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Oncotarget
By Oncotarget PodcastScience
Oncotarget episodes
- GLS2 Shapes Ferroptosis in Hepatocellular CarcinomaBUFFALO, NY- October 19, 2023 – A new editorial paper was published in Oncotarget's Volume 14 on October 19, 2023, entitled, “GLS2 shapes ferroptosis in hepatocellular carcinoma.”In their new editorial, researchers Sawako Suzuki, Divya Venkatesh, Tomoaki Tanaka, and Carol Prives from Columbia University discuss ferroptosis regulation of GLS2 as a potential therapeutic strategy against liver diseases.“More than a decade has passed since our group (1) as well as Hu et al., (2) identified glutaminase (GLS2) as a p53 target gene that promotes the tricarboxylic acid cycle (TCA) via α-ketoglutarate (αKG) and lowers oxidative stress via increasing glutathione (GSH) [1, 2].”Two years after this Dixon et al., [3] described a form of cell death they named ferroptosis which is caused by iron-mediated lipid peroxidation. Then, three years later, Gao et al., reported that GLS2 but not GLS1 is an inducer of ferroptosis in human cancer cells [4]. Ferroptosis had first been shown to be regulated by p53 via repression of SLC7A11 [5]. The circle was closed by a study from the Murphy group who reported that a cancer-related nonsynonymous mutation in p53 (P47S) is correlated with failure to either activate GLS2 expression or produce ferroptosis [6].“Our recent study (Suzuki et al.) [7] has validated the ability of GLS2 to promote ferroptosis in murine models.”DOI - https://doi.org/10.18632/oncotarget.28526Correspondence to - Carol Prives - [email protected]Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28526Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - cancer, ferroptosis, hepatocellular carcinoma, GLS2, p53, tumor suppressionAbout OncotargetOncotarget (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.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/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/Media Contact180092209573 min
- The Nuclear Envelope and Breast Cancer MetastasisBUFFALO, NY- October 18, 2023 – A new editorial paper was published in Oncotarget's Volume 14 on April 14, 2023, entitled, “The nuclear envelope and metastasis.”In their new editorial, researchers Emily Hansen and James M. Holaska from Rowan University discuss nuclear morphology — one of the basic visual criteria used by pathologists to diagnose breast cancer. Immunofluorescence staining of the nuclear structural proteins lamin B and emerin was recommended as an effective diagnostic tool for both thyroid and breast cancer, suggesting nuclear structure is intimately tied to malignant transformation. But what role nuclear morphology plays in cancer transformation and progression remains unclear.“The most likely explanation for why cancer cells present with distinct nuclear morphology is thought to be related to the most likely route of cancer spread: the vasculature.”For a tumor to metastasize, cancer cells need to enter and exit the blood and lymphatic vessels by squeezing through extremely small gaps in the endothelium, most of which are 1.2–2 µm in diameter. While the cytoplasm is very flexible and the cytoskeleton can rearrange to fit through openings as narrow as 1 µm, the nuclear diameter (10–20 µm) and its considerable stiffness (2–10x stiffer than the cytoplasm) represent physical barriers to this process.“Thus, to enable metastasis, cancer cells must also increase their nuclear malleability.”Studies have shown that nuclear softening is associated with tumor aggressiveness and metastasis. Although nuclear softening is one of the ‘hallmarks of cancer’ it remains poorly understood. Nuclear shape and stiffness are governed by a complex set of structural proteins that serve as both scaffolds and signaling proteins to influence almost all aspects of nuclear function.The best studied nucleostructural proteins are lamins, which are frequently downregulated in cancer. However, it is difficult to ascertain whether specific functional consequences are due to lamins or due to displacement of lamin-interacting proteins upon lamin loss. For example, nuclear size and shape is also governed by emerin, which binds to lamins at the nuclear envelope (NE) and upon lamin loss is retained in the endoplasmic reticulum. Like lamins, emerin is frequently mutated in cancer, with mutations in its transmembrane and actin-binding domains.“We found that in breast cancer, emerin expression in tumor tissue is significantly correlated to survival time [16]. These data suggest emerin plays a central role in pathogenic transformation and progression of malignant breast tissue.”DOI - https://doi.org/10.18632/oncotarget.28375Correspondence to - James M. Holaska - [email protected]Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28375Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - cancer, emerin, metastasis, mechanotransduction, breast cancer, nucleoskeletonAbout OncotargetOncotarget (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.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/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/Media Contact180092209574 min
- GBP3-STING Interaction in Glioblastoma Coordinates Poor Response to TemozolomideBUFFALO, NY- October 17, 2023 – A new editorial paper was published in Oncotarget's Volume 14 on May 19, 2023, entitled, “GBP3-STING interaction in glioblastoma coordinates autophagy, anti-oxidative, and DNA repair programs in response to temozolomide.”In their recent editorial, researchers Jun Ma, Ziyu Wang, Clark C. Chen, and Ming Li from the University of Minnesota discussed the methylating agent, Temozolomide (TMZ). TMZ is the standard adjuvant chemotherapeutic drug for glioblastoma, which constitutes 17.7% of overall primary central nervous system tumors. The survival rate of this WHO Grade IV tumor has achieved a clinically significant prolongation of 2.5 months overall and an increase of 16.3% 2-year survival rate. However, one intractable challenge is the diverse reactions to temozolomide treatment.“The acquired resistance to the standard adjutant radiochemotherapy including temozolomide has favored the recurrence of some glioblastoma cases and has kept the milestone from moving forward for more than 15 years.”Guanylate-binding proteins (GBPs) are a group of dynamin-related large (~65 kDa) GTPases expressed in response to interferon and mediate intracellular immunity. Consisting of 7 members in humans, little is known about the function of GBPs beyond their role in innate cellular immunity. After recent years of dedication to the GBP family, its role in glioblastoma’s development and recurrence has drawn great attention.“More recently, Li’s lab did informatic analysis of clinically annotated glioblastoma datasets, laboratory studies of protein-protein interaction, and functional characterization after depletion or exogenous expression.”GBP family members such as GBP1, GBP2, GBP3, and GBP5 are highly elevated and play pro-tumor roles through multiple mechanisms in glioblastoma. Although other GBP family members did not show a prominent relationship with treatment resistance at the present stage, GBP3 showed significant up-regulation in response to temozolomide. Furthermore, it’s revealed that high levels of GBP3 expression in glioblastoma was associated with a worsened survival after temozolomide treatment. Consistent with this observation, exogenous expression of GBP3 induced temozolomide resistance in independent patient-derived glioblastoma neurosphere lines, while GBP3 silencing conferred temozolomide sensitivity, both in vitro and in vivo.“This sensitivity was associated with the accumulation of cytoplasmic DNA fragments, suggesting the involvement of Stimulator of interferon genes (STING).”DOI - https://doi.org/10.18632/oncotarget.28370Correspondence to - Ming Li - [email protected]Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28370Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - cancer, GBP3, MGMT, glioblastoma, temozolomide resistance, STINGAbout OncotargetOncotarget (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.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/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/Media Contact180092209574 min
- HER3: A Vital Target in Cancer TreatmentDr. Omkar Desai, from the Department of Surgery at Case Western Reserve University and University Hospitals Cleveland Medical Center, describes a research perspective he co-authored with Dr. Rui Wang that was published by Oncotarget in Volume 14, entitled, “HER3- A key survival pathway and an emerging therapeutic target in metastatic colorectal cancer and pancreatic ductal adenocarcinoma.”DOI - https://doi.org/10.18632/oncotarget.28421Correspondence to - Rui Wang - [email protected]Author video - https://www.youtube.com/watch?v=3-02jt7-MW8Sign 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 Contact180092209579 min
- Suppression of Cancer Stemness & Drug Resistance via BRAF/EGFR/MEK Inhibition in Colorectal CancerBUFFALO, NY- October 11, 2023 – A new research paper was published in Oncotarget's Volume 14 on October 4, 2023, entitled, “Inhibiting BRAF/EGFR/MEK suppresses cancer stemness and drug resistance of primary colorectal cancer cells.”Drug resistance is a major barrier against successful treatments of cancer patients. Gain of stemness under drug pressure is a major mechanism that renders treatments ineffective. Identifying approaches to target cancer stem cells (CSCs) is expected to improve treatment outcomes for patients. In their new study, researchers Astha Lamichhane, Gary D. Luker, Seema Agarwal, and Hossein Tavana from The University of Akron, University of Michigan and Georgetown University aimed to elucidate the role of cancer stemness in resistance of colorectal cancer cells to targeted therapies.“[...] we developed spheroid cultures of patient-derived BRAFmut and KRASmut tumor cells and studied resistance mechanisms to inhibition of MAPK pathway through phenotypic and gene and protein expression analysis.”They found that treatments enriched the expression of CSC markers CD166, ALDH1A3, CD133, and LGR5 and activated PI3K/Akt pathway in cancer cells. The team examined various combination treatments to block these activities and found that a triple combination against BRAF, EGFR, and MEK significantly reduced stemness and activities of oncogenic signaling pathways. This study demonstrates the feasibility of blocking stemness-mediated drug resistance and tumorigenic activities in colorectal cancer.“Our approach to identify mechanisms of drug resistance of patient-derived cancer cells to targeted therapies and develop effective treatments is promising toward cancer precision medicine.”DOI - https://doi.org/10.18632/oncotarget.28517Correspondence to - Hossein Tavana - [email protected]Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28517Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - cancer, drug resistance, cancer stem cells, patient-derived tumor model, colorectal cancer, combination treatmentAbout OncotargetOncotarget (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.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/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/Media Contact180092209573 min
- STAT3 as a Target in H3K27M-mutant DMGsBUFFALO, NY- October 9, 2023 – A new editorial perspective was published in Oncotarget's Volume 14 on October 4, 2023, entitled, “STAT3 as a biologically relevant target in H3K27M-mutant diffuse midline glioma.”Pediatric H3K27M-mutant diffuse midline gliomas (DMGs), including those formerly classified as diffuse intrinsic pontine gliomas (DIPG), are uniformly lethal central nervous system malignancies. Children diagnosed with these tumors have an extremely poor prognosis, with a median survival of approximately 12 months. The current standard of care for DMG includes possible biopsy for diagnostic confirmation and a 6-week course of palliative radiation. Despite enormous effort toward the development of novel therapeutics in DMG, chemotherapy remains ineffective in this disease.“Indeed, over 100 clinical trials for chemotherapeutics in DMG have failed to show therapeutic benefit [5].”In their new editorial perspective, researchers Jacob B. Anderson, Samantha M. Bouchal, Liang Zhang, and David J. Daniels from the Mayo Clinic discussed the currently available literature and their recent study on the Signal Transducer and Activator of Transcription (STAT) as a biologically relevant therapeutic target in H3K27M-mutant DMGs. In their recently published manuscript, the lab performed a screen of drugs currently in clinical use or clinical trials for efficacy against a library of H3K27Mmutant and H3-wildtype patient-derived cell lines. The results of this drug screen identified the STAT3 signaling pathway as a novel target in DMG.“Until recently, however, STAT3 was not a druggable target.”DOI - https://doi.org/10.18632/oncotarget.28516Correspondence to - David J. Daniels - [email protected]Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28516Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - cancer, H3K27M, DMG, DIPG, midline glioma, STAT3About OncotargetOncotarget (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.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/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/Media Contact180092209573 min
- Blog: Genetic Insights into Early Breast Cancer in KazakhstanBreast cancer (BC) is one of the most common and deadly cancers worldwide, affecting millions of women every year. However, not all women share the same risk of developing breast cancer. There are many factors that influence this disease, including age, lifestyle, family history, and genetic makeup.One of the most important aspects of breast cancer research is to identify the genetic factors that predispose some women to develop breast cancer at an early age, especially in different ethnic groups that may have unique genetic variants. This can help to improve the prevention, diagnosis and treatment of breast cancer, as well as to reduce the health disparities among different populations.In a new study, researchers Gulnur Zhunussova, Nazgul Omarbayeva, Dilyara Kaidarova, Saltanat Abdikerim, Natalya Mit, Ilya Kisselev, Kanagat Yergali, Aigul Zhunussova, Tatyana Goncharova, Aliya Abdrakhmanova, and Leyla Djansugurova from the Institute of Genetics and Physiology, Kazakh Institute of Oncology and Radiology, Al-Farabi Kazakh National University, and Asfendiyarov Kazakh National Medical University aimed to determine the genetic predisposition to early breast cancer in women from Kazakhstan — a population that has not been well studied before. On October 4, 2023, their research paper was published in Oncotarget, entitled, “Determination of genetic predisposition to early breast cancer in women of Kazakh ethnicity.”“Our study may reveal previously uncharacterized population-specific variants that may increase the risk of BC in the Kazakh population.”Full blog - https://www.oncotarget.org/2023/10/05/genetic-insights-into-early-breast-cancer-in-kazakhstan/Paper DOI - https://doi.org/10.18632/oncotarget.28518Correspondence to - Gulnur Zhunussova - [email protected], and Nazgul Omarbayeva - [email protected]Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28518Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - cancer, breast cancer, early-onset breast cancer, triple negative breast cancer, next-generation sequencing, pathogenic variant, Kazakh populationAbout OncotargetOncotarget (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.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/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/Media Contact180092209577 min
- UGDH in Clinical Oncology and Cancer BiologyBUFFALO, NY- October 4, 2023 – A new review paper was published in Oncotarget's Volume 14 on September 28, 2023, entitled, “UDP-glucose dehydrogenase (UGDH) in clinical oncology and cancer biology.”UDP-glucose-6-dehydrogenase (UGDH) is a cytosolic, hexameric enzyme that converts UDP-glucose to UDP-glucuronic acid (UDP-GlcUA), a key reaction in hormone and xenobiotic metabolism and in the production of extracellular matrix precursors.In this review, researchers Meghan J. Price, Annee D. Nguyen, Jovita K. Byemerwa, Jasmine Flowers, César D. Baëta, and C. Rory Goodwin from Johns Hopkins Hospital, Duke University, Stanford University, Duke Center for Brain and Spine Metastasis, and Duke Cancer Institute classify UGDH as a molecular indicator of tumor progression in multiple cancer types, describe its involvement in key canonical cancer signaling pathways, and identify methods to inhibit UGDH, its substrates, and its downstream products.“As such, we position UGDH as an enzyme to be exploited as a potential prognostication marker in oncology and a therapeutic target in cancer biology.”DOI - https://doi.org/10.18632/oncotarget.28514Correspondence to - C. Rory Goodwin - [email protected]Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28514Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - cancer, UDP-6 glucose dehydrogenase, UGDH, oncology, cancer biologyAbout OncotargetOncotarget (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.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/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/Media Contact180092209573 min
- An Ancient Anti-cancer Mechanism: DISEBUFFALO, NY- October 3, 2023 – A new editorial paper was published in Oncotarget's Volume 14 on September 25, 2023, entitled, “DISE, an ancient anti-cancer mechanism that senses mutational load in cancerous cells?”In their new editorial, researchers Monal Patel and Marcus E. Peter from Northwestern University discuss a recent breakthrough in cancer therapy. Despite the multiple advances in therapy, cancer remains one of the most common causes of death globally. It is a systemic disease affecting people of all ages and originates at the level of single cells which, upon acquisition of mutations, become neo-plastically transformed.Cell division is the biggest risk factor for the accumulation of mutations, explaining why all multicellular organisms which evolved about 2 billion years ago, are prone to cancer. Given the recent achievements in cancer treatment with immune checkpoint blockade therapies, multicellular organisms may have developed the immune system as a mechanism to eradicate cancerous cells.“However, the immune system arose relatively recent, ~500 million years ago [3].”Moreover, studies have shown that cancer cells can become resistant to the anticancer activity of both the innate and the adaptive immune system. Therefore, while the immune system is important, it is likely not the most vital machinery that emerged in multicellular organisms to prevent cancer formation. The researchers believe that there are other more effective and archaic anti-cancer mechanisms that are conserved during evolution.Of note, RNA interference (RNAi) is a highly conserved biological mechanism for silencing gene expression. While RNAi likely emerged as a defense tool against viruses and other foreign nucleic acids, it has also evolved to have other activities in the cells. The team’s research has identified a new evolutionarily conserved RNAi-based form of cell death that targets essential survival genes: Death Induced by Survival gene Elimination (DISE).“DISE was discovered through our work on CD95 and its ligand, CD95L, where we found that more than 80% of 26 different short interfering RNAs (siRNAs) and short hairpin RNAs (shRNAs) derived from the two genes, killed multiple cancer cell lines via simultaneous activation of multiple cell death pathways; and we were unable to find a way to inhibit this form of cell death [9].”DOI - https://doi.org/10.18632/oncotarget.28466Correspondence to - Marcus E. Peter - [email protected]Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28466Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - cancer, cell death, evolution, RNAi, short RNAsAbout OncotargetOncotarget (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.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/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/Media Contact180092209574 min
- Reassessing COVID-19 Precautions in 2023BUFFALO, NY- September 27, 2023 – A new editorial paper was published in Oncotarget's Volume 14 on September 22, 2023, entitled, “Reassessing the risks and benefits of COVID-19 precautions in 2023.”The COVID-19 pandemic has killed over one million Americans with many dying during the Omicron wave. By now most Americans have either had COVID-19 and/or been vaccinated against it. Despite the availability of updated immunizations, only 16.7% of Americans are now up-to-date on bivalent boosters. In their new editorial, researchers Thomas A. Ollila, Rashida Taher and Prashanth Moku from the Alpert Medical School of Brown University and Rhode Island Hospital discuss the current state of COVID-19 treatment.“At our cancer center, we treat many patients with hematologic malignancies, most of whom are older adults.”Patients with hematologic malignancies, especially lymphoma, are at increased risk of poor response to vaccination and worse outcomes from COVID-19 infection. The researchers state that most of their patients have been abundantly cautious since the onset of the pandemic and some have avoided ever becoming infected. Patients in their clinic frequently inquire about the safety of being outdoors, spending time with their families during large gatherings (Christmas, Thanksgiving, etc.), and methods to prevent the contraction of COVID-19.“Despite these precautions, too many patients reached remission from cancer only to then perish from COVID-19 in the first years of the pandemic.”The concerns behind their questions are very real, but understanding how to best answer them is not always easy and their abundance of caution is not without cost. Grandchildren’s birthdays went uncelebrated, weddings were forgone, and memorable moments with loved ones were lost. With both aging and malignancy, an acute awareness of the limited days means that there may not be years ahead to make up for all that was missed.“Although COVID-19 continues to pose a serious threat, medical advancements have now allowed for a more in-depth risk-benefit discussion to weigh the risk of infection versus the challenges of social isolation.”DOI - https://doi.org/10.18632/oncotarget.28468Correspondence to - Thomas A. Ollila - [email protected]Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28468Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - cancer, COVID, immunosuppression, coronavirus, vaccination, lymphomaAbout OncotargetOncotarget (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.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/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/Media Contact180092209574 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/