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Oncotarget
By Oncotarget PodcastScience
Oncotarget episodes
- BORIS Gene Mutation and Expression: Link to Breast Cancer ProgressionA new research paper was published in Oncotarget's Volume 14 on May 26, 2023, entitled, “Association of mutation and expression of the brother of the regulator of imprinted sites (BORIS) gene with breast cancer progression.”The brother of the regulator of imprinted sites (BORIS), 11 zinc-finger transcription factors, is a member of the cancer-testis antigen (CTA) family. It is mapped to chromosome number 20q13.2 and this region is genetically linked to the early onset of breast cancer.In the current study, researchers Mohammad Salman Akhtar, Naseem Akhter, Arshi Talat, Raed A. Alharbi, Abdulmajeed A.A. Sindi, Faisal Klufah, Hanan E. Alyahyawi, Abdulmohsen Alruwetei, Abrar Ahmad, Mazin A. Zamzami, SVS Deo, Syed Akhtar Husain, Osama A. Badi, and Mohammad Jahir Khan from Al-Baha University, Jamia Millia Islamia, ITS Dental College, Qassim University, King Abdulaziz University, All India Institute of Medical Sciences (AIIMS), Henry Ford Health System, and Jawahar Lal Nehru University analyzed the correlation between BORIS mutations and the expression of the protein in breast cancer cases.“The present study is to find out the mutations of BORIS genes in hot spot exons by PCR-SSCP and by automated DNA sequencing in breast cancer tissue samples along with adjacent normal samples.”A population-based study including a total of 155 breast cancer tissue samples and an equal number of normal adjacent tissues from Indian female breast cancer patients was carried out. Mutations of the BORIS gene were detected by polymerase chain reaction-single standard confirmation polymorphisms (PCR-SSCP) and automated DNA sequencing and by immunohistochemistry for BORIS protein expression were performed. The observed findings were correlated with several clinicopathological parameters to find out the clinical relevance of associations.“The BORIS mutations and high protein expression occur frequently in carcinoma of the breast suggesting their association with the onset and progression of breast carcinoma. Further, the BORIS has the potential to be used as a biomarker.”DOI - https://doi.org/10.18632/oncotarget.28442Correspondence to - Mohammad Salman Akhtar - [email protected], [email protected]Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28442Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - BORIS, breast cancer, mutation, transcription factor, PCR-SSCPAbout OncotargetOncotarget is a primarily oncology-focused, peer-reviewed, open access journal. Papers are published continuously within yearly volumes in their final and complete form, and then quickly released to Pubmed. On September 15, 2022, Oncotarget was accepted again for indexing by MEDLINE. Oncotarget is now indexed by Medline/PubMed and PMC/PubMed.To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us:SoundCloud - https://soundcloud.com/oncotargetFacebook - https://www.facebook.com/Oncotarget/Twitter - https://twitter.com/oncotargetInstagram - https://www.instagram.com/oncotargetjrnl/YouTube - https://www.youtube.com/@OncotargetJournalLinkedIn - https://www.linkedin.com/company/oncotargetPinterest - https://www.pinterest.com/oncotarget/Reddit - https://www.reddit.com/user/Oncotarget/Media Contact180092209574 min
- Deconstructing the Role of MALAT1 in MAPK-Signaling in MelanomaA new research paper was published in Oncotarget's Volume 14 on May 26, 2023, entitled, “Deconstructing the role of MALAT1 in MAPK-signaling in melanoma: insights from antisense oligonucleotide treatment.”The long non-coding RNA (lncRNA) MALAT1 is a regulator of oncogenesis and cancer progression. MAPK-pathway upregulation is the main event in the development and progression of human cancer, including melanoma and recent studies have shown that MALAT1 has a significant impact on the regulation of gene and protein expression in the MAPK pathway. However, the role of MALAT1 in regulation of gene and protein expression of the MAPK-pathway kinases RAS, RAF, MEK, and ERK in melanoma is largely unknown.In this study, researchers Valentin Feichtenschlager, Yixuan James Zheng, Wilson Ho, Linan Chen, Ciara Callanan, Christopher Chen, Albert Lee, Jose Ortiz, Klemens Rappersberger, and Susana Ortiz-Urda from the University of California San Francisco and Medical University Vienna demonstrated the impacts of antisense oligonucleotide (ASO)-based MALAT1-inhibition on MAPK-pathway gene regulation in melanoma.“Our results showed that MALAT1-ASO treatment decreased BRAF RNA expression and protein levels, and MALAT1 had increased correlation with MAPK-pathway associated genes in melanoma patient samples compared to healthy skin.”Additionally, drug-induced MAPK inhibition upregulated MALAT1-expression, a finding that resonates with a paradigm of MALAT1-expression presented in this work: MALAT1 is downregulated in melanoma and other cancer types in which MALAT1 seems to be associated with MAPK-signaling, while MALAT1-ASO treatment strongly reduced the growth of melanoma cell lines, even in cases of resistance to MEK inhibition. MALAT1-ASO treatment significantly inhibited colony formation in vitro and reduced tumor growth in an NRAS-mutant melanoma xenograft mouse model in vivo, while showing no aberrant toxic side effects.“Our findings demonstrate new insights into MALAT1-mediated MAPK-pathway gene regulation and a paradigm of MALAT1 expression in MAPK-signaling-dependent cancer types. MALAT1 maintains essential oncogenic functions, despite being downregulated.”DOI - https://doi.org/10.18632/oncotarget.28447Correspondence to - Valentin Feichtenschlager - [email protected]Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28447Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - MALAT1, MAPK-pathway, BRAF, melanoma, antisense oligonucleotidesAbout OncotargetOncotarget is a primarily oncology-focused, peer-reviewed, open access journal. Papers are published continuously within yearly volumes in their final and complete form, and then quickly released to Pubmed. On September 15, 2022, Oncotarget was accepted again for indexing by MEDLINE. Oncotarget is now indexed by Medline/PubMed and PMC/PubMed.To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us:SoundCloud - https://soundcloud.com/oncotargetFacebook - https://www.facebook.com/Oncotarget/Twitter - https://twitter.com/oncotargetInstagram - https://www.instagram.com/oncotargetjrnl/YouTube - https://www.youtube.com/@OncotargetJournalLinkedIn - https://www.linkedin.com/company/oncotargetPinterest - https://www.pinterest.com/oncotarget/Reddit - https://www.reddit.com/user/Oncotarget/Media Contact180092209574 min
- Can the Creatine Shuttle be Targeted to Fight Colorectal Cancer?Blog summary: “Role of creatine shuttle in colorectal cancer cells.”_____________________________________________Since the 1992 Barcelona Olympics, creatine supplementation has increased in popularity and grown to widespread use among the mainstream public. Creatine is a naturally occurring compound, primarily stored in skeletal muscle and involved in energy production for high-intensity activities—enhancing performance and supporting muscle growth and strength. The process by which creatine is transported into the muscles and utilized for energy production is referred to as the creatine shuttle. While it is a useful mechanism for healthy muscles, the creatine shuttle has also been implicated in cancer.“The creatine shuttle is highlighted in cancer as a source of energy for cancer cells that display aggressive proliferation, and aberrant creatine kinase (CK) levels are known to be associated with many malignancies and mitotic control [7].”In a new study, researchers Mayu Kita, Rina Fujiwara-Tani, Shingo Kishi, Shiori Mori, Hitoshi Ohmori, Chie Nakashima, Kei Goto, Takamitsu Sasaki, Kiyomu Fujii, Isao Kawahara, Ujjal Kumar Bhawal, Yi Luo, and Hiroki Kuniyasu from Nara Medical University, Saveetha University and Nantong University hypothesized that the creatine shuttle is involved in energy metabolism and other adenosine triphosphate (ATP) supply in cancer cells. On May 19, 2023, their new research paper was published in Oncotarget’s Volume 14, entitled, “Role of creatine shuttle in colorectal cancer cells.”Full blog - https://www.oncotarget.org/2023/05/25/can-the-creatine-shuttle-be-targeted-to-fight-colorectal-cancer/DOI - https://doi.org/10.18632/oncotarget.28436Correspondence to - Hiroki Kuniyasu - [email protected], and Rina Fujiwara-Tani - [email protected]Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28436Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - creatine kinase B, mitochondrial creatine kinase, ATP metabolism, phosphorylation signal, stemnessAbout OncotargetOncotarget is a primarily oncology-focused, peer-reviewed, open access journal. Papers are published continuously within yearly volumes in their final and complete form, and then quickly released to Pubmed. On September 15, 2022, Oncotarget was accepted again for indexing by MEDLINE. Oncotarget is now indexed by Medline/PubMed and PMC/PubMed.To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us:SoundCloud - https://soundcloud.com/oncotargetFacebook - https://www.facebook.com/Oncotarget/Twitter - https://twitter.com/oncotargetInstagram - https://www.instagram.com/oncotargetjrnl/YouTube - https://www.youtube.com/@OncotargetJournalLinkedIn - https://www.linkedin.com/company/oncotargetPinterest - https://www.pinterest.com/oncotarget/Reddit - https://www.reddit.com/user/Oncotarget/Media Contact180092209577 min
- Behind the Study: Molecular Dialogue Between Tumor Cells and FibroblastsDr. Gopal C. Kundu from KIIT Deemed to be University in Odisha, India, describes a recent editorial he co-authored that was published by Oncotarget in Volume 14, entitled, “The molecular dialogue between the tumor cells and fibroblasts.”DOI - https://doi.org/10.18632/oncotarget.28405Correspondence to - Gopal C. Kundu - [email protected]Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28405Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - CAFs, heterogeneity, myofibroblasts, drug resistance, osteopontinAbout OncotargetOncotarget is a primarily oncology-focused, peer-reviewed, open access journal. Papers are published continuously within yearly volumes in their final and complete form, and then quickly released to Pubmed. On September 15, 2022, Oncotarget was accepted again for indexing by MEDLINE. Oncotarget is now indexed by Medline/PubMed and PMC/PubMed.To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us:SoundCloud - https://soundcloud.com/oncotargetFacebook - https://www.facebook.com/Oncotarget/Twitter - https://twitter.com/oncotargetInstagram - https://www.instagram.com/oncotargetjrnl/YouTube - https://www.youtube.com/@OncotargetJournalLinkedIn - https://www.linkedin.com/company/oncotargetPinterest - https://www.pinterest.com/oncotarget/Reddit - https://www.reddit.com/user/Oncotarget/Media Contact180092209577 min
- HER3: Survival Pathway and Therapeutic Target in Metastatic Colorectal and Pancreatic CancerA new research perspective was published in Oncotarget's Volume 14 on May 10, 2023, entitled, “HER3- A key survival pathway and an emerging therapeutic target in metastatic colorectal cancer and pancreatic ductal adenocarcinoma.”Colorectal cancer (CRC) and pancreatic ductal adenocarcinoma (PDAC) are highly metastatic cancers with poor survival rates. The tumor microenvironment has been shown to play a critical role in cancer progression and response to therapies. Endothelial cells (ECs) are a key component of the tumor microenvironment and promote cancer cell survival by secreting soluble factors that activate cancer-promoting signaling pathways.In this new perspective, researchers Omkar Desai and Rui Wang from Case Western Reserve University and University Hospitals Cleveland Medical Center discuss their studies and others that have identified HER3 as a key mediator of liver EC-induced chemoresistance and cancer cell growth in metastatic CRC and PDAC.“In complement to our studies, prior preclinical studies have shown that HER3-targeted therapies with antibodies and inhibitors have been effective in blocking tumor growth in several types of cancers [22, 23], specifically breast cancer [24], head and neck squamous cell carcinoma (HNSCC) [25], PDAC [25], and non-small cell lung cancer (NSCLC) [26]. However, translating the preclinical findings to clinical studies has shown limited impact on patient outcomes.”In this article, the researchers discuss that HER3-targeted therapies may be effective in treating patients with HER3-expressing CRC and PDAC, and highlight the importance of applying HER3 expression as a predictive biomarker for patient response to HER3-targeted therapies. They also discuss the challenges encountered in past clinical trials of HER3-targeted therapies, including the role of NRG1 gene fusions, alternative HER3 activation mechanisms, and adaptive resistance mechanisms. Finally, the team concludes by suggesting the future directions of HER3-targeted therapies, including novel approaches to overcome chemoresistance and promote cancer cell death.“In summary, we discovered that the surrounding liver EC microenvironment plays a key role in activating HER3 and promoting cell survival in mCRC and mPDAC, and potentially other types of cancer that metastasize to the liver.”DOI - https://doi.org/10.18632/oncotarget.28421Correspondence to - Rui Wang - [email protected]Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28421Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - HER3, colorectal, pancreatic cancer, metastasis, microenvironmentAbout OncotargetOncotarget is a primarily oncology-focused, peer-reviewed, open access journal. Papers are published continuously within yearly volumes in their final and complete form, and then quickly released to Pubmed. On September 15, 2022, Oncotarget was accepted again for indexing by MEDLINE. Oncotarget is now indexed by Medline/PubMed and PMC/PubMed.To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us:SoundCloud - https://soundcloud.com/oncotargetFacebook - https://www.facebook.com/Oncotarget/Twitter - https://twitter.com/oncotargetInstagram - https://www.instagram.com/oncotargetjrnl/YouTube - https://www.youtube.com/@OncotargetJournalLinkedIn - https://www.linkedin.com/company/oncotargetPinterest - https://www.pinterest.com/oncotarget/Reddit - https://www.reddit.com/user/Oncotarget/Media Contact180092209574 min
- GPR141 Regulates Breast Cancer Progression via Oncogenic Mediators and the p-mTOR/p53 AxisA new research paper was published in Oncotarget's Volume 14 on May 19, 2023, entitled, “G-protein-coupled receptor 141 mediates breast cancer proliferation and metastasis by regulating oncogenic mediators and the p-mTOR/p53 axis.”Breast cancer morbidity is surging towards the peak in females across the globe. An inherent property of cancer cells is enhanced cell proliferation rate and migration capability, leading to deregulated cell signaling cascades. G-protein-coupled receptors (GPCRs) have recently emerged as a hot-spot target in cancer research.Researchers Monalisa Parija, Amit K. Adhya and Sandip K. Mishra from the Institute of Life Sciences, Regional Centre for Biotechnology and All India Institute of Medical Sciences identified aberrant expression of G-protein-coupled receptor 141 (GPR141) in different breast cancer subtypes that correlate with poor prognosis. However, the molecular mechanism via which GPR141 advances breast cancer remains elusive. Increased GPR141 expression enhances the migratory behavior of breast cancer, driving oncogenic pathways both in vitro and in vivo through activation of epithelial to mesenchymal transition (EMT), oncogenic mediators and regulation of p-mTOR/p53 signaling.“Our study unveils a molecular mechanism for p53 downregulation and activation of p-mTOR1 and its substrates in GPR141 overexpressed cells, accelerating breast tumorigenesis.”In their current study, the researchers found that an E3 ubiquitin ligase, Cullin1, partly mediates p53 degradation via proteasomal pathway. Co-immunoprecipitation results show that the phosphorylated form of 40S ribosome protein S6 (ps6., a p-mTOR1 substrate) forms a complex with Cullin1. These findings suggest an interplay between Cullin1 and p-mTOR1 in GPR141 overexpressed cells that downregulates p53 expression, thus inducing tumor growth.GPR141 silencing restores p53 expression and attenuates p-mTOR1 signaling events, thereby impeding proliferation and migration in breast cancer cells. Their findings describe the role of GPR141 in breast cancer proliferation, and metastasis, as well as in influencing the tumor microenvironment. Modulating GPR141 expression could pave the way for a better therapeutic approach to regulating breast cancer progression and metastasis.“In conclusion, our research highlights the gain of function of GPR141 drives breast tumorigenesis by inducing tumor cell properties via the p-mTOR1/p53 axis, altering EMT markers, and enhancing oncogenic mediators.”DOI - https://doi.org/10.18632/oncotarget.28433Correspondence to - Sandip K. Mishra - [email protected]Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28433Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - G-protein-coupled receptor 141, cell migration, metastasis, p-mTOR, p53About OncotargetOncotarget is a primarily oncology-focused, peer-reviewed, open access journal. Papers are published continuously within yearly volumes in their final and complete form, and then quickly released to Pubmed. On September 15, 2022, Oncotarget was accepted again for indexing by MEDLINE. Oncotarget is now indexed by Medline/PubMed and PMC/PubMed.To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us:SoundCloud - https://soundcloud.com/oncotargetFacebook - https://www.facebook.com/Oncotarget/Twitter - https://twitter.com/oncotargetInstagram - https://www.instagram.com/oncotargetjrnl/YouTube - https://www.youtube.com/@OncotargetJournalLinkedIn - https://www.linkedin.com/company/oncotargetPinterest - https://www.pinterest.com/oncotarget/Reddit - https://www.reddit.com/user/Oncotarget/Media Contact180092209574 min
- Targeting Cellular Respiration as a Therapeutic Strategy in GlioblastomaA new research perspective was published in Oncotarget's Volume 14 on May 4, 2023, entitled, “Targeting cellular respiration as a therapeutic strategy in glioblastoma.”While glycolysis is abundant in malignancies, mitochondrial metabolism is significant as well. Mitochondria harbor the enzymes relevant for cellular respiration, which is a critical pathway for both regeneration of reduction equivalents and energy production in the form of ATP.In this research perspective, researchers Enyuan Shang, Trang Thi Thu Nguyen, Mike-Andrew Westhoff, Georg Karpel-Massler, and Markus D. Siegelin from Columbia University Medical Center, City University of New York and Ulm University Medical Center discuss their recent finding that FDA-approved HDAC-inhibitors may have a profound impact on energy metabolism in solid tumor cells, including glioblastoma (GBM).“Because of the impact of HDAC-inhibitors on metabolism we hypothesized that imipridones, which suppress cellular respiration, might synergize with these compounds to significantly enhance killing of GBM cells [38]. Indeed, we found that imipridones reversed HDAC-inhibitor induced activation of cellular respiration and in turn the combination treatment facilitated induction of intrinsic apoptosis in a manner that was partially reliant on the anti-apoptotic Bcl-2 family members.”The oxidation of NADH2 and FADH2 are fundamental since NAD and FAD are the key components of the TCA-cycle that is critical to entertain biosynthesis in cancer cells. The TCA-cycle itself is predominantly fueled through carbons from glucose, glutamine, fatty acids and lactate.Targeting mitochondrial energy metabolism appears feasible through several drug compounds that activate the CLPP protein or interfere with NADH-dehydrogenase, pyruvate-dehydrogenase, enzymes of the TCA-cycle and mitochondrial matrix chaperones. While these compounds have demonstrated anti-cancer effects in vivo, recent research suggests which patients most likely benefit from such treatments.“In summary, targeting tumor cell metabolism is relevant and future research needs to identify patient populations that particularly benefit from such treatments. Moreover, while most studies related to metabolism still rest predominantly on the tumor cells it is critical to extend such observations to the microenvironment of the tumors, especially with regards to the immune system [41, 42].”DOI - https://doi.org/10.18632/oncotarget.28424Correspondence to - Markus D. Siegelin - [email protected]Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28424Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - glioblastoma, metabolism, lactate, carbon tracing, central carbon metabolismAbout OncotargetOncotarget is a primarily oncology-focused, peer-reviewed, open access journal. Papers are published continuously within yearly volumes in their final and complete form, and then quickly released to Pubmed. On September 15, 2022, Oncotarget was accepted again for indexing by MEDLINE. Oncotarget is now indexed by Medline/PubMed and PMC/PubMed.To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us:SoundCloud - https://soundcloud.com/oncotargetFacebook - https://www.facebook.com/Oncotarget/Twitter - https://twitter.com/oncotargetInstagram - https://www.instagram.com/oncotargetjrnl/YouTube - https://www.youtube.com/@OncotargetJournalLinkedIn - https://www.linkedin.com/company/oncotargetPinterest - https://www.pinterest.com/oncotarget/Reddit - https://www.reddit.com/user/Oncotarget/Media Contact180092209574 min
- Impact Journals (Oncotarget's Publisher) at SSP 45th Annual MeetingImpact Journals (Oncotarget's publisher) will be participating as an exhibitor at the Society for Scholarly Publishing (SSP) 45th Annual Meeting, which convenes on May 31–June 2, 2023, at the Oregon Convention Center & Hyatt Regency Portland in Portland, Oregon, USA. This year, the SSP’s meeting theme is: “Transformation, Trust, and Transparency.”“The pace of change in our industry continues unabated, with seismic shifts in areas such as the dissemination of research, business models, and the nature of the workplace. And yet, while pressure for change has become the new normal, fundamental change has proved more elusive. We invite you to join us in highlighting the Trust and Transparency issues that underlie many of the challenges we face and exploring what it takes to create more meaningful Transformation in scholarly publishing.” (Source: sspnet.org)Visit booth No. 216 at the SSP 45th Annual Meeting to connect with members of the Impact Journals team.About Impact Journals:Impact Journals publishes scholarly journals in the biomedical sciences with a focus on all areas of cancer and aging research. Our mission is to provide scientists with the opportunity to share their exceptional discoveries, to offer services that enable rapid dissemination of results, and to present vital findings from the many fields of biomedical science. Our goal is life without disease.To learn more about Impact Journals, visit www.ImpactJournals.com.Connect with us on social media to stay updated on journals published by Impact Journals:Oncotarget Twitter – https://twitter.com/OncotargetAging Twitter – https://twitter.com/AgingJrnlOncotarget Facebook – https://www.facebook.com/OncotargetAging Facebook – https://www.facebook.com/AgingUSOncotarget YouTube – https://www.youtube.com/@OncotargetJournalAging YouTube – https://www.youtube.com/@AgingJournalOncotarget LinkedIn – https://www.linkedin.com/company/oncotarget/Aging LinkedIn – https://www.linkedin.com/company/agingFor media requests, please contact [email protected].2 min
- Automated, Accurate Reporting for NGS-Based Clonality TestingA new research paper was published in Oncotarget's Volume 14 on May 12, 2023, entitled, “Development and implementation of an automated and highly accurate reporting process for NGS-based clonality testing.”B and T cells undergo random recombination of the VH/DH/JH portions of the immunoglobulin loci (B cell) and T-cell receptors before becoming functional cells. When one V-J rearrangement is over-represented in a population of B or T cells indicating an origin from a single cell, this indicates a clonal process. Clonality aids in the diagnosis and monitoring of lymphoproliferative disorders and evaluation of disease recurrence.In a new study, researchers Sean T. Glenn, Phillip M. Galbo Jr., Jesse D. Luce, Kiersten Marie Miles, Prashant K. Singh, Manuel J. Glynias, and Carl Morrison from Roswell Park Comprehensive Cancer Center aimed to develop objective criteria, which can be automated, to classify B and T cell clonality results as positive (clonal), No evidence of clonality, or invalid (failed).“Using clinical samples with “gold standard” clonality data obtained using PCR/CE testing, we ran NGS-based amplicon clonality assays and developed our own model for clonality reporting.”To assess the performance of their model, the researchers analyzed the NGS results across other published models. Their model for clonality calling using NGS-based technology increases the assay’s sensitivity, more accurately detecting clonality. In addition, they built a computational pipeline to use their model to objectively call clonality in an automated fashion.“Collectively the results outlined below will have a direct clinical impact by expediting the review and sign-out process for concise clonality reporting.”DOI - https://doi.org/10.18632/oncotarget.28429Correspondence to - Sean T. Glenn - [email protected]Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28429Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - clonality, NGS, bioinformatics, molecular diagnostics, leukemiaAbout OncotargetOncotarget is a primarily oncology-focused, peer-reviewed, open access journal. Papers are published continuously within yearly volumes in their final and complete form, and then quickly released to Pubmed. On September 15, 2022, Oncotarget was accepted again for indexing by MEDLINE. Oncotarget is now indexed by Medline/PubMed and PMC/PubMed.To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us:SoundCloud - https://soundcloud.com/oncotargetFacebook - https://www.facebook.com/Oncotarget/Twitter - https://twitter.com/oncotargetInstagram - https://www.instagram.com/oncotargetjrnl/YouTube - https://www.youtube.com/@OncotargetJournalLinkedIn - https://www.linkedin.com/company/oncotargetPinterest - https://www.pinterest.com/oncotarget/Reddit - https://www.reddit.com/user/Oncotarget/Media Contact180092209573 min
- Reaching the Brain Through the Groin: A Novel Approach to Brain CancerBlog summary: “From the groin to the brain: a transfemoral path to blood-brain barrier opening.”___________________________________________Just a small number of molecules, including alcohol and caffeine, are able to cross the blood-brain barrier (BBB). The BBB is a highly selective semipermeable membrane that separates circulating blood from extracellular fluid in the brain. It plays a critical role in protecting the brain from harmful substances in the blood while also maintaining a stable and consistent environment for neuronal function. Without the BBB, humans would be at the mercy of any harmful toxin, pathogen and unwanted substance that could cross from the bloodstream into the brain.This protective function also makes it difficult to deliver therapeutic agents to the brain, as the majority of drugs and other molecules are unable to cross the BBB. This is particularly problematic for the treatment of brain-localized diseases, including brain cancers and neurological disorders, which require high concentrations of drugs to effectively target sites in the brain. In a new editorial paper, researchers Thomas C. Chen, Weijun Wang and Axel H. Schönthal from the University of Southern California‘s Keck School of Medicine discuss a series of preclinical studies that introduced the novel concept of intraarterial (IA) injection of NEO100—a promising strategy aimed at temporarily and safely opening the BBB up for therapeutic treatment. Their editorial was published in Oncotarget’s Volume 14 on May 4, 2023, entitled, “From the groin to the brain: a transfemoral path to blood-brain barrier opening.”“It is believed that procedures to open the BBB in a controlled and safe fashion might provide tremendous advantages by allowing optimal brain entry of any and all circulating therapeutics.”Full blog - https://www.oncotarget.org/2023/05/11/reaching-the-brain-through-the-groin-a-novel-approach-to-brain-cancer/Paper DOI - https://doi.org/10.18632/oncotarget.28414Correspondence to - Thomas C. Chen - [email protected], and Axel H. Schönthal - [email protected]Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28414Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - brain metastases, glioma, NEO100, perillyl alcohol, transfemoral cannulationAbout OncotargetOncotarget is a primarily oncology-focused, peer-reviewed, open access journal. Papers are published continuously within yearly volumes in their final and complete form, and then quickly released to Pubmed. On September 15, 2022, Oncotarget was accepted again for indexing by MEDLINE. Oncotarget is now indexed by Medline/PubMed and PMC/PubMed.To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us:SoundCloud - https://soundcloud.com/oncotargetFacebook - https://www.facebook.com/Oncotarget/Twitter - https://twitter.com/oncotargetInstagram - https://www.instagram.com/oncotargetjrnl/YouTube - https://www.youtube.com/@OncotargetJournalLinkedIn - https://www.linkedin.com/company/oncotargetPinterest - https://www.pinterest.com/oncotarget/Reddit - https://www.reddit.com/user/Oncotarget/Media Contact180092209579 min
About Oncotarget
From the publisher's feed
Oncotarget is a primarily oncology-focused, peer-reviewed, open access journal. Papers are published continuously within yearly volumes in their final and complete form and then quickly released to Pubmed.
Oncotarget is now indexed by MEDLINE, PubMed and PMC/PubMed.
Read about the Oncotarget Scientific Integrity Process: https://www.oncotarget.com/scientific_integrity/