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Oncotarget
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Oncotarget episodes
- ER Expression Multiclonality in DCIS: Clinical & Future InsightsDr. Mangesh A. Thorat from Guy’s Hospital in London, Queen Mary University of London, and King’s College London, describes a recent #editorial he authored that was #published by Oncotarget in Volume 14, entitled, “Multiclonality of ER expression in DCIS – Implications for clinical practice and future research.”#author #interview #authorinterview #researcher #cancer #cancerresearch #breastcancer #research #recurrence #clonality #ductalcarcinoma #ER #openaccess #openscience #peerreview #journal #publication #meded #publishing #researcher #videoDOI - https://doi.org/10.18632/oncotarget.28450Correspondence to - Mangesh A. Thorat - [email protected]; [email protected]Video interview - https://www.youtube.com/watch?v=TGeiFcKjbaQSign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28450Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - cancer, ductal carcinoma in situ (DCIS), invasive breast cancer, ER, recurrence, clonalityAbout 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/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 Contact180092209576 min
- Editorial: A Macrophage is a Macrophage is a Macrophage—in MetastasisA new editorial paper was published in Oncotarget's Volume 14 on June 6, 2023, entitled, “A macrophage is a macrophage is a macrophage—in metastasis.”In this new editorial, researcher Thomas T. Tapmeier from Monash University, Hudson Institute of Medical Research and University of Oxford discusses a recent study he co-authored on how lung macrophages evolve during metastatic growth of lung colonies in a mouse model of melanoma. Macrophages have important roles in the response to infection or injury and can orchestrate the appropriate response after sampling their microenvironment, devouring anything untoward and presenting ingested antigens to T cells to elicit an adaptive immune response. In adult life, they develop from bone marrow-derived precursors and circulating monocytes, which differentiate into macrophages within tissue.“Apart from their role in clearing challenges to tissue integrity, macrophages have an essential role in growth-related processes such as angiogenesis and vascular remodelling, neural patterning, and ductal growth of developing glands [2].”However, their powers can be usurped by tumors, which cannot grow beyond a certain size or metastasis without the help of macrophages. This is crucial, as the primary tumor might be amenable to treatment—so that patients can live with it—but metastasis is yet untreatable and inevitably becomes incompatible with survival. Macrophages perform a range of physiological functions and are able to activate function-specific gene repertoires; however, surface markers for selectively targeting macrophages of one or another function are still elusive, despite recent advances in the field.“Thus, therapy attempts based on countering macrophages try to target the surface receptors that recruit them to sites of infection, inflammation or growth [5].”DOI - https://doi.org/10.18632/oncotarget.28423Correspondence to - Thomas T. Tapmeier - [email protected]Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28423Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - cancer, metastasis, macrophages, melanoma, CCRAbout 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/Twitter - https://twitter.com/oncotargetInstagram - https://www.instagram.com/oncotargetjrnl/YouTube - https://www.youtube.com/@OncotargetJournalLinkedIn - https://www.linkedin.com/company/oncotargetPinterest - https://www.pinterest.com/oncotarget/Reddit - https://www.reddit.com/user/Oncotarget/Media Contact180092209573 min
- Aggressive Luminal Breast Cancer: Are Cis-Spliced Fusion Proteins Pathological?A new editorial paper was published in Oncotarget's Volume 14 on June 12, 2023, entitled, “Are cis-spliced fusion proteins pathological in more aggressive luminal breast cancer?”A vast majority of breast cancers (~70%) are estrogen receptor-alpha positive (ER+), for which endocrine therapy is the common treatment. However, recurrence often occurs leading to tumor progression, metastasis and eventually patient death, and the underlying molecular mechanisms remain poorly understood. In this new editorial, researchers Chia-Chia Liu and Xiao-Song Wang from the University of Pittsburgh discuss their recent study regarding recurrent gene fusions — hallmarks of some cancers that resulted either from chromosomal rearrangements or from cis- or trans-splicing.“Importantly, selected oncogenic fusions have been matched with effective targeted therapy in several solid tumors. For instance, EML4-ALK, one of the most important oncogenic driver genes of non-small cell lung cancer (NSCLC) uncovered in recent years.”In addition to gene fusions resulting from genomic rearrangements, a read-through SLC45A3-ELK4 fusion transcript has been identified in prostate cancer which is associated with disease progression and metastasis. Although the whole genome and RNA sequencing provide an effective way to detect fusion genes, the downstream identification and validation of fusion genes or their products in solid tumors remains a major challenge. Through analysis of RNA-seq data from TCGA, the authors of this editorial and their co-authors recently identified a neoplastic fusion transcript RAD51AP1-DYRK4 in luminal B breast cancer (~17.5%) showing higher ki67 expression which is an indication of aggressive clinical characteristics.“In this study, we examined the utility of MEK inhibitor trametinib (Mekinist) currently used for treating melanoma with BRAF mutations, in blocking the MEK-ERK signaling driven by RAD51AP1-DYRK4 fusion. Interestingly [...] RAD51AP1-DYRK4 may endow sensitivity to MEK inhibition in luminal B breast cancer [13]. To our knowledge, this is one of the few non-traditional fusions generated by read-through events in the absence of DNA rearrangement that play an important role in tumorigenesis.”DOI - https://doi.org/10.18632/oncotarget.28438Correspondence to - Xiao-Song Wang - [email protected]Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28438Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - cancer, luminal B breast cancer, RAD51AP1-DYRK4, MEK inhibitor, chimerical transcriptAbout 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/Twitter - https://twitter.com/oncotargetInstagram - https://www.instagram.com/oncotargetjrnl/YouTube - https://www.youtube.com/@OncotargetJournalLinkedIn - https://www.linkedin.com/company/oncotargetPinterest - https://www.pinterest.com/oncotarget/Reddit - https://www.reddit.com/user/Oncotarget/Media Contact180092209574 min
- Inhibiting Glutamine Metabolism Impacts Tumor Cells or the Microenvironment?A new editorial paper was published in Oncotarget's Volume 14 on August 10, 2023, entitled, “Inhibition of glutamine metabolism: acting on tumoral cells or on tumor microenvironment?”Cancer cell growth and survival relies on metabolites and metabolic routes different from those used by healthy cells. Glucose and glutamine (Gln) uptake and consumption is increased by many cancer types in order to support their high growth rate. Besides being metabolized to tricarboxylic acid (TCA) cycle precursors, Gln is necessary also for the generation of nitrogen-containing metabolites, such as nucleotides, glucosamine-6-phosphate or nonessential amino acids. Indeed, nitrogen supply has been widely described as limiting for cell cycle progression.As mitochondrial glutaminase (GLS) directs Gln into the TCA cycle, its inhibition has been suggested as a potential strategy for targeting and blocking Gln metabolism in cancer cells. In fact, GLS inhibitors block cancer cell growth in vivo and in vitro. Based on this premise, several clinical studies have been conducted to test if Gln dysregulation increases cancer patients’ survival. So far, these treatments have not been able to induce a great overall benefit for patients due to the ability of tumor cells to alter their metabolism.Different authors have described an increase in the oxidative stress after alterations in Gln metabolism in vivo, suggesting the possibility to combine glutamine dysregulation strategies with some other therapies increasing reactive oxidative species to promote cancer cell death. In his new editorial, researcher Raul Peña from Institut Hospital del Mar d'Investigacions Mèdiques (IMIM) discusses a novel mechanism by which Gln, usually concentrated at the tumor periphery, acts as a chemoattractant for cancer-associated fibroblasts (CAFs), enhancing extracellular matrix degradation and facilitating epithelial cancer cell migration and metastasis in vivo.“Recently, we described a new action of Gln on cancer-associated fibroblasts (CAFs) in breast cancer. [...] In our study, we determined that mesenchymal-like epithelial breast tumor cells and CAFs present a higher dependence on Gln than tumor epithelial breast cancer cells.”DOI - https://doi.org/10.18632/oncotarget.28443Correspondence to - Raúl Peña - [email protected]Video short - https://www.youtube.com/watch?v=HcI9CpUdbysSign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28443Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - cancer, glutamine, tumor microenvironment, fibroblasts, CAF, snail1About 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/Twitter - https://twitter.com/oncotargetInstagram - https://www.instagram.com/oncotargetjrnl/YouTube - https://www.youtube.com/@OncotargetJournalLinkedIn - https://www.linkedin.com/company/oncotargetPinterest - https://www.pinterest.com/oncotarget/Reddit - https://www.reddit.com/user/Oncotarget/Media Contact180092209574 min
- Guiding Therapies for HPV Malignancies: Tumor Burden SurrogatesA new review paper was published in Oncotarget's Volume 14 on August 10, 2023, entitled, “Peripheral surrogates of tumor burden to guide chemotherapeutic and immunotherapeutic strategies for HPV-associated malignancies.”With the rapid adoption of immunotherapy into clinical practice for HPV-associated malignancies, assessing tumor burden using “liquid biopsies” would further our understanding of clinical outcomes mediated by immunotherapy and allow for tailoring of treatment based on real-time tumor dynamics.In their new review, researchers Meghali Goswami, Jeffrey Schlom and Renee N. Donahue from the National Cancer Institute examine translational studies on peripheral surrogates of tumor burden derived from peripheral blood in HPV-associated malignancies, including levels and methylation of circulating tumor DNA (ctDNA), miRNA derived from extracellular vesicles, circulating tumor cells (CTCs), and HPV-specific antibodies and T cell responses.“We review their utility as prognostic and predictive biomarkers of response to chemotherapy and radiation, with a focus on how they may inform and guide immunotherapies to treat locally advanced and metastatic HPV-associated malignancies. We also highlight unanswered questions that must be addressed to translate and integrate these peripheral tumor biomarkers into the clinic.”DOI - https://doi.org/10.18632/oncotarget.28487Correspondence to - Jeffrey Schlom - [email protected]Video short - https://www.youtube.com/watch?v=b9FhlVB6iY0Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28487Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - cancer, HPV-associated malignancies, immunotherapy, circulating tumor DNA, circulating tumor cells, HPV-specific antibodiesAbout 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/Twitter - https://twitter.com/oncotargetInstagram - https://www.instagram.com/oncotargetjrnl/YouTube - https://www.youtube.com/@OncotargetJournalLinkedIn - https://www.linkedin.com/company/oncotargetPinterest - https://www.pinterest.com/oncotarget/Reddit - https://www.reddit.com/user/Oncotarget/Media Contact180092209573 min
- Blog: Whole-Genome Doubling and Aneuploidy in Human CancerWhole-genome doubling (WGD) and aneuploidy are two common genomic alterations that occur in human cancers. WGD is a macro-evolutionary event that results in the duplication of the entire genome, while aneuploidy is a micro-evolutionary event that results in the gain or loss of individual chromosomes or chromosome arms. Both WGD and aneuploidy can have profound effects on cellular physiology, gene expression and genome stability, and are associated with tumor initiation, progression and drug resistance.However, the relationship between WGD and aneuploidy is complex and context-dependent. In a new editorial paper, researchers Kavya Prasad and Uri Ben-David from Tel Aviv University discuss a recent study exploring how WGD shapes the aneuploidy landscape of human cancers. Their editorial was published in Oncotarget on April 26, 2023, and entitled, “A balancing act: how whole-genome doubling and aneuploidy interact in human cancer.”“It is known that tumors that have undergone WGD are more permissive to aneuploidy, but whether WGD also affects aneuploidy patterns has remained an open question.”Full blog - https://www.oncotarget.org/2023/08/10/whole-genome-doubling-and-aneuploidy-in-human-cancer/Editorial DOI - https://doi.org/10.18632/oncotarget.28374Correspondence to - Uri Ben-David - [email protected]Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28374Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - cancer, cancer genetics, whole-genome doubling, chromosomal instabilityAbout 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/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 Contact180092209576 min
- CDK9 Inhibitors: A Promising Combination Partner in Treating Hematological MalignanciesA new research perspective was published in Oncotarget's Volume 14 on August 7, 2023, entitled, “CDK9 INHIBITORS: a promising combination partner in the treatment of hematological malignancies.”In their new perspective, researchers Daniel Morillo, Gala Vega and Victor Moreno from Hospital Fundación Jiménez Díaz discuss Cyclin-dependent kinases (CDK) in hematological malignancies. CDKs belong to a family of serine/threonine kinases that need to form heterodimeric complexes with cyclins to perform their functions. These kinases are involved in multiple processes within cells, including cell cycle, apoptosis, transcription and differentiation. These kinases are often overexpressed in different malignancies, making them potential targets for new drugs.Most hematological malignancies are characterized by overexpression of certain cancer promoting genes, such as MYC, MCL1 and cyclin D1. Preclinical studies in animal models have shown that CDK9 inhibitors suppress the transcription of these anti-apoptotic and pro-survival proteins, and suggest their potential synergism with other drugs. In its first in-human trial, enitociclib demonstrated clinical activity in a small cohort of patients with high grade B lymphoma with MYC and BCL2 and/or BCL6 rearrangements, inducing complete responses in 2 of 7 subjects (29%) in monotherapy.“In summary, most hematological malignancies are characterized by overexpression of certain cancer promoting genes, such as MYC and MCL1. CDK9 inhibitors are relatively new drugs that inhibit transcription of these anti-apoptotic and pro-survival proteins.”DOI - https://doi.org/10.18632/oncotarget.28473Correspondence to - Victor Moreno - [email protected]Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28473Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - cancer, cyclin-dependent kinases (CDK), CDK9, hematological malignanciesAbout 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/Twitter - https://twitter.com/oncotargetInstagram - https://www.instagram.com/oncotargetjrnl/YouTube - https://www.youtube.com/@OncotargetJournalLinkedIn - https://www.linkedin.com/company/oncotargetPinterest - https://www.pinterest.com/oncotarget/Reddit - https://www.reddit.com/user/Oncotarget/Media Contact180092209573 min
- AGO2 in T-prolymphocytic Leukemia (T-PLL)A new editorial paper was published in Oncotarget's Volume 14 on May 4, 2023, entitled, “AGO2 in T-prolymphocytic leukemia: its canonical and noncanonical deregulation and function.”In their new editorial, researchers Till Braun, Hanna Klepzig and Marco Herling from University of Cologne and University of Leipzig T-prolymphocytic leukemia (T-PLL) — a mature T-cell neoplasm with an aggressive and treatment refractory course.“In light of limited therapeutic options median overall survival times from diagnosis is hardly longer than 2 years.”There is currently no FDA- or EMA-approved drug for the treatment of T-PLL. Although 80–90% of patients experience a response to the most efficient single agent Alemtuzumab, relapses are common within the first 12–24 months following this first-line treatment. One of the defining characteristics of T-PLL is the presence of the chromosomal aberrations inv(14) or t(14;14), which lead to constitutive expression of the proto-oncogene T-cell leukemia 1A (TCL1A).This adapter molecule is centrally implicated in the enhanced T-cell receptor (TCR) signaling that is observed in the memorytype malignant T-cell. Other recurrent genomic alterations that have been identified in T-PLL affect the genes ataxia telangiectasia mutated (ATM), Janus kinase (JAK), signal transducer and activator of transcription (STAT), and MYC. In a recent study published by Braun et al., the team made significant advances in the understanding of the biology of T-PLL at the level of post-transcriptional gene regulation.“For the first time, descriptive and mechanistic data implicated the involvement of molecules of the RNA interference (RNAi) machinery in T-PLL’s leukemogenesis and by that refined our current disease model by concepts beyond protein-coding genes.”DOI - https://doi.org/10.18632/oncotarget.28378Correspondence to - Marco Herling - [email protected]Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28378Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - cancer, leukemia, T-PLL, AGO2, microRNAAbout 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/Twitter - https://twitter.com/oncotargetInstagram - https://www.instagram.com/oncotargetjrnl/YouTube - https://www.youtube.com/@OncotargetJournalLinkedIn - https://www.linkedin.com/company/oncotargetPinterest - https://www.pinterest.com/oncotarget/Reddit - https://www.reddit.com/user/Oncotarget/Media Contact180092209573 min
- Epigenetically Guided Cancer Therapy: Targeting H3K27me3 Loss in Pediatric Brain TumorsA new editorial paper was published in Oncotarget's Volume 14 on May 12, 2023, entitled, “Targeting H3K27me3 loss in pediatric brain tumors - a perspective on epigenetically guided cancer therapy.”High-grade tumors of the central nervous system, including medulloblastoma, ependymoma and DMG (diffuse midline glioma, formerly known as DIPG (diffuse intrinsic pontine glioma)), constitute a major challenge in pediatric oncology. They are characterized by an aggressive growth and high relapse rates and claim the lives of many pediatric cancer patients.Both medulloblastoma and ependymoma are treated with surgical resection followed by adjuvant radiation therapy. DMG, on the other hand, diffusely infiltrates the brain stem making a resection virtually impossible. Thus, radiotherapy is the primary treatment modality for this tumor. While radiation temporarily attenuates the progression of DMG this brain cancer remains incurable and most children succumb to their disease.In his new editorial, Dr. Michael Goldstein from Johns Hopkins University School of Medicine discusses the extensively investigated molecular profiles of the aforementioned pediatric brain tumors demonstrating distinct epigenetic traits.“Strikingly, a global loss of H3K27 tri-methylation (H3K27me3) as a result of the dominant-negative histone H3K27M mutation was found to be a hallmark of DMG occurring in the majority of the tumors.”H3K27me3 is a product of the EZH2 histone methyltransferase affecting multiple cellular processes including transcription, chromatin structure and DNA damage response. Similarly, the aggressive PFA ependymoma subgroup is characterized by a lack of H3K27me3 due to an overexpression of the EZHIP protein that acts as an EZH2 inhibitor whereas less aggressive PFB tumors retain normal H3K27me3 levels. However, no comprehensive analysis of H3K27me3 expression patterns in medulloblastoma has been performed and the significance of this epigenetic mark in pediatric brain tumors has remained unknown.“To address this, we have investigated the levels of the H3K27me3 histone mark and its role in treatment response of non-WNT/SHH medulloblastoma comprising group 3 and group 4 tumors. We demonstrated that about 50% of the tumors in patients with group 3 and group 4 medulloblastoma are H3K27me3 deficient. Strikingly, loss of H3K27me3 was associated with high relapse rates and poor survival.”DOI - https://doi.org/10.18632/oncotarget.28427Correspondence to - Michael Goldstein - [email protected]Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28427Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - cancer, epigenetics, brain tumor, EZH2, H3K27me3, radiation therapyAbout 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/Twitter - https://twitter.com/oncotargetInstagram - https://www.instagram.com/oncotargetjrnl/YouTube - https://www.youtube.com/@OncotargetJournalLinkedIn - https://www.linkedin.com/company/oncotargetPinterest - https://www.pinterest.com/oncotarget/Reddit - https://www.reddit.com/user/Oncotarget/Media Contact180092209574 min
- Multiclonality of Estrogen Receptor Expression in Ductal Carcinoma in Situ (DCIS)A new editorial paper was published in Oncotarget's Volume 14 on July 20, 2023, entitled, “Multiclonality of ER expression in DCIS – Implications for clinical practice and future research.”Estrogen receptor (ER) expression is not routinely evaluated in ductal carcinoma in situ (DCIS). This may be because the prognostic role of ER in DCIS was unclear until the UK/ ANZ DCIS trial in 2021 showed that lack of ER expression in DCIS was associated with a greater than 3-fold risk of ipsilateral recurrence. This was the largest (to date) case-control study nested in a DCIS randomized trial.The meticulous study design eliminated treatment allocation bias as well as treatment-related confounding. This was also the first-ever study to show that ER expression in DCIS is multi-clonal — having very important clinical and research implications. A small proportion of otherwise ER-positive DCIS also contained carcinoma in situ (CIS) duct/s that completely lacked ER expression.“This admixture of clearly ER-positive and ER-negative ducts is not the same as heterogeneity in ER expression and I labeled such DCIS cases as multiclonal DCIS even if just one CIS duct in the entire section lacked ER expression.”In his new editorial, Dr. Mangesh A. Thorat from Guy's and St Thomas' NHS Foundation Trust, Queen Mary University of London and King's College London discusses this study in greater detail, the clinical implications of ER status in DCIS, the potential for avoiding overtreatment and undertreatment based on ER expression, and the importance of simple clinical observations in research.“In summary, ER is a strong and independent prognostic biomarker in DCIS and our novel clonal method is a more accurate method to assess ER status in DCIS.”DOI - https://doi.org/10.18632/oncotarget.28450Correspondence to - Mangesh A. Thorat - [email protected]; [email protected]Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28450Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - cancer, ductal carcinoma in situ (DCIS), invasive breast cancer, ER, recurrence, clonalityAbout 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/Twitter - https://twitter.com/oncotargetInstagram - https://www.instagram.com/oncotargetjrnl/YouTube - https://www.youtube.com/@OncotargetJournalLinkedIn - https://www.linkedin.com/company/oncotargetPinterest - https://www.pinterest.com/oncotarget/Reddit - https://www.reddit.com/user/Oncotarget/Media Contact180092209573 min
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