Oncotarget

Oncotarget

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Oncotarget episodes

  • Tumor Dormancy Initiated by Lymphovascular Embolus
    BUFFALO, NY- October 30, 2024 – A new #research paper was #published in Oncotarget's Volume 15 on October 11, 2024, entitled “Initiation of tumor dormancy by the lymphovascular embolus.”
    Researchers Yin Ye, Justin Wang, Michael G. Izban, Billy R. Ballard, and Sanford H. Barsky from Meharry Medical College in Nashville, TN, and Scripps Mercy Hospital in San Diego, CA, uncovered critical mechanisms that lead to tumor dormancy in breast cancer. This study sheds light on how certain cancer cells can remain dormant for years before potentially reawakening as metastatic tumors.
    Using breast cancer patient-derived organoids and tumor samples, the research team discovered that tumor dormancy in breast cancer can be triggered by specific signaling changes within small cell clusters, called tumor emboli, which detach from the primary tumor and travel through the bloodstream. These emboli can remain inactive, sometimes for years, before reawakening in other parts of the body. Key changes include reduced activity of mTOR, a metabolic regulator, and structural shifts in E-cadherin, a molecule involved in cell adhesion. This study also suggests these changes are regulated by the PI3K pathway and occur within the unique three-dimensional structure of tumor spheroids, shedding light on the interactions within dormant cell clusters.
    As a conclusion, this work not only identifies mTOR and E-cadherin as key components in maintaining dormancy but also offers a promising roadmap for future therapies. By targeting these pathways, there may be potential to keep cancer cells in a dormant state, reducing the risk of late-stage recurrence and improving patient outcomes.
    DOI - https://doi.org/10.18632/oncotarget.28658
    Correspondence to - Sanford H. Barsky - [email protected]
    Video short - https://www.youtube.com/watch?v=z6ex7Yl8r5Q
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    Keywords - cancer, dormancy, lymphovascular embolus, mTOR, E-cadherin proteolysis
    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
  • Complete Response to Encorafenib + Binimetinib in BRAF V600E-Mutant Tumor
    BUFFALO, NY- October 29, 2024 – A new #casereport was #published in Oncotarget's Volume 15 on October 11, 2024, entitled “Complete response to encorafenib plus binimetinib in a BRAF V600E-mutant metastasic malignant glomus tumor.”
    As highlighted in the abstract, glomus tumors (GT) are rare mesenchymal neoplasms originating in dermal arteriovenous structures involved in thermoregulation. While generally benign, some can exhibit malignant features, leading to aggressive behavior, metastasis, and limited response to standard chemotherapy. The identification of the BRAF V600E mutation in certain malignant GT cases offers a promising therapeutic target.
    In their paper, researchers Marta Arregui, Antonio Calles, María del Mar Galera, Ana Gutiérrez, Carlos López-Jiménez, Carolina Agra, Adriana Fernández, Natalia Gutiérrez, María de Toro and Rosa Álvarez from Gregorio Marañón University Hospital and Fundación Jiménez Díaz University Hospital in Madrid, Spain, document a remarkable clinical and metabolic response in a case of metastatic BRAF V600E-mutated glomangiosarcoma treated with the combination of encorafenib and binimetinib.
    They report on a 45-year-old male patient with stage IV malignant GT carrying a BRAF V600E mutation, who was treated systemically with encorafenib and binimetinib. This approach led to a swift clinical and radiological improvement.
    “To our knowledge, our patient represents the first reported case of a metastatic malignant GT successfully treated with BRAF and MEK inhibitors, achieving a long-lasting complete morpho-metabolic response.”
    DOI - https://doi.org/10.18632/oncotarget.28654
    Correspondence to - Carlos López-Jiménez - [email protected]
    Video short - https://www.youtube.com/watch?v=xjbj3Iu16P4
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    Keywords - cancer, malignant glomus tumor, glomangiosarcoma, BRAF V600E, agnostic treatment, targeted therapy
    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
  • Behind the Study: Molecular Chaperones & Tumor Suppressor Stability
    Drs. Mehdi Mollapour, Jennifer Heritz, and Sarah Backe from SUNY Upstate Medical University (Syracuse, NY) discuss a review they co-authored that was published by Oncotarget in Volume 15, entitled, “Molecular chaperones: Guardians of tumor suppressor stability and function.”
    DOI - https://doi.org/10.18632/oncotarget.28653
    Correspondence to - Mehdi Mollapour - [email protected]
    Video interview - https://www.youtube.com/watch?v=vEHmyemWgNo
    Video transcript - https://www.oncotarget.net/2024/10/24/behind-the-study-molecular-chaperones-tumor-suppressor-stability/
    Abstract
    The term ‘tumor suppressor’ describes a widely diverse set of genes that are generally involved in the suppression of metastasis, but lead to tumorigenesis upon loss-of-function mutations. Despite the protein products of tumor suppressors exhibiting drastically different structures and functions, many share a common regulatory mechanism—they are molecular chaperone ‘clients’. Clients of molecular chaperones depend on an intracellular network of chaperones and co-chaperones to maintain stability. Mutations of tumor suppressors that disrupt proper chaperoning prevent the cell from maintaining sufficient protein levels for physiological function. This review discusses the role of the molecular chaperones Hsp70 and Hsp90 in maintaining the stability and functional integrity of tumor suppressors. The contribution of cochaperones prefoldin, HOP, Aha1, p23, FNIP1/2 and Tsc1 as well as the chaperonin TRiC to tumor suppressor stability is also discussed. Genes implicated in renal cell carcinoma development—VHL, TSC1/2, and FLCN—will be used as examples to explore this concept, as well as how pathogenic mutations of tumor suppressors cause disease by disrupting protein chaperoning, maturation, and function.
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    Keywords - cancer, molecular chaperone, tumor suppressor, renal cell carcinoma, Birt-Hogg-Dubé (BHD) syndrome, TSC syndrome
    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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    7 min
  • Next-Generation Antibodies for Cancer Therapy
    Cancer research has made remarkable progress in recent years, with monoclonal antibody (mAb) therapy emerging as one of the most promising advancements. These treatments are designed to precisely target cancer cells, offering a more focused approach that helps patients fight different malignancies with fewer side effects compared to traditional chemotherapy.
    Despite this progress, a major challenge remains: targeting cancer-related molecules inside cells rather than on the surface, which has been the main focus of available mAb therapies until now. This is where the groundbreaking research in the paper “Next-generation cell-penetrating antibodies for tumor targeting and RAD51 inhibition,” published in Volume 15 of Oncotarget on October 1, 2024, comes into play.
    Full blog - https://www.oncotarget.org/2024/10/24/next-generation-antibodies-for-cancer-therapy/
    Paper DOI - https://doi.org/10.18632/oncotarget.28651
    Correspondence to - Peter M. Glazer - [email protected]
    Video short - https://www.youtube.com/watch?v=sTHjJ0Qq0YQ
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    Keywords - cancer, 3E10, cell penetration, nucleic acid binding, nucleic acid delivery, RAD51
    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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    9 min
  • How Blood Cancer Cells Rewire to Evade Drug Treatment
    BUFFALO, NY- October 23, 2024 – A new #editorial was #published in Oncotarget's Volume 15 on October 11, 2024, entitled, “Gene regulatory network and signalling pathway rewiring: How blood cancer cells shift their shapes to evade drug treatment.”
    As highlighted in the paper, Acute Myeloid Leukemia (AML) is a complex and diverse disease caused by multiple mutations in genes that regulate transcription and growth. These mutations lead to extensive rewiring of the gene regulatory network (GRN), which alters the identity of hematopoietic stem and progenitor cells, ultimately blocking normal myeloid differentiation. A key feature of AML is the presence of mutations in growth factor receptor and signaling genes, such as FLT3, KIT, and RAS. Notably, FLT3 is one of the most commonly mutated genes in AML, with around 25% of cases showing an internal tandem duplication (ITD) that causes the receptor to remain constantly active.
    In their paper, researchers Constanze Bonifer and Peter N. Cockerill from the Institute of Cancer and Genomic Sciences at the University of Birmingham, UK, and the Murdoch Children’s Research Institute, Royal Children’s Hospital in Melbourne, Australia, discuss recent publications from their group addressing this issue through a multi-omics study. The authors investigated how gene regulatory networks (GRNs) in FLT3-ITD patients were rewired compared to normal cells and in response to FLT3 inhibitor treatment. Several key findings stood out, including: 1) Mapping of open chromatin regions revealed that patients initially responsive to FLT3 inhibition showed significant rewiring of their GRNs, forming new connections between transcription factors (TFs) and target genes, while non-responsive patients did not; 2) Chromatin immunoprecipitation (ChIP) experiments showed that drug treatment led to the loss of binding of RUNX1, the master regulator of hematopoiesis, and the MAP-Kinase (MAPK)-inducible TF AP-1; 3) Disruption of AP-1 binding via a dominant-negative version of the TF (dnFOS) also abolished RUNX1 binding at hundreds of sites, indicating that RUNX1 binding is AP-1 dependent; and 4) Inhibition of both AP-1 and RUNX1 led to a pronounced cell cycle block.
    “In summary, drugs that target individual signalling pathways in AML often fail to stop proliferation malignant growth, due to the wide variety, redundancy and cross talk between multiple pathways regulating and differentiation.”
    DOI - https://doi.org/10.18632/oncotarget.28662
    Correspondence to - Constanze Bonifer - [email protected]
    Video short - https://www.youtube.com/watch?v=5c_uT6aE36A
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    Keywords - cancer, acute myeloid leukemia, gene regulatory networks, aberrant growth factor signaling, transcription, RUNX1/AP-1 axis
    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
  • Tribute to Dr. Mikhail (Misha) Blagosklonny
    It is with great sadness and heavy heart that we announce the recent passing of Dr. Mikhail (Misha) V. Blagosklonny, our beloved Editor-in-Chief. Misha succumbed to metastatic lung cancer after a courageous battle.
    Dr. Blagosklonny will be remembered as a brilliant and extraordinary scientist who dedicated his life to science. He was a visionary thinker, who made highly original contributions to cancer and aging research that were often ahead of their time.
    Dr. Blagosklonny was born into a family of scientists. His mother, Professor of Medicine Yanina V. Blagosklonnaya, specialized in endocrinology and was a talented teacher, mentoring several generations of medical students. His father, Professor Vladimir M. Dilman, was a brilliant gerontologist, endocrinologist and oncologist, known for being a very charismatic person. He was the first person to encourage Misha to think about nature, aging, and philosophy.
    Misha was a theorist by nature. While in school, he was deeply interested in physics and dreamed of becoming a theoretical physicist. Eventually, he chose biology, driven to study aging and age-related diseases, including cancer. He started as an experimentalist, but over the years, he became a theoretical biologist. In a way, his dream came true.
    Full tribute to Misha: https://www.oncotarget.com/news/pr/tribute-to-dr-mikhail-misha-blagosklonny/
    13 min
  • Next-Gen Cell-Penetrating Antibodies for Tumor Targeting and RAD51 Inhibition
    BUFFALO, NY- October 21, 2024 – A new #research paper was #published in Oncotarget's Volume 15 on October 1, 2024, entitled, “Next-generation cell-penetrating antibodies for tumor targeting and RAD51 inhibition.”
    As highlighted in the abstract, monoclonal antibody therapies for cancer have shown extraordinary clinical success in recent years. However, these strategies are primarily limited to targeting specific cell surface antigens, despite many disease targets being located intracellularly.
    In their paper, researchers Madison Rackear, Elias Quijano, Zaira Ianniello, Daniel A. Colón-Ríos, Adam Krysztofiak, Rashed Abdullah, Yanfeng Liu, Faye A. Rogers, Dale L. Ludwig, Rohini Dwivedi, Franziska Bleichert, and Peter M. Glazer from the Departments of Therapeutic Radiology and Genetics at Yale University School of Medicine, Gennao Bio, and the Department of Molecular Biophysics and Biochemistry at Yale University report on the humanization of the full-length, nucleic acid-binding monoclonal lupus-derived autoantibody 3E10, which exhibits a novel mechanism for cell penetration and tumor-specific targeting.
    The authors compare humanized variants of 3E10 and demonstrate that cell uptake relies on the nucleoside transporter ENT2. They also find that faster cell uptake and superior in vivo tumor targeting are associated with higher affinity nucleic acid binding.
    “We show that one human variant retains the ability of the parental 3E10 to bind RAD51, serving as a synthetically lethal inhibitor of homology-directed repair in vitro.”
    DOI - https://doi.org/10.18632/oncotarget.28651
    Correspondence to - Peter M. Glazer - [email protected]
    Video short - https://www.youtube.com/watch?v=sTHjJ0Qq0YQ
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    Keywords - cancer, 3E10, cell penetration, nucleic acid binding, nucleic acid delivery, RAD51
    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
  • Molecular Chaperones: Guardians of Tumor Suppressor Stability
    BUFFALO, NY- October 16, 2024 – A new #review was #published in Oncotarget's Volume 15 on October 1, 2024, entitled, “Molecular chaperones: Guardians of tumor suppressor stability and function.”
    As highlighted in the abstract of this paper, "tumor suppressor" describes a diverse set of genes typically involved in suppressing metastasis, but which can lead to tumorigenesis when loss-of-function mutations occur. Despite the varied structures and functions of tumor suppressor proteins, many share a common regulatory mechanism—they are "clients" of molecular chaperones, and they rely on an intracellular network of chaperones and co-chaperones to maintain their stability. Mutations in tumor suppressors that disrupt proper chaperoning prevent cells from maintaining sufficient protein levels for normal physiological function.
    In their review, researchers Jennifer A. Heritz, Sarah J. Backe, and Mehdi Mollapour from SUNY Upstate Medical University and New York VA Health Care in Syracuse, New York, discuss the role of molecular chaperones Hsp70 and Hsp90 in maintaining the stability and functional integrity of tumor suppressors. They also detail the contributions of co-chaperones prefoldin, HOP, Aha1, p23, FNIP1/2, and Tsc1, as well as the chaperonin TRiC, to tumor suppressor stability.
    “Overall, it is clear that oncogenesis can result from the dysregulation of tumor suppressor stabilization by chaperones.”
    DOI - https://doi.org/10.18632/oncotarget.28653
    Correspondence to - Mehdi Mollapour - [email protected]
    Video short - https://www.youtube.com/watch?v=V5OFjeqaH3A
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    Keywords - cancer, molecular chaperone, tumor suppressor, renal cell carcinoma, Birt-Hogg-Dubé (BHD) syndrome, TSC syndrome
    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
  • TP53 Mutated AML: Transplant or No Transplant
    BUFFALO, NY- October 11, 2024 – A new #editorial was #published in Oncotarget's Volume 15 on October 1, 2024, entitled, “Transplant or no transplant for TP53 mutated AML.”
    As highlighted in this editorial, TP53 mutations (mut) occur in 10–15% of acute myeloid leukemia (AML) cases, commonly associated with therapy-related AML (t-AML) and complex cytogenetics (CG). TP53-mut AML is inherently resistant to conventional chemotherapies and continues to show a poor prognosis, even with venetoclax-based therapies. Allogeneic hematopoietic stem cell transplant (allo-HCT) remains a potential curative option, though only 10–15% of patients receive it. In a recent study, allo-HCT was the only variable significantly improving survival, despite only 16% of patients successfully bridging to it.
    In their editorial, researchers Talha Badar, Moazzam Shahzad, Ehab Atallah, Mark R. Litzow, and Mohamed A. Kharfan-Dabaja from the Division of Hematology-Oncology and Blood and Marrow Transplantation and Cellular Therapy Program at Mayo Clinic (Jacksonville, Florida) evaluated the outcomes of TP53-mutated AML patients based on data from the Consortium of Myeloid Malignancies and Neoplastic Diseases (COMMAND). The study found a “dismal” survival rate of 8.5 months, with no significant difference among treatment types, and allo-HCT was the only variable associated with improved survival.
    The authors also report on the “better long-term outcomes” when allo-HCT was performed during Complete Remission 1 (CR1) in previous observations. They acknowledge the limitations of their retrospective analysis, including selection bias, data heterogeneity from participating institutions, and the lack of complete molecular data prior to allo-HCT that might have influenced the results. Nevertheless, the findings are encouraging and suggest that allo-HCT improves long-term outcomes in this poor prognostic disease, where effective therapies remain limited.
    “In summary, this study reported improved survival when allo-HTC was performed in CR1 versus after later lines of therapy.”
    DOI - https://doi.org/10.18632/oncotarget.28652
    Correspondence to - Talha Badar - [email protected]
    Video short - https://www.youtube.com/watch?v=OQue9gbqsxE
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    Keywords - cancer, AML, TP53 mutation, allogeneic stem cell transplant
    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
  • Targeting Stem Cell-like Traits: How miR-10b Inhibition Treats Metastatic Breast Cancer
    While there have been significant improvements in breast cancer detection and treatment, the outlook for metastatic breast cancer remains bleak, with only a 30% five-year survival rate. This is largely due to existing therapies’ inability to effectively target the unique characteristics of metastatic cells. One key factor in metastasis is miR-10b, a small noncoding RNA known to influence cancer cell invasion, migration, viability, and proliferation.
    In their paper, 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, shared findings showing that inhibiting miR-10b impairs breast cancer cell stemness. Their research paper, entitled, “Inhibition of miR-10b treats metastatic breast cancer by targeting stem cell-like properties” was published in Volume 15 of Oncotarget on August 26, 2024.
    Full blog - https://www.oncotarget.org/2024/10/11/targeting-stem-cell-like-traits-how-mir-10b-inhibition-treats-metastatic-breast-cancer/
    Research 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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    7 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.