mouse cancer cachexia model that we previously established [14] to examine the status of cancer-derived myocardial impairment reported in literature, and validate our model for studying cancer-derived myocardial impairment.”
The Study
Some causes of cancer-derived myocardial impairment have been reported as cancer-induced cytokines, oxidative stress, depletion of antioxidants, and protein catabolism as a result of AKT/mTOR inhibition.
“Despite these advances in our understanding, the multifactorial mechanisms underlying cancer-derived myocardial impairment remain incompletely understood, necessitating further investigations to elucidate the molecular mechanisms and prevent myocardial damage in cancer patients.”
The researchers previously established a mouse cancer cachexia model. In this study, they aimed to validate their model by employing it in the examination of cancer-derived myocardial impairment that has been reported in previous literature. Their study enlisted the mouse model, CT26 colon cancer cell cultures, protein extraction, histological analysis, immunoblot analysis, enzyme-linked immunosorbent assay (ELISA), mitochondrial stress tests (Seahorse assay), glycolytic stress tests, and statistical analysis.
Conclusion
“In summary, our established mouse cachexia model showed various myocardial changes associated with cancer cachexia such as oxidative stress in the myocardium, energy metabolism, autophagy, and inflammatory cytokines.”
Results obtained by the researchers in this study using their mouse cachexia model are congruent with previously reported results about cancerous myocardial damage, and therefore provide reasonable evidence that it may be used in future studies.
“The established mouse cachexia model can therefore be considered useful for analyzing cancer-derived myocardial damage.”
Click here to read the full scientific study, published in Oncotarget.
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Oncotarget is a unique platform designed to house scientific studies in a journal format that is available for anyone to read—without a paywall making access more difficult. This means information that has the potential to benefit our societies from the inside out can be shared with friends, neighbors, colleagues and other researchers, far and wide.
Researchers review different varieties of cannabinoids, the signaling pathways they affect, and their role in different types of cancer.
Close up of female Cannabis flower with a high production of cannabinoid resin
The Top-Performer series highlights research literature published in Oncotarget that has generated a high Altmetric score. Altmetric scores, located at the top-left of trending Oncotarget papers, provide an at-a-glance indication of the volume and type of online attention the research has received. Read Oncotarget’sTop 100 Altmetric papers.
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In a high-rated paper published in 2014 in Oncotarget, researchers from India’s Sanjay Gandhi Post Graduate Institute of Medical Sciences and the United States’ Ohio State University reviewed cannabinoids, their role in different types of cancer, and the signaling pathways they affect. Today, this paper currently presents with an Altmetric Attention score of 200.
“In this review article, we will focus on a broad range of cannabinoids, their receptor dependent and receptor independent functional roles against various cancer types with respect to growth, metastasis, energy metabolism, immune environment, stemness and future perspectives in exploring new possible therapeutic opportunities.”
Cannabinoids and Receptors
“[The] Cannabis sativa plant has been used for several hundreds of years both recreationally and medicinally.”
Researchers trace the earliest archaeological evidence of cannabis medical use back to ancient China, during the Han Dynasty. The use of this plant was recommended for rheumatic pain, constipation, disorders of the female reproductive tract, and malaria, among other conditions. Cannabis sativa contains three major classes of bioactive molecules; flavonoids, terpenoids, and 100+ types of cannabinoids.
Cannabinoids are a family of complex chemicals that activate and bind to two receptors in mammals named central cannabinoid receptor one (CB1) and peripheral cannabinoid receptor two (CB2). These receptors are found abundantly throughout the central nervous system and immune system.
“CB1/2 receptors are also responsible for proliferation, motility, invasion, adhesion and apoptosis of cancer cells both in vitro and in vivo.”
CB1 and CB2 receptors have been used as targets for the treatment of various diseases, including neurodegenerative diseases such as Alzheimer’s, Parkinson’s, and Huntington’s disease, neuropathic and inflammatory pain, glaucoma, multiple sclerosis, cardiovascular disorders, obesity, and more. Today, in addition to inhibiting nausea and emesis, stimulating appetite, improving mood, and relieving pain and insomnia that cancer patients face, cannabinoids used in the targeted killing of tumor cells has been a major discovery in cancer treatment.
“In this review article we focused on the role of cannabinoids in different cancer types and the respective signaling pathways.”
Endocannabinoids
“Endogenous cannabinoids which are produced in our body include lipid molecules containing long-chain polyunsaturated fatty acids, amides, esters and ethers that bind to CB1 or CB2 receptors.”
Endocannabinoids act primarily as neuromodulators, or reverse messengers, which can affect the release of neurotransmitters. They also play important role in regulating inflammation, insulin, and fat and energy metabolism, which affects our mood, appetite, pain sensation, inflammation response, and memory.
Phytocannabinoids
“Phytocannabinoids are only known to occur naturally in significant quantities in the cannabis plant, and are concentrated in a viscous resin that is produced in glandular structures known as trichomes.”
Over 120 phytocannabinoids are capable of interacting within the body’s own biological systems because their structures and behaviors mimic those of endocannabinoids (cannabinoids that are synthesized by our own bodies). The most prevalent natural cannabinoids are delta-9-tetrahydrocannabinol (∆9-THC), cannabidiol (CBD), and cannabinol (CBN).
Synthetic Cannabinoids
“Synthetic cannabinoids are classified on the basis of chemical structure of molecules and they are capable of a more selective activation of cannabinoid receptors [28].”
The researchers explain that synthetic cannabinoids have been used extensively in pharmacology to gain better insight about their action in order to evaluate the potential use of cannabinoids clinically.
Within the synthetic category, classical cannabinoids are compounds isolated from the Cannabis sativa plant or its synthetic analogs. Nonclassical cannabinoids “are a family of AC-bicyclic and ACD-tricyclic cannabinoid analogs.” Aminoalkylindoles are non-cannabinoid molecules given cannabis-mimicking capabilities. Eicosanoids are compounds that can enhance or inhibit physiological and pathophysiological responses. These lipid mediators also have an affinity for CB1 and CB2 receptors.
Cannabinoids in Cancer
Multiple studies have shown that THC, CBD, and synthetic cannabinoids can inhibit breast cancer cell proliferation and drive them toward apoptosis.
“It [breast cancer] is classified into three main subtypes according to their molecular profiles: hormone receptor-positive, HER2-positive (ErbB2-positive, a member of EGFR family) and triple-negative tumors [42-43]. Cannabinoid-based medicines have been useful for the treatment of these three breast cancer subtypes.”
In prostate cancer, CB1 and CB2 expression levels are often higher in prostate cancer tissues and several cell lines compared to normal prostate epithelial cells. Studies have found that cannabinoids have either induced cell death or activated pathways that lead to growth inhibition and increased patient survival.
Preclinical cancer models have shown that cannabinoids can alter gene expression, block enzymes, inhibit signaling pathways, and induce apoptosis in mice with lung cancer. In skin and pancreatic cancers, researchers have found that the activation of CB1/2 receptors induced the apoptotic death of tumorigenic cells, without affecting the normal cells. In bone cancer studies, researchers found that cannabinoids reduced pain and bone loss in mice.
“Cannabinoids could halt tumor development without side effects via specific targeting of CB1/CB2 receptor.”
Cannabinoids have anti-tumorigenic properties in glioma, lymphoma, oral cancers, and thyroid carcinoma. In young people, marijuana smoking has been found to increase the incidence of head and neck cancer, however, cannabinoids have anti-tumor properties.
Conclusion
“Cannabinoids exert a direct anti-proliferative effect on tumors of different origin.”
Given that cannabinoid receptors are often demonstrated to be expressed higher in tumor cells than in normal cells, cannabinoids are more specific to cancer cells than to normal cells. The researchers conclude their review by noting that it is important to identify which cannabinoids are most compatible with an individual cancer or disorder to have the greatest impact on patient outcome.
“It is important to understand which of the cannabinoid receptors are expressed and activated in different tumors as each receptor follows a different signaling mechanism.”
Click here to read the full scientific review, published in Oncotarget.
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Oncotarget is a unique platform designed to house scientific studies in a journal format that is available for anyone to read—without a paywall making access more difficult. This means information that has the potential to benefit our societies from the inside out can be shared with friends, neighbors, colleagues and other researchers, far and wide.
Oncotarget Special Collection: Lung CancerListen to an audio version of this post
Lung cancer is still the leading cause of cancer-related mortality worldwide. According to the CDC, smoking cigarettes is linked to 80-90% of lung cancer deaths in the United States. In non-smokers, lung cancer can be caused by exposure to radon, secondhand smoke, air pollution, asbestos, diesel exhaust, and other chemicals and factors.
Some symptoms of lung cancer include pain in chest or ribs, frequent respiratory infections, shortness of breath, wheezing, fatigue or loss of appetite. As numerous research studies about lung cancer are currently underway, we hope this Special Collection will set future research in motion to discover more causes and treatments for this disease.
Special Collections: Lung Cancer
Oncotarget publishes open access peer-reviewed literature about research studies, clinical studies, reviews, case reports, and meta-analyses on a variety of different topics pertaining to cancer. Lung cancer continues to be an area of interest for researchers, therefore, the Special Collection on Lung Cancer was created by Oncotarget for scientists and researchers to discover new biomarkers, mechanisms, and therapies to treat this cancer.
All content submitted for publication has been reviewed by a diligent board of academic editors and world-renowned scientists and researchers. In this Special Collection, the content focussing on lung cancer is organized together in one place, including papers such as “Molecular pathways and therapeutic targets in lung cancer” by Emma Shtivelman, Thomas Hensing, George R. Simon, Phillip A. Dennis, Gregory A. Otterson, Raphael Bueno, and Ravi Salgia. This review is a summary of the pathways and mechanisms involved in current treatment methods for lung cancer of various types.
Oncotarget is a unique platform designed to house scientific studies in a journal format that is available for anyone to read—without a paywall making access more difficult. This means information that has the potential to benefit our societies from the inside out can be shared with friends, neighbors, colleagues and other researchers, far and wide.
As you may know, Oncotarget is a scientific journal that publishes oncology-focused review and research papers every week on its open access platform — available at no cost to readers. Recently, a new Special Collections series debuted, and the first collection launched in honor of breast cancer awareness.
What makes our collections special?
Oncotarget carefully selects the most credible and insightful studies to publish on Oncotarget.com, while also choosing papers that link different fields of oncology, cancer research, and biomedical sciences together to eliminate borders between specialties. The term “oncotarget” encompasses all molecules, pathways, cellular functions, cell types, and tissues that can be viewed as targets relevant to cancer, as well as other diseases. This journal is a resource for oncology researchers and the larger scientific community.
Before a study is published in Oncotarget, selected papers are meticulously peer-reviewed by an editorial board of award-winning scientific editors from academic universities and institutions well-known for their excellence and precision. Click here for a complete list of Oncotarget Editorial Board members.
Breast cancer research
Each year, over 40,000 women and men lose the fight against breast cancer in the United States. After skin cancer, breast cancer is the most commonly diagnosed cancer in women. The spread of breast cancer awareness and increase in research funding has helped develop advances and discoveries in the diagnosis and treatment of this proliferous cancer.
The new Special Collections by Oncotarget are yet another tool researchers and science readers alike may use as a resource to learn more about breast cancer. The creators of these collections also hope that they may be used by scientists to discover new biomarkers, mechanisms, and therapies to improve our quality of life and better treat cancer and diseases.
Click here to explore the Special Collection on breast cancer.
A recent breakthrough medical study has revealed that exercise has been proven to combat breast cancer. The paper, entitled “Anticancer effect of physical activity is mediated by modulation of extracellular microRNA in blood,” was recently published in a June 2020 issue of the free online open-access medical journal Oncotarget. It was authored by an international team of medical researchers, headed by Dr. Alessandra Pulliero of the University of Genoa in Italy, and included Doctors Ming You, Pradeep Chaluvally-Raghavan, Barbara Marengo, Cinzia Domenicotti, Barbara Banelli, Paolo Degan, Luigi Molfetta, Fabio Gianiorio, and Alberto Izzotti.
While previous
medical studies have shown that physical activity reduces the risk of cancer,
particularly breast cancer, it’s been a mystery up to now exactly how this
happens. Medical researchers have long suspected that this healing process is
triggered by microRNAs, cellular fragments of RNA (ribonucleic acid) also known
as miRNAs.
What’s RNA?
Like DNA (deoxyribonucleic acid), RNA is one of the building blocks of life. It
acts as a messenger transmitting instructions that control the synthesis of
proteins. MicroRNAs stop a particular protein from being produced by binding
to, and then destroying, the messenger RNA that would have produced this
protein.
It is known
that miRNAs are incredibly important when it comes to carcinogenesis (the
creation of cancer) and cancer outcomes. In addition, MiRNAs regulate the creation
of muscle tissueand muscle mass,
and it’s been learned that structured exercise controls the creation of miRNA,
especially in skeletal muscle.
The research
team endeavored to test how exercise in breast cancer patients changed the
production of miRNA in their bodies. To begin, 30 women from northern Italy
between 54 and 78 years old walked for 45 minutes on the treadmill under
identical conditions. Blood samples were taken from them both before and after
the exercise sessions.
THE RESULTS
A technique
known as microarray analysis revealed that structured exercise modified 14
different extracellular miRNAs related to cancer. Structured exercise caused
all these miRNAs to decrease, except for a miRNA called miR-206, which
increased. The researchers discovered that the most striking effects induced by
exercise were changes in two miRNAs involved in breast cancer progression.
When the
researchers investigated the biological effects of these two miRNAs on human
breast cancer cells, they conclusively learned that working together, the
changes in these two microRNAs activated by a physical exercise program
suppressed breast cancer cells. Since too many miRNAs are linked to triggering
inflammation and the creation of lymphocytes (white blood cells in the lymph
system, which can influence breast cancer), the researchers also believe that
structured exercise might reduce inflammation by modulating miRNA in the blood.
They also found
that structured exercise improved blood pressure and glucose levels (cancerous
tumors feed on glucose) among participants. The doctors discovered that these
improvements in blood pressure and glucose levels helped regulate the miRNAs
being studied, and in turn helped the miRNAs combat cancer.
This
international team of researchers is confident that by testing for the levels
of these miRNAs in patients’ blood, they’ve achieved a non-invasive way of
establishing biomarkers (a measurable sign of whether a disease is present or
how severe it is) to prevent breast cancer. This is potentially a significant
breakthrough in breast cancer prevention and treatment.
As a result of
this study, the medical community now knows that structured exercise fights
breast cancer, and it’s been given a non-invasive way to diagnose and battle breast
cancer—and possibly other forms of cancers as well.
ABOUT ONCOTARGET
This important study was able to be published, and noticed so quickly, because it was made available by Impact Journals’ free, open-access cancer research journal Oncotarget. Currently, over 20,000 Oncotarget papers are also searchable on PubMed, a widely used free search engine for life sciences and biomedical research.
Because Oncotargetis open-access, it is free for everyone in the world to read. Most medical journals charge authors for publishing their work, and then in turn charge readers to access what could be all-important, life-saving information. With its revolutionary publishing model, Impact Journals, through publications like Oncotarget, makes it easy for anyone with important medical discoveries to communicate them to the public in the fastest and most effective way possible—possibly saving, prolonging, and improving many people’s lives in the process.
With the goal
of a life without disease, Impact Journals allows scientists to share their
exceptional discoveries, offers services that enable rapid dissemination of
results, and presents vital findings from the many fields of biomedical
science. It shares scientific findings through a comprehensive publication
process entailing peer review, manuscript preparation, and publication
promotion.
In addition, Oncotarget is well-known for publishing papers by Nobel Prize winners. The 2019 Nobel Prize in Physiology or Medicine was awarded jointly to Oncotarget Editorial Board members William G. Kaelin Jr., and Gregg L. Semenza for their discoveries of “how cells sense and adapt to oxygen availability,” which can help us understand and potentially treat a range of conditions like cancer, heart attack, stroke, and anemia. (They shared the Prize with UK physician-scientist Sir Peter J. Ratcliffe.) Both William G. Kaelin and Gregg L. Semenza are founding members of Oncotarget, where Gregg L. Semenza has published eight papers.
Another notable Oncotarget Nobel Prize winner is endocrinologist Andrew V. Schally, a member of Oncotarget’s Editorial Board who won the Nobel Prize in Physiology or Medicine in 1977 and who has published 12 papers in Oncotarget. Of Oncotarget’s work, he remarked: “Oncotarget is an outstanding and most important journal in the field of oncology and cancer research. Oncotarget is performing an extremely useful function for those of us working not only in cancer research, but also on other important topics in the field of medicine. Oncotarget deserves strong support from investigators working in the area of oncology as well as from the National Institutes of Health (NIH).”
If you would like to be first to learn about some of the most exciting new discoveries in medical science, consider investigating the groundbreaking work being published by Impact Journals, including its flagship publication, Oncotarget.
