Sign up to save your podcasts
Or
Share Oncotarget
Share to email
Share to Facebook
Share to X
Share to email
Share to Facebook
Share to X
Or
Oncotarget
By Oncotarget PodcastScience
Oncotarget episodes
- Mapping the Hidden Structure of Glioma Research: What Are We Missing?Glioma research has evolved rapidly over the past decade, driven by breakthroughs in molecular biology, imaging technologies, and computational tools. Today, clinicians can classify tumors with far greater precision than ever before, using genetic mutations, epigenetic markers, and advanced diagnostic frameworks. Yet, despite this progress, an important question remains: are we truly capturing the full picture of what shapes patient outcomes?Traditionally, glioma classification has focused on what can be measured in the tumor itself—its histology, molecular profile, and biological behavior. While these factors are undeniably critical, they may not fully explain why patients with similar tumors can experience very different clinical trajectories. Increasingly, researchers are beginning to recognize that broader influences—particularly social and environmental factors—may also play a role. Understanding how these different layers of information connect is becoming an important challenge in neuro-oncology.A review was published in Volume 17 of Oncotarget on March 31, 2026, titled “Bibliometric mapping of glioma classification research through main path, key route, and K-core analyses.” The study was led by first and corresponding author Kayode Ahmed from The University of Texas MD Anderson Cancer Center, in collaboration with Juan E. Núñez-Ríos from Universidad Panamericana.Full blog - https://www.oncotarget.org/2026/05/05/mapping-the-hidden-structure-of-glioma-research-what-are-we-missing/Paper DOI - https://doi.org/10.18632/oncotarget.28851Correspondence to - Kayode Ahmed - [email protected]Abstract video - https://www.youtube.com/watch?v=v8h2z3eEMFMSign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28851Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - cancer, glioma research, social network analysis, socio-clinical domains, web of science, networksTo learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us on social media:Facebook - https://www.facebook.com/Oncotarget/X - 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/Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh6 min
- Targeted Therapies Drive Long-Term Decline in Multiple Myeloma Mortality in the U.S.BUFFALO, NY – April 29, 2026 – A new #research paper was #published in Volume 17 of Oncotarget on April 28, 2026, titled “Targeted therapeutics and U.S. population-level mortality trends in multiple myeloma: A SEER-based analysis from 1975 to 2023.”The study was led by first and corresponding author Navkirat Kahlon from the Mass General Cancer Center at Wentworth-Douglass Hospital, in collaboration with researchers from multiple U.S. institutions. In this study, the researchers examined how mortality trends in multiple myeloma have changed in the United States over nearly five decades, using population-level data from the SEER database. Multiple myeloma, a cancer of plasma cells, has historically been associated with poor survival outcomes, but treatment options have evolved dramatically over time.The analysis revealed a clear shift in mortality trends that closely parallels major therapeutic advances. Between 1975 and the mid-1990s, mortality rates steadily increased, reflecting the limited effectiveness of early treatments such as alkylating agents and corticosteroids. A turning point emerged in the 1990s with the introduction of autologous stem cell transplantation, which marked the first meaningful improvement in survival outcomes.Over the following years, the development of targeted therapies—including immunomodulatory drugs and proteasome inhibitors—was associated with a more pronounced decline in mortality. These treatments introduced new mechanisms of action, such as immune modulation and enhanced cancer cell apoptosis, significantly improving disease control.More recent years have seen further progress with the introduction of monoclonal antibodies, maintenance therapies, and combination treatment strategies. Notably, the steepest decline in mortality occurred between 2021 and 2023, coinciding with the clinical adoption of advanced immunotherapies such as CAR T-cell therapies and bispecific antibodies. These treatments have shown the ability to induce deep and durable responses, even in heavily pretreated patients.“Our findings highlight the real-world impact of targeted therapies on population-level outcomes and underscore the urgent need for care models that ensure accessibility, affordability, and long-term sustainability in the era of precision oncology.”Importantly, while these therapeutic advances have improved survival, they have also introduced new challenges. Many patients now require long-term treatment, which can be associated with cumulative toxicities and a significant financial burden. In addition, access to these therapies remains uneven, influenced by geographic, socioeconomic, and healthcare system factors.Overall, this study provides a comprehensive, real-world view of how advances in cancer treatment have translated into measurable improvements in survival at the population level. At the same time, it highlights the need to ensure that these benefits are both sustainable and accessible to all patients as the field continues to evolve.DOI - https://doi.org/10.18632/oncotarget.28877Correspondence to - Navkirat Kahlon - [email protected]; (ORCID: https://orcid.org/0000-0003-1115-2029)Abstract video - https://www.youtube.com/watch?v=-TNWkG9FyUoSubscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us on social media:Facebook - https://www.facebook.com/Oncotarget/X - 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/Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh4 min
- SCD1 Inhibition Strategy Shows Potent Synergy with Regorafenib and Metformin in Tumor Cell KillingCancer has long been understood through a variety of biological frameworks, including genetic mutations, dysregulated signaling pathways, and uncontrolled cell proliferation. Yet, these models often capture the visible consequences of disease rather than the deeper metabolic dependencies that sustain tumor survival. Despite major advances in targeted therapies, a central challenge remains: what underlying mechanisms make cancer cells vulnerable to treatment, and how can these vulnerabilities be exploited more effectively? Increasing attention has shifted toward cellular metabolism—particularly lipid regulation and energy-sensing pathways such as AMPK—as critical determinants of tumor behavior. Scientists are now taking a closer look at how metabolism works together with stress responses like autophagy—and how this connection could be used to develop better cancer treatments.A new research paper was published in Volume 17 of Oncotarget, titled “The SCD1 inhibitor aramchol interacts with regorafenib and metformin to kill tumor cells.” The study was led by first author Michael R. Booth and corresponding author Paul Dent from Virginia Commonwealth University, in collaboration with Laurence Booth and Jane L. Roberts from Virginia Commonwealth University and John M. Kirkwood from the University of Pittsburgh Cancer Institute.Full blog - https://www.oncotarget.org/2026/04/21/scd1-inhibition-strategy-shows-potent-synergy-with-regorafenib-and-metformin-in-tumor-cell-killing/Paper DOI - https://doi.org/10.18632/oncotarget.28861Correspondence to - Paul Dent - [email protected]Abstract video - https://www.youtube.com/watch?v=lmX_c2e_-HYSign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28861Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - cancer, macroautophagy, ER stress, aramchol, regorafenib, BIDTo learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us:Facebook - https://www.facebook.com/Oncotarget/X - 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/Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh6 min
- Epigenetic Dysregulation of PDX1 Drives Prostate Cancer ProgressionBUFFALO, NY – April 15, 2026 – A new #research paper was #published in Volume 17 of Oncotarget on March 31, 2026, titled “Epigenetic dysregulation and biological function of PDX1 in prostate cancer.”The study was led by first author Tayo A. Adeyika and corresponding author Bernard Kwabi-Addo from Howard University, Washington, DC. The team explored the role of the pancreatic and duodenal homeobox 1 (PDX1) gene in prostate cancer, with a focus on its epigenetic regulation and biological function. Their analysis identified PDX1 as differentially hypermethylated in prostate cancer tissues compared to normal prostate samples, alongside a paradoxical increase in protein expression in tumor tissues.Experiments in prostate cancer cell lines showed that PDX1 overexpression significantly enhanced cell proliferation and migration, while knockdown of PDX1 suppressed these tumor-associated behaviors. These findings point to a clear role for PDX1 in promoting aggressive cancer phenotypes.The work further shows that PDX1 regulates key metabolic, inflammatory, and epithelial–mesenchymal transition (EMT) pathways, including genes such as INSR, IGF1R, TWIST1, and SNAI1. Notably, these effects were more pronounced under high-glucose conditions, suggesting a link between metabolic state and prostate cancer progression.“Overall, our findings suggest that PDX1 plays a tumor-promoting role in human PCa cells by influencing expression of metabolites in insulin, inflammatory, and epithelial-mesenchymal transition (EMT) signaling pathways.”The authors conclude that PDX1 may represent a potential therapeutic target, particularly in the context of metabolic disorders such as obesity and diabetes, which are known to influence prostate cancer risk and progression. Their findings provide new insight into the interplay between epigenetics, metabolism, and tumor biology in prostate cancer.DOI - https://doi.org/10.18632/oncotarget.28854Correspondence to - Bernard Kwabi-Addo - [email protected]Abstract video - https://www.youtube.com/watch?v=itYVsyXJJoESign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28854Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - cancer, PDX1, DNA methylation prostate cancer, shRNA knockdown, over-expression, glucoseTo learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us:Facebook - https://www.facebook.com/Oncotarget/X - 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/Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh3 min
- Cancer Care in Conflict Zones Remains Critically NeglectedBUFFALO, NY – April 13, 2026 – A new #review was #published in Volume 17 of Oncotarget on March 31, 2026, titled “Cancer without borders: Policy frameworks for oncology care in humanitarian and conflict settings.”The study—led by corresponding author Pragnesh Parmar, along with Gunvanti Rathod from AIIMS Bibinagar, Telangana, India—brings together evidence from peer-reviewed studies, global health reports, and case examples from regions such as Gaza, Sudan, and Ukraine to examine the structural, ethical, and policy barriers limiting access to cancer care in humanitarian settings. Their findings show that oncology services are often excluded from emergency health priorities, resulting in delayed diagnosis, treatment interruptions, and reduced access to palliative care.The review further highlights that disrupted infrastructure, legal constraints, and fragmented policies disproportionately impact vulnerable populations—including women, children, and the elderly—who often present with advanced disease stages due to delays in care.“Addressing cancer in humanitarian contexts is not merely a technical challenge but a moral imperative.”The authors conclude that integrating oncology into humanitarian response frameworks is essential to ensure equitable access to care and improve outcomes for displaced populations. They emphasize the need for coordinated global strategies, including cross-border care models, tele-oncology, and policy reform, to address this critical gap in global health systems.DOI - https://doi.org/10.18632/oncotarget.28856Correspondence to - Pragnesh Parmar - [email protected]; (ORCID: orcid.org/0000-0002-8402-8435)Abstract video - https://www.youtube.com/watch?v=zXlhIBZyJ6QSign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28856Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - cancer, cancer care, humanitarian crisis, tele-oncology, global health policy, oncology triageTo learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us on social media:Facebook - https://www.facebook.com/Oncotarget/X - 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/Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh3 min
- Oncotarget Editorial Highlights Advances in Scientific Integrity and Publishing TransparencyBUFFALO, NY – April 10, 2026 – A new #editorial perspective was #published in Volume 17 of Oncotarget on April 8, 2026, titled “Oncotarget: Past, Present and Future: Trends in the publishing industry.”Authored by the Scientific Integrity Office at Oncotarget, the editorial comprehensively analyzes the journal’s evolving approach to scientific integrity. It addresses historical challenges in scholarly publishing and discusses the necessity of modern image forensics tools to meet the most rigorous standards of scientific integrity.The Scientific Integrity Office describes how advances in digital technologies—particularly image forensics tools such as ImageTwin and analytical platforms like Argos—have transformed the ability to detect problematic data and analyze the quality of published research.The editorial emphasizes that the lack of adequate image tools in the “pre-tools” era limited journals’ ability to detect image-related issues, underscoring the importance of recent technological advancements. It also highlights that Argos provides a good opportunity to obtain a more objective picture across different journals in both the pre- and post-tools era.Looking forward, Oncotarget advocates indexes for broader adoption of independent analytical and AI-based tools in journal evaluation. In the public interest, it also encourages open discussion of how indexes select, deselect, and reevaluate journals.DOI - https://doi.org/10.18632/oncotarget.28852Correspondence to - Scientific Integrity Office - [email protected]Introduction video - https://www.youtube.com/watch?v=hgxvr2Q_ZPMSign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28852Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - Scientific Integrity, Academic Publishing, Open Access, Peer Review, ResearchTo learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us on social media:Facebook - https://www.facebook.com/Oncotarget/X - 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/Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh2 min
- CREB5: A Master Regulator of Stem Cell-Like Programs in Prostate Cancer ProgressionAndrogen receptor (AR) signaling has long been the central driver of prostate cancer progression and the primary target of therapies for advanced disease. Yet, a significant subset of tumors either fail to respond or develop resistance, often by switching to AR-independent programs that resemble basal or stem cell-like states. Understanding what drives these aggressive, therapy-resistant phenotypes is a critical challenge in oncology.A research paper, titled “CREB5 regulates stem cell-like transcriptional programs to enhance tumor progression in prostate cancer” was published in Volume 17 of Oncotarget by a multi-institutional team of researchers, identifies a key molecular regulator of this process and reveals how it promotes tumor progression.Full blog - https://www.oncotarget.org/2026/04/07/creb5-a-master-regulator-of-stem-cell-like-programs-in-prostate-cancer-progression/Paper DOI - https://doi.org/10.18632/oncotarget.28826Correspondence to - Emmanuel S. Antonarakis - [email protected], Justin Hwang - [email protected]Abstract video - https://www.youtube.com/watch?v=Zywrj5hV4hoSign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28826Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - cancer, prostate cancer, CREB5, basal-like, stem cell-like, AP-1 transcription factorsTo learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us on social media:Facebook - https://www.facebook.com/Oncotarget/X - 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/Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh11 min
- Adjuvant PD-1/PD-L1 Inhibitors Show Efficacy but Highlight Safety Considerations in Solid CancersBUFFALO, NY – April 7, 2026 – A new #research paper was #published in Volume 17 of Oncotarget on March 31, 2026, titled “Efficacy and safety of PD-1/ PD-L1 inhibitors as adjuvants in the treatment of patients with solid cancers: A systematic review and meta-analysis of randomized controlled trials.”Led by first author Maryam Aleid from Imam Abdulrahman Bin Faisal University, and corresponding author Dhai Almuteri from King Fahad Specialist Hospital, the researchers evaluated 13 randomized controlled trials involving 9,850 patients to assess the efficacy and safety of PD-1 and PD-L1 inhibitors as adjuvant therapy following tumor resection.The analysis demonstrated that immune checkpoint inhibitors significantly improved key clinical outcomes, including disease-free survival and distant metastasis-free survival. However, no clear improvement in overall survival was observed across studies. The study also identified a reduction in recurrence and metastasis risk, supporting the role of these therapies in early-stage cancer management. At the same time, variability across tumor types suggests that benefits may differ depending on cancer subtype and patient population.“Adjuvant PD-1 and PD-L1 inhibitors improve disease-free and distant metastasis-free survival in selected patients with high-risk solid tumors.”In terms of safety, the findings highlight an increased incidence of adverse events associated with PD-1/PD-L1 inhibitors, including fatigue, nausea, pruritus, and hypothyroidism, emphasizing the importance of careful monitoring during treatment. The authors conclude that while PD-1/PD-L1 inhibitors offer meaningful benefits in reducing recurrence and metastasis in high-risk solid tumors, the clinical benefit must be balanced against higher toxicity rates. Future research is needed to refine patient selection, evaluate long-term survival outcomes, and better understand differences across tumor types to optimize the use of these therapies in clinical practice.DOI - https://doi.org/10.18632/oncotarget.28855Correspondence to - Dhai Almuteri - [email protected]Abstract video - https://www.youtube.com/watch?v=4Ce07bHfjB4Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28855Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - cancer, PD-1, PD-L1, adjuvant immunotherapy, solid tumorTo learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us:Facebook - https://www.facebook.com/Oncotarget/X - 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/Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh3 min
- Bibliometric Mapping Reveals the Evolution of Glioma Classification ResearchBUFFALO, NY – April 6, 2026 – A new #review was #published in Volume 17 of Oncotarget on March 31, 2026, titled “Bibliometric mapping of glioma classification research through main path, key route, and K-core analyses.”Led by first and corresponding author Kayode Ahmed from The University of Texas MD Anderson Cancer Center, and Juan E. Núñez-Ríos from Universidad Panamericana, the study uses bibliometric network analysis to map how glioma classification research has evolved across clinical, molecular, and social domains. The authors analyzed Web of Science data using direct citation networks and applied main path analysis, key route analysis, and K-core analysis to identify influential papers, critical routes, and densely connected thematic clusters.The network comprised 46,204 nodes and 231,432 arcs, highlighting the prominent role of DNA methylation profiling in molecular biomarker-based classification models. The authors also found that advanced imaging and molecular techniques were key drivers of the field, while the subset of glioma classification studies that incorporate social factors remained relatively scarce. Their analysis, therefore, points not only to the major intellectual structure of the literature but also to a thematic gap in how social determinants are represented in glioma classification research.“Through quantitative network analysis complemented by narrative interpretation, we uncovered patterns and substructures that offer deep insights into the evolving research landscape.”The authors conclude that their framework offers a more integrative view of glioma classification research than approaches centered only on citation counts or h-index–style metrics. By identifying the evolutionary logic of the field and the limited but notable presence of social factors, the study suggests future glioma classification models may benefit from incorporating clinical, molecular, and social dimensions more explicitly.DOI - https://doi.org/10.18632/oncotarget.28851Correspondence to - Kayode Ahmed - [email protected]Abstract video - https://www.youtube.com/watch?v=v8h2z3eEMFMSign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28851Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - cancer, glioma research, social network analysis, socio-clinical domains, web of science, networksTo learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us on social media:Facebook - https://www.facebook.com/Oncotarget/X - 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/Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh3 min
- The SCD1 Inhibitor Aramchol, Regorafenib, and Metformin Combine to Kill Uveal Melanoma CellsBUFFALO, NY – March 31, 2026 – A new #research paper was #published in Volume 17 of Oncotarget on March 27, 2026, titled “The SCD1 inhibitor aramchol interacts with regorafenib and metformin to kill tumor cells.”Led by Michael R. Booth, Laurence Booth, and Jane L. Roberts from Virginia Commonwealth University, with corresponding author Paul Dent from the same institution and John M. Kirkwood from the University of Pittsburgh Cancer Institute, the study examines how aramchol interacts with regorafenib and metformin to kill tumor cells, particularly patient-derived uveal melanoma (UM) cells and cholangiocarcinoma cells.The authors report that aramchol, regorafenib, and metformin interact to enhance tumor cell killing, with the strongest effects seen when metformin is added to aramchol plus regorafenib. In patient-derived UM cells and LD-1 cholangiocarcinoma cells, the three-drug combination increased autophagosome formation and autophagic flux, while knockdown of Beclin1, ATG5, or LAMP2 reduced autophagosome and autolysosome formation and lowered cell killing. The study also found that BID contributes to the lethal response, supporting a multifactorial mechanism involving macroautophagy and death-receptor signaling.“Our data demonstrates that UM cells are killed by treatment with aramchol plus regorafenib plus metformin via enhanced autophagic flux and that this combination may have the potential to control UM tumors that have metastasized to the liver.”The authors also note that while SCD1 knockdown increased baseline tumor cell death, it did not replicate the full anticancer effects of aramchol, suggesting additional molecular targets contribute to its activity. They emphasize the need for further in vivo studies to evaluate the therapeutic potential of this combination in metastatic uveal melanoma, particularly in liver-targeted disease.DOI - https://doi.org/10.18632/oncotarget.28861Correspondence to - Paul Dent - [email protected]Abstract video - https://www.youtube.com/watch?v=lmX_c2e_-HYSign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28861Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - cancer, macroautophagy, ER stress, aramchol, regorafenib, BIDTo learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us:Facebook - https://www.facebook.com/Oncotarget/X - 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/Spotify - https://open.spotify.com/show/0gRwT6BqYWJzxzmjPJwtVh3 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/