Oncotarget

Oncotarget

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Oncotarget episodes

  • Zika Virus as a Treatment for Brain Cancer: A Systematic Review
    BUFFALO, NY- October 9, 2024 – A new #review was #published in Oncotarget's Volume 15 on September 30, 2024, entitled, “Zika virus and brain cancer: Can Zika be an effective treatment for brain cancer? A systematic review.”
    As highlighted in the introduction of this review, many studies have identified oncolytic viruses as a promising new class of therapeutic agents for central nervous system (CNS) tumors, particularly glioblastomas (GBM). Zika virus (ZIKV) proteins, specifically targeting certain stem cells, have shown promising results in both in vitro and animal model studies.
    In their review, researchers Mateus Gonçalves de Sena Barbosa, Beatriz Rodrigues Messias, Rafael Trindade Tatit, Maycon Cristian Gomes de Paula, Valdecir Boeno Spenazato Júnior, Maria Gabriella Borges Braga, Caio Vinícius Marcolino Santos, Luiza D'Ottaviano Cobos, Vinícius Otávio da Silva, Eberval Gadelha Figueiredo, Nicollas Nunes Rabelo, and Bipin Chaurasia from Atenas University Center, Passos; University of Israelita de Ciências da Saúde Albert Einstein; University of Sapucaí Valley; Atenas University Center, Sete Lagoas; Nove de Julho University, Campus Vergueiro; José do Rosário Vellano University, Alfenas; School of Medicine-University of São Paulo (FMUSP), Hospital das Clínicas/FMUSP; and Neurosurgery Clinic in Birgunj, evaluated the efficacy and safety of using ZIKV for treating CNS tumors. Data from in vivo studies were extracted and assessed for bias using the Robins-I tool, evaluating factors such as selection, performance, detection, attrition, and reporting bias.
    The 14 studies demonstrated that ZIKV reduced cell viability, inhibited the growth and proliferation of glioma stem cells (GSCs), and decreased Bcl2 expression, potentially enhancing chemotherapy and radiotherapy effects. ZIKV caused cytopathic effects, induced tumor cell damage, showed oncolytic properties, and selectively killed GSCs safely. This ultimately led to significant tumor remission and improved long-term survival through an enhanced T-cell response.
    “Although current evidence suggests ZIKV as a promising treatment for CNS tumors and may improve survival when combined with surgery and radiotherapy.”
    DOI - https://doi.org/10.18632/oncotarget.28647
    Correspondence to - Bipin Chaurasia - [email protected]
    Video short - https://www.youtube.com/watch?v=JINORGdqAO4
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    Keywords - cancer, Zika, neurotropism, glioblastoma, glioma, brain tumor
    About Oncotarget
    Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.
    Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).
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    4 min
  • Lessons from ACDC-RP Trial: Designing Neoadjuvant Therapy Trials for Prostatectomy
    Oncotarget #published this #editorial on September 30, 2024, in Volume 15, entitled “Lessons from the ACDC-RP trial: Clinical trial design for radical prostatectomy neoadjuvant therapy trials” by Rashid K. Sayyid and Neil E. Fleshner from the Division of Urologic Oncology, Princess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada.
    DOI - https://doi.org/10.18632/oncotarget.28648
    Correspondence to - Rashid K. Sayyid - [email protected]
    Video short - https://www.youtube.com/watch?v=APkPoTlXBWY
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    Keywords - cancer, clinical trial, prostatic neoplasms, neoadjuvant therapy, chemotherapy; androgen receptor agonist
    About Oncotarget
    Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.
    Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).
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    4 min
  • Key Roles of MIF, DDT, and CD74 in Melanoma Prognosis and Therapy
    Macrophage Migration Inhibitory Factor (MIF) and its homolog D-dopachrome Tautomerase (DDT) have been implicated as drivers of tumor progression in various cancers. Recent evidence suggests that MIF could be a therapeutic target in immune checkpoint inhibition (ICI) resistant melanomas; however, clinical evidence for MIF, and particularly for DDT, remains limited.
    Researchers Caroline Naomi Valdez, Gabriela Athziri Sánchez-Zuno, Lais Osmani, Wael Ibrahim, Anjela Galan, Antonietta Bacchiocchi, Ruth Halaban, Rajan P. Kulkarni, Insoo Kang, Richard Bucala, and Thuy Tran from Yale University; Oregon Health and Science University; Cancer Early Detection Advanced Research Center (CEDAR); and the Department of Veterans Affairs Portland Health Care System analyzed 97 patients treated at Yale for melanoma between 2002–2020. Their research paper was published in Oncotarget’s Volume 15 on July 19, 2024, entitled, “Prognostic and therapeutic insights into MIF, DDT, and CD74 in melanoma.”
    Full blog - https://www.oncotarget.org/2024/08/28/key-roles-of-mif-ddt-and-cd74-in-melanoma-prognosis-and-therapy/
    Paper DOI - https://doi.org/10.18632/oncotarget.28615
    Correspondence to - Thuy Tran - [email protected]
    Video short - https://www.youtube.com/watch?v=ULlzscn0PvQ
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    Keywords - cancer, MIF, DDT, melanoma, immune checkpoint inhibition, cancer transcriptomics
    About Oncotarget
    Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.
    Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).
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    5 min
  • miR-10b Inhibition: A Strategy for Treating Metastatic Breast Cancer
    BUFFALO, NY- August 28, 2024 – A new #research paper was #published in Oncotarget's Volume 15 on August 26, 2024, entitled, “Inhibition of miR-10b treats metastatic breast cancer by targeting stem cell-like properties.”
    As stated within the Abstract of the paper, despite advances in breast cancer screening and treatment, the prognosis for metastatic disease remains dismal, with only a 30% five-year survival rate. This poor outcome is largely due to the failure of current therapeutics to target the unique properties of metastatic cells. One of the key drivers of metastasis is miR-10b, a small noncoding RNA implicated in cancer cell invasion, migration, viability, and proliferation.
    Researchers Alan Halim, Nasreen Al-Qadi, Elizabeth Kenyon, Kayla N. Conner, Sujan Kumar Mondal, Zdravka Medarova, and Anna Moore from Michigan State University’s Precision Health Program, College of Human Medicine, and College of Veterinary Medicine, and Transcode Therapeutics Inc. in Newton, Massachusetts, provide transcriptional evidence that inhibiting miR-10b with MN-anti-miR10b—a nanodrug designed to deliver anti-miR-10b antisense oligomers to cancer cells—activates developmental processes in cancer cells. They observed increased miR-10b expression in stem-like cancer cells.
    In mouse models of metastatic triple-negative breast cancer, MN-anti-miR10b has been shown to prevent the onset of metastasis and eliminate existing metastases when combined with chemotherapy, even after treatment has been discontinued.
    "Our results demonstrate that inhibition of miR-10b using MN-anti-miR10b decreases the stemness of breast cancer cells, supporting dedifferentiation as a mechanism through which the nanodrug may function as a therapy."
    DOI - https://doi.org/10.18632/oncotarget.28641
    Correspondence to - Anna Moore - [email protected]
    Video short - https://www.youtube.com/watch?v=BtaZd_iV8dI
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    Keywords - cancer, breast cancer, metastasis, stem-like cells, nanoparticle, miR-10b
    About Oncotarget
    Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.
    Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).
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    3 min
  • Artificial Intelligence: Revolutionizing Precision Oncology
    BUFFALO, NY- August 27, 2024 – A new #editorial was #published in Oncotarget's Volume 15 on August 26, 2024, entitled, “Artificial intelligence: A transformative tool in precision oncology.”
    Artificial intelligence (AI) is revolutionizing society and healthcare, opening new possibilities for precision medicine. In oncology, immunotherapy (IO) has similarly transformed cancer treatment with novel therapeutic mechanisms, but it has also introduced atypical response patterns that challenge traditional evaluation methods.
    In this editorial, researchers Jeremy McGale, Matthew J. Liao, Egesta Lopci, Aurélien Marabelle, and Laurent Dercle from the Department of Radiology at Columbia University in New York, explore AI's role in addressing these challenges. They focus on the development of new biomarkers for precise disease characterization, particularly those using imaging for the early response assessment of cancer patients treated with IO.
    Additionally, the researchers highlight a comprehensive review that applied AI/radiomics to cross-sectional imaging (PET, CT, MRI) showcasing the current landscape in IO treatment. They also determined that of 87 relevant studies, most utilized algorithms to predict treatment response or prognosticate survival at predetermined time points.
    “In conclusion, although AI/Radiomics in IO is a rapidly advancing field, there remains significant room for improvement.”
    DOI - https://doi.org/10.18632/oncotarget.28639
    Correspondence to - Jeremy McGale - [email protected], and Laurent Dercle - [email protected]
    Video short - https://www.youtube.com/watch?v=FyZVKeUaUOs
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    Keywords - cancer, immunotherapy, oncology, artificial intelligence, radiomics, lactate, dehydrogenase, PET, MRI, CT, SPECT
    About Oncotarget
    Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.
    Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).
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    3 min
  • Genotype Matters: Tailored Screening for Germline CHEK2 Variants
    BUFFALO, NY- August 26, 2024 – A new #editorial was #published in Oncotarget's Volume 15 on July 10, 2024, entitled, “Genotype matters: Personalized screening recommendations for germline CHEK2 variants.”
    Recognized as a moderate-risk gene, CHEK2—responsible for encoding the CHK2 protein, which plays a crucial role in the repair of DNA double-strand breaks—is associated with a 20–40% lifetime risk of breast cancer (BC) by age 85. While CHEK2 pathogenic variants (PVs) were previously linked to an increased risk of colorectal cancer (CRC), two recent studies have not observed this association.
    In their recent work, researchers Adela Rodriguez Hernandez, Rochelle Scheib, Judy E. Garber, Huma Q. Rana and Brittany L. Bychkovsky from Dana-Farber Cancer Institute and Harvard Medical School in Boston, found that a CHEK2 PV does not increase the CRC risk compared with controls (odds ratio 0.62 (0.51–0.76), p < .001).
    The cancer risks associated with CHEK2 PVs vary depending on the variant type, and risk management strategies should reflect this variability. The CHEK2 c.1100del is the most studied truncating variant and has been crucial to our understanding of the cancer phenotype. Cancer risks seem to be higher with truncating variants compared to missense variants.
    “In our study, we postulated that these differences were driven by three common low-risk (LR) missense variants: p.I157T, p.S428F, and p.T476M, all of which have a BC odds ratio of <1.4.”
    In summary, CHEK2 is recognized as a moderate-risk gene for breast cancer. Further large-scale, prospective studies are needed to clarify its potential associations with prostate, kidney, and thyroid cancers, as well as to establish appropriate screening measures.
    DOI - https://doi.org/10.18632/oncotarget.28604
    Correspondence to - Brittany L. Bychkovsky - [email protected]
    Video short - https://www.youtube.com/watch?v=KYHCdGz8c3I
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    Keywords - cancer, CHEK2, pathogenic or likely pathogenic variants, germline
    About Oncotarget
    Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.
    Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).
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    3 min
  • Disrupting NKG2A:HLA-E Interactions for Enhanced Anti-Cancer Immunity
    BUFFALO, NY- August 21, 2024 – A new #editorial was #published in Oncotarget's Volume 15 on July 17, 2024, entitled, “Strategies to disrupt NKG2A:HLA-E interactions for improved anti-cancer immunity.”
    Two studies using CRISPR screens in cancer cells identified HLA-E as a critical negative regulator of NK cell interactions with cancer cells. Consistent with this, IFNγ signaling was associated with NK cell resistance due to increased STAT1 activation and enhanced HLA-E expression. This effect is also evident in the murine homolog of HLA-E, Qa-1b, which was upregulated by inflammatory signals across all cell types tested.
    In addition to inflammatory signals, researchers Jack G. Fisher, Lara V. Graham, and Matthew D. Blunt from Clinical and Experimental Sciences, Faculty of Medicine at the University of Southampton, UK, recently demonstrated that surface expression of HLA-E is increased by lymph node-associated signals IL-4 and CD40L on primary chronic lymphocytic leukaemia (CLL) cells.
    Additionally, two recent studies have shown that HLA-E can protect circulating tumor cells from NK cell lysis via NKG2A, suggesting that targeting the NKG2A axis could be a promising strategy for preventing metastasis in solid tumors.
    “In conclusion, there is strong preclinical evidence that disruption of NKG2A interactions with HLA-E can stimulate both NK cell and cytotoxic T cell effector functions against cancer.”
    DOI - https://doi.org/10.18632/oncotarget.28610
    Correspondence to - Matthew D. Blunt - [email protected]
    Video short - https://www.youtube.com/watch?v=iQREIa-RToU
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    Keywords - cancer, Natural killer (NK) cells, immunotherapy, NKG2A, immune checkpoint blockade, HLA-E
    About Oncotarget
    Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.
    Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).
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    3 min
  • Role of the Gut Barrier in Colorectal Cancer Treatment
    BUFFALO, NY- August 19, 2024 – A new #review was #published in Oncotarget's Volume 15 on August 14, 2024, entitled, “The gut barrier as a gatekeeper in colorectal cancer treatment.”
    Colorectal cancer (CRC) is highly prevalent and a major cause of cancer-related deaths worldwide. The primary curative treatment for CRC is surgical resection of the affected bowel segment. However, postoperative complications often include a weakened gut barrier and the dissemination of bacterial proinflammatory lipopolysaccharides.
    Researchers Roy Hajjar, Carole Richard, and Manuela M. Santos from Centre de recherche du Centre hospitalier de l’Université de Montréal (CRCHUM), Québec; Centre hospitalier de l’Université de Montréal (CHUM), Québec; Université de Montréal, Québec; and Institut du cancer de Montréal, Québec, discuss how gut microbiota and microbial metabolites regulate basal inflammation levels in the gut and the healing process of the bowel after surgery.
    “We and others have shown in the last few years that gut microbiota influences the healing process of the bowel and the restoration of the gut barrier after surgery.”
    The researchers further elaborate on the restoration of gut barrier function in CRC patients and how this potentially impacts the dissemination and implantation of CRC cells in extracolonic tissues, thereby contributing to worse survival outcomes after surgery.
    “Based on our recent work, we believe that weakened gut barrier function, namely due to poor healing after surgery, leads to persistent systemic low-grade inflammation and a higher risk of local and systemic cancer recurrence.”
    DOI - https://doi.org/10.18632/oncotarget.28634
    Correspondence to - Roy Hajjar - [email protected]
    Video short - https://www.youtube.com/watch?v=HgWx_11K6Kw
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    Keywords - cancer, colorectal cancer, gut microbiome, gut barrier, colorectal surgery, anastomotic leak
    About Oncotarget
    Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.
    Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).
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    3 min
  • Nanobody Inhibits Metastasis of Breast Tumor Cells to Lung in Mice
    BUFFALO, NY- August 15, 2024 – A new #research paper was #published in Oncotarget's Volume 15 on August 14, 2024, entitled, “A nanobody against the V-ATPase c subunit inhibits metastasis of 4T1-12B breast tumor cells to lung in mice.”
    The vacuolar H+-ATPase (V-ATPase) is an ATP-dependent proton pump that functions to control the pH of intracellular compartments as well as to transport protons across the plasma membrane of various cell types, including cancer cells.
    Researchers Zhen Li, Mohammed A. Alshagawi, Rebecca A. Oot, Mariam K. Alamoudi, Kevin Su, Wenhui Li, Michael P. Collins, Stephan Wilkens, and Michael Forgac from Tufts University School of Medicine; Tufts University; Dana Farber Cancer Institute, Harvard Medical School; University of Minnesota School of Medicine; Prince Sattam Bin Abdulaziz University; Korro Bio; SUNY Upstate Medical University; and Foghorn Therapeutics, have previously shown that selective inhibition of plasma membrane V-ATPases in breast tumor cells inhibits the invasion of these cells in vitro. They have now developed a nanobody directed against an extracellular epitope of the mouse V-ATPase c subunit.
    “We show that treatment of 4T1-12B mouse breast cancer cells with this nanobody inhibits V-ATPase-dependent acidification of the media and invasion of these cells in vitro.”
    The research team further found that injecting this nanobody into mice implanted with 4T1-12B cells orthotopically in the mammary fat pad inhibited the metastasis of tumor cells to the lungs.
    “In conclusion, our results indicate that a nanobody directed against an extracellular epitope expressed on the surface of the V-ATPase is able to inhibit activity of cell surface V-ATPases in 4T1-12B breast cancer cells, inhibit in vitro invasion of these cells and inhibit metastasis of these cells to lung following their implantation in the mammary fat pad of mice.”
    DOI - https://doi.org/10.18632/oncotarget.28638
    Correspondence to - Michael Forgac - [email protected]
    Video short - https://www.youtube.com/watch?v=4eLGqvSfAgg
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    Keywords - cancer, vacuolar ATPase, breast cancer, invasion, tumor metastasis, tumor growth
    About Oncotarget
    Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.
    Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).
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    3 min
  • Response of BRAF-Mutated Spindle Cell Sarcoma to BRAF/MEK Inhibitors
    BUFFALO, NY- August 14, 2024 – A new #casereport was #published in Oncotarget's Volume 15 on July 17, 2024, entitled, “Rapid but nondurable response of a BRAF exon 15 double-mutated spindle cell sarcoma to a combination of BRAF and MEK inhibitors.”
    As noted in the introduction of the Abstract, the BRAF V600E substitution predicts a cancer's sensitivity to BRAF inhibitor therapy, though the mutation is rarely found in soft-tissue sarcomas.
    Researchers Kseniya Sinichenkova, Iliya Sidorov, Nataliya Kriventsova, Dmitriy Konovalov, Ruslan Abasov, Nataliya Usman, Alexander Karachunskiy, Galina Novichkova, Dmitriy Litvinov, and Alexander Druy from the Dmitriy Rogachev National Medical Research Center of Pediatric Hematology, Oncology, Immunology (Ministry of Healthcare of Russian Federation) and the Research Institute of Medical Cell Technologies in Yekaterinburg, Russia, describe a case of undifferentiated spindle cell sarcoma that exhibited primary insensitivity to standard chemotherapy and a pronounced but non-sustained response to BRAF/MEK inhibitors at recurrence.
    The case presentation involved a 13-year-old girl that was diagnosed with low-grade spindle cell sarcoma of pelvic localization, BRAF exon 15 double-mutated: c.1799T>A p.V600E and c.1819T>A p.S607T in cis-position.
    “This is the first report of spindle cell sarcoma BRAF V600E/S607T double-mutated, responding to a combination of B-Raf and MEK inhibitors.”
    DOI - https://doi.org/10.18632/oncotarget.28606
    Correspondence to - Kseniya Sinichenkova - [email protected]
    Video short - https://www.youtube.com/watch?v=QWEAaaixPxE
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    Keywords - cancer, undifferentiated sarcoma, BRAF V600E mutation, low grade spindle cell sarcoma, abdominal cocoon
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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.