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Oncotarget
By Oncotarget PodcastScience
Oncotarget episodes
- Blog: The Obesity Paradox, Metformin and Lung CancerListen to a blog summary of an editorial published in Volume 14 of Oncotarget, entitled, "Obesity paradox and lung cancer, metformin-based therapeutic opportunity?"__________________________________________________________________The strong correlation between obesity and a myriad of life-limiting diseases and conditions, including type 2 diabetes, is widely recognized and acknowledged in the research community. A less defined correlation is that between obesity, diabetes and lung cancer. Whether this association is directly causal or if there are underlying contributing factors is not yet clear.“Although obesity and type 2 diabetes mellitus (T2DM) have been associated with lung cancer (LC) development, several confounding factors, such as chronic inflammation, high insulin levels, microbiome, as well as the oncogenic potential of growth and sexual hormones, have introduced uncertainty and avoid the fully recognition of this relationship [1, 2].”Given the existence of this association, scientists are testing therapeutic regimens that may have the potential to fight all three issues — together. Metformin, a drug commonly prescribed to treat type 2 diabetes, helps lower blood sugar levels by improving insulin sensitivity and reducing glucose production in the liver. The metabolic-modifying properties of metformin aid in treating diabetes and obesity. Metformin has also garnered attention for its potential anti-aging properties and may hold promise for treating age-related diseases, including cancer. Lately, there has been growing interest in testing metformin in combination therapies to combat cancer-promoting conditions induced by obesity.The "Obesity Paradox"While the link between morbidity and obesity may seem cut-and-dry, researchers have discovered a surprising trend. The "obesity paradox" suggests that, in certain instances, individuals classified as overweight or mildly obese seem to fare better or have a survival advantage compared to those with normal weight or even underweight counterparts. This paradox has been particularly observed in certain chronic illnesses, such as heart failure, chronic kidney disease, and even in the context of aging. Researchers are still striving to understand the underlying mechanisms driving this phenomenon.Full blog: https://www.oncotarget.org/2023/07/27/the-obesity-paradox-metformin-and-lung-cancer/Paper DOI: https://doi.org/10.18632/oncotarget.28432Corresponding author: Oscar Arrieta - [email protected]Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28477Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - metformin, tyrosine-kinase inhibitors, BMI, EGFR, obesity paradoxAbout 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 Contact180092209577 min
- KIAA0930: A Cachexic Phenotype Inducer in Cancer CellsA new research paper was published in Oncotarget's Volume 14 on July 20, 2023, entitled, “The uncharacterized transcript KIAA0930 confers a cachexic phenotype on cancer cells.”Patients with cancer cachexia have a poor prognosis and impaired quality of life. Numerous studies using preclinical models have shown that inflammatory cytokines play an important role in the development of cancer cachexia; however, no clinical trial targeting cytokines has been successful. Therefore, it is essential to identify molecular mechanisms to develop anti-cachexia therapies.In this new study, researchers Takahiro Yamakawa, Guoxiang Zhang, Liza Bengrine Najjar, Chun Li, and Keiichi Itakura from the Beckman Research Institute of City of Hope identified the uncharacterized transcript KIAA0930 as a candidate cachexic factor based on analyses of microarray datasets and an in vitro muscle atrophy assay.“We here report the initial characterization of KIAA0930.”While conditioned media from pancreatic, colorectal, gastric, and tongue cancer cells caused muscle atrophy in vitro, conditioned medium from KIAA0930 knockdown cells did not. The PANC-1 orthotopic xenograft study showed that the tibialis anterior muscle weight and cross-sectional area were increased in mice bearing KIAA0930 knockdown cells compared to control mice. Interestingly, KIAA0930 knockdown did not cause consistent changes in the secretion of inflammatory cytokines/chemokines from a variety of cancer cell lines. An initial characterization experiment showed that KIAA0930 is localized in the cytosol and not secreted from cells.“These data suggest that the action of KIAA0930 is independent of the expression of cytokines/chemokines and that KIAA0930 could be a novel therapeutic target for cachexia.”Read the full study: DOI: https://doi.org/10.18632/oncotarget.28476Correspondence to: Takahiro Yamakawa - [email protected]Keywords: KIAA0930, cancer cachexia, muscle atrophy, inflammatory cytokines/chemokines, protein secretionAbout 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.To learn more about Oncotarget, visit Oncotarget.com and connect with us on social media: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/Sign up for free Altmetric alerts about this article: https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28476For media inquiries, please contact: [email protected].3 min
- A Multiplex Assay to Assess Activated p300/CBP in Circulating Prostate Tumor CellsA new research paper was published in Oncotarget's Volume 14 on July 20, 2023, entitled, “Development of a multiplex assay to assess activated p300/CBP in circulating prostate tumor cells.”Reduced SIRT2 deacetylation and increased p300 acetylation activity leads to a concerted mechanism of hyperacetylation at specific histone lysine sites (H3K9, H3K14, and H3K18) in castration-resistant prostate cancer (CRPC). In this new study, researchers Mikolaj Filon, Bing Yang, Tanaya A. Purohit, Jennifer Schehr, Anupama Singh, Marcelo Bigarella, Peter Lewis, John Denu, Joshua Lang, and David F. Jarrard from the University of Wisconsin examined whether circulating tumor cells (CTCs) identify patients with altered p300/CBP acetylation.“In the current study, employing a novel Exclusion-based Sample Preparation (ESP) technology (9) (Supplementary Figure 1) to isolate CTCs, we evaluated p300 activity, SIRT2 expression and H3K18 acetylation in CTCs in a series of patients with sensitivity or resistance to ADT.”CTCs were isolated from 13 advanced PC patients using Exclusion-based Sample Preparation (ESP) technology. Bound cells underwent immunofluorescent staining for histone modifying enzymes (HMEs) of interest and image capture with NIS-Elements software. Using the cBioPortal PCF/SU2C dataset, the response of CRPC to androgen receptor signaling inhibitors (ARSI) was analyzed in 50 subjects.Staining optimization and specificity revealed clear expression of acetyl-p300, acetyl-H3K18, and SIRT2 on CTCs (CK positive, CD45 negative cells). Exposure to A-485, a selective p300/CBP catalytic inhibitor, reduced p300 and H3K18 acetylation. In CRPC patients, a-p300 strongly correlated with its target acetylated H3k18 (Pearson’s R = 0.61), and SIRT2 expression showed robust negative correlation with a-H3k18 (R = −0.60).A subgroup of CRPC patients (6/11; 55%) demonstrated consistent upregulation of acetylation based on these markers. To examine the clinical impact of upregulation of the CBP/p300 axis, CRPC patients with reduced deacetylase SIRT2 expression demonstrate shorter response times to ARSI therapy (5.9 vs. 12 mo; p = 0.03). A subset of CRPC patients demonstrate increased p300/CBP activity based on a novel CTC biomarker assay.“With further development, this biomarker suite may be used to identify candidates for CBP/p300 acetylation inhibitors in clinical development.”Read the full study: DOI: https://doi.org/10.18632/oncotarget.28477Correspondence to: David F. Jarrard - [email protected]Keywords: prostate cancer, circulating tumor cells, p300/CBPAbout 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.To learn more about Oncotarget, visit Oncotarget.com and connect with us on social media: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/Sign up for free Altmetric alerts about this article: https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28477For media inquiries, please contact: [email protected].5 min
- Novel Therapeutic Strategy Against Melanoma: Combined Targeting of Hedgehog Signaling and BRD4A new editorial paper was published in Oncotarget's Volume 14 on May 26, 2023, entitled, “Combined targeting of HEDGEHOG signaling and BRD4 as a novel therapeutic option against melanoma.”The Hedgehog-GLI (HH/GLI) pathway is aberrantly activated in several types of cancer. Canonical HH/ GLI pathway is triggered by binding of HH ligands to the twelve-pass transmembrane receptor Patched 1 (PTCH1), which retrieves its inhibition on the seven-pass transmembrane G protein-coupled receptor Smoothened (SMO), leading to the activation of the GLI transcription factors. Small molecules inhibitors targeting the essential pathway transducer SMO (e.g., vismodegib, sonidegib) have demonstrated therapeutic efficacy in HH-dependent tumors, such as basal cell carcinoma (BCC) and medulloblastoma (MB).However, the therapeutic efficacy of these SMO antagonists is limited by the development of acquired resistance and recurrence after drug withdrawal, and by additional oncogenic signals responsible for noncanonical activation of GLI transcription factors [1]. In this new editorial, researchers Silvia Pietrobono and Barbara Stecca from the University of Verona and the Institute for Cancer Research and Prevention (CRL-ISPRO) state that they subscribe to the idea that targeting non-canonical HH/GLI signaling will improve the response rate and durability of therapeutic effects exerted by SMO inhibition. Therefore, they propose that the identification of novel targetable regulators that function downstream of SMO, especially those acting at the transcriptional level, is of critical importance to effectively inhibit the HH pathway and prevent tumor relapse.“Collectively, the findings presented by Pietrobono et al. pave the path for the development of a novel therapeutic strategy in tumors having both canonical and non-canonical HH/GLI signaling activation, such as melanoma.”DOI - https://doi.org/10.18632/oncotarget.28441Correspondence to - Silvia Pietrobono - [email protected], and Barbara Stecca - [email protected]Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28441Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - cancer, melanoma, hedgehog signaling, BRD4, SOX2, GLI1About 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
- Case Report: Intrathoracic Synovial Sarcoma with BRAF V600E MutationA new case report was published in Oncotarget's Volume 14 on July 7, 2023, entitled, “Intrathoracic synovial sarcoma with BRAF V600E mutation.”Synovial sarcoma (SS) is a highly malignant mesenchymal tumor that occurs mainly in adolescents and young adults. The treatment of SS is multimodal, involving surgery, radiotherapy and chemotherapy. The overall prognosis is generally quite satisfactory in children and adolescents with localized SS at diagnosis. However, the outcome remains poor for patients who relapse, with a reported 5-year post-relapse survival of around 30%.In this new paper, researchers Ida Russo, Sabina Barresi, Pier Luigi Di Paolo, Valentina Di Ruscio, Giada Del Baldo, Annalisa Serra, Silvia Vallese, Evelina Miele, Angela Mastronuzzi, Rita Alaggio, Andrea Ferrari, and Giuseppe Maria Milano from Italy’s Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) report the case of a 15-year-old boy with intrathoracic synovial sarcoma who relapsed after standard chemotherapy, surgery and radiotherapy. The molecular analysis of the tumor identified a BRAF V600E mutation at time of progression of relapsed disease under third line systemic treatment.This mutation is commonly seen in melanomas and papillary thyroid cancers, but less prevalent (typically <5%) across a variety of other cancer types. The patient underwent selective BRAF inhibitor Vemurafenib treatment achieving partial response (PR) with a progression free survival (PFS) ratio of 1.6 months and an overall survival of 19 months, alive in continuous PR. This case highlights the role of routine next generation sequencing (NGS) used to drive treatment choice and to investigate SS tumors for BRAF mutations.“Our data highlight the importance of implementing molecular tests in SS patients to evaluate BRAF mutational actual incidence in these neoplasms.”DOI - https://doi.org/10.18632/oncotarget.28475Correspondence to - Giuseppe Maria Milano - [email protected]Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28475Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - synovial sarcoma, next-generation sequencing, BRAF V600E mutation, targeted 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 Contact180092209573 min
- Targeting Ras in Cancer Therapies: Advances in Protein EngineeringRas plays a crucial role in controlling various cellular processes by switching between active (Ras-GTP) and inactive (Ras-GDP) states with the help of specific molecules. In its active form, Ras interacts with multiple effector proteins, initiating downstream events. Humans have three Ras genes, resulting in four isoforms that have distinct expression patterns and unique functions in different tissues. Posttranslational modifications target Ras to the cell membrane, where it can form dimers and interact with effectors through common domains. Ras mutations, commonly found in pancreatic, colorectal and lung cancers, lock Ras in an active state, promoting continuous cell division and proliferation. Ras signaling disruption occurs through reduced catalytic activity, altered effector binding and decreased affinity for other regulatory proteins.Although Ras has been considered difficult to target, recent advancements have identified potential binding pockets that can be addressed by small molecules, peptidomimetics and proteins. Inhibitors designed to covalently bind to the Ras G12C mutant have shown promise, leading to FDA-approved drugs for specific lung cancers. Additionally, protein-based inhibitors that target Ras and its interactions with effectors, regulatory proteins and guanine nucleotide exchange factors offer alternative strategies for therapeutic intervention. These developments have challenged the notion that Ras is “undruggable” and highlight the potential for effective treatments against various cancer types.On July 1, 2023, researchers Atilio Tomazini and Julia M. Shifman from The Hebrew University of Jerusalem published a new review paper in Oncotarget, entitled, “Targeting Ras with protein engineering.” The authors provide an overview of the challenges associated with targeting Ras proteins with small molecules and discuss how protein engineering has emerged as a promising method to overcome these challenges.“While the development of small-molecule Ras inhibitors has been reviewed elsewhere [40], we focus our review on protein-based Ras inhibitors, describing the methods for their engineering, various scaffolds used for inhibitor design, and prospects for delivery of the designed Ras inhibitors into the cellular cytoplasm, where Ras is located.”Full blog - https://www.oncotarget.org/2023/07/14/targeting-ras-in-cancer-therapies-advances-in-protein-engineering/Paper DOI - https://doi.org/10.18632/oncotarget.28469Correspondence to - Julia M. Shifman - [email protected]Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28469Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - Ras oncogene, anti-Ras therapeutics, Ras targeting, protein engineering, protein designAbout 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 Contact180092209579 min
- Cetuximab's Effectiveness and Toxicity in Advanced Cutaneous Squamous Cell Skin CancerA new research paper was published in Oncotarget's Volume 14 on July 7, 2023, entitled, “Effectiveness and toxicity of cetuximab with concurrent RT in locally advanced cutaneous squamous cell skin cancer: a case series.”Treatment for locally advanced cutaneous squamous cell cancers (laCSCC) remains poorly defined. Most laCSCC tumors express high levels of epidermal growth factor receptors (EGFR). Cetuximab has activity in other EGFR expressing cancers and enhances the effectiveness of radiotherapy.In this new study, researchers Mark Chang, Wolfram Samlowski and Raul Meoz from University Medical Center of Southern Nevada, Comprehensive Cancer Centers of Nevada, University of Nevada Las Vegas, and University of Nevada Reno conducted a retrospective review of institutional data and identified 18 patients with laCSCC treated with cetuximab induction and concurrent radiotherapy.“We performed a retrospectively review of treatment outcome and toxicity in our patients who received concurrent cetuximab and radiotherapy to show an additional potentially effective treatment option for patients with laCSCC. The goal is also to provide data to inform the design of potential prospective clinical trials.”The loading dose of cetuximab was 400 mg/m² IV. Subsequent weekly doses of 250 mg/m² IV were infused throughout the period of radiation. The treatment doses ranged from 4500–7000 cGy, with a dose fraction of 200-250 cGy. The objective response rate was 83.2% with 55.5% complete responses and 27.7% partial responses.Median progression-free survival was 21.6 months. Progression-free survival was 61% at 1 year and 40% at 2 years. With longer follow-up, some patients developed a local recurrence (16.7%), distant metastases (11.1%) or a second primary cancer (16.3%). Cetuximab was well tolerated, with 68.4% patients experienced only mild acneiform skin rash or fatigue (Grade 1 or 2). Radiotherapy produced expected side effects (skin erythema, moist desquamation, mucositis).“Cetuximab plus radiotherapy represents an active and tolerable treatment option for laCSCC, including patients with contraindications for checkpoint inhibitor therapy.”DOI - https://doi.org/10.18632/oncotarget.28470Correspondence to - Wolfram Samlowski - [email protected]Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28470Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - keratinocyte carcinoma, squamous cell skin cancer, cetuximab, epidermal growth factor receptor, radiation therapyAbout 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.To learn more about Oncotarget, visit Oncotarget.com and connect with us on social media: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/For media inquiries, please contact: [email protected].4 min
- Deciphering Progesterone’s Mechanisms of Action in Breast CancerA new research perspective was published in Oncotarget's Volume 14 on July 1, 2023, entitled, “Deciphering the mechanisms of action of progesterone in breast cancer.”A practice-changing, randomized, controlled clinical study established that preoperative hydroxyprogesterone administration improves disease-free and overall survival in patients with node-positive breast cancer. In this new perspective, researchers Gaurav Chakravorty, Suhail Ahmad, Mukul S. Godbole, Sudeep Gupta, Rajendra A. Badwe, and Amit Dutt from Tata Memorial Centre, Homi Bhabha National Institute and MIT World Peace University summarized evidence from their studies that preoperative hydroxyprogesterone administration may improve disease-free and overall survival in patients with node-positive breast cancer by modulating cellular stress response and negative regulation of inflammation.“This research perspective is aimed to highlight the multipronged roles of progesterone in breast cancer that underlie the associated clinical response. We also present our opinion on the role of progesterone in overcoming endocrine resistance in the patients, especially by countering the genomic effects of overexpression and mutation of ESR1 and its targets.”Non-coding RNAs, particularly DSCAM-AS1, play a regulatory role in this process, along with the upregulation of the kinase gene SGK1 and activation of the SGK1/AP-1/NDRG1 axis. Progesterone-induced modification of the progesterone receptor and estrogen receptor genomic binding pattern is also involved in orchestrating estrogen signaling in breast cancer, preventing cell migration and invasion, and improving patient outcomes. The team continues on to highlight the role of progesterone in endocrine therapy resistance, which could lead to novel treatment options for patients with hormone receptor-positive breast cancer and for those who develop resistance to traditional endocrine therapies.“Overall, while preoperative hydroxyprogesterone administration appears to be a promising strategy for improving the prognosis of patients with node-positive breast cancer, the investigation of the mechanism of actions of progesterone in breast cancer remains an important area of research that holds great promise for improving patient outcomes.”DOI - https://doi.org/10.18632/oncotarget.28455Correspondence to - Amit Dutt - [email protected]Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28455Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - breast cancer, progesterone, DSCAM-AS1, endocrine 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
- Turning Immunosuppressive Tumors to Immunostimulatory: Nerofe and Doxorubicin's ImpactA new research paper was published in Oncotarget's Volume 14 on July 1, 2023, entitled, “Transformation of immunosuppressive mtKRAS tumors into immunostimulatory tumors by Nerofe and Doxorubicin.”Members of the rat sarcoma viral oncogene (RAS) subfamily KRAS are frequently mutated oncogenes in human cancers and have been identified in pancreatic ductal, colorectal, and lung adenocarcinomas. Recently, two drugs that specifically target KRAS G12C, sotorasib (Lumakras™) and adagrasib (Krazati™), have received accelerated approval by the FDA for the treatment of adult patients with KRAS G12C-mutated locally advanced or metastatic NSCLC, who have received at least one prior systemic therapy. These drugs are the first RAS GTPase family inhibitors to be approved for clinical use, representing a major breakthrough in the field of precision oncology.In this new study, researchers Joel Ohana, Uziel Sandler, Orly Devary, and Yoram Devary from Immune System Key (ISK) and Jerusalem College of Technology show that a derivative of the hormone peptide Tumor Cell Apoptosis Factor (TCApF), Nerofe™ (dTCApFs), in combination with Doxorubicin (DOX) substantially reduces viability of tumor cells.“The objective of the present study was to investigate the synergistic effect of the combination of Nerofe and DOX in colorectal cancer and its underlying mechanism.”It was observed that the combination of Nerofe and DOX downregulated KRAS signaling via miR217 upregulation, resulting in enhanced apoptosis of tumor cells. In addition, the combination of Nerofe and DOX also resulted in activation of the immune system against tumor cells, manifested by an increase in the immunostimulatory cytokines IL-2 and IFN-γ as well as the recruitment of NK cells and M1 macrophages to the tumor site.“In conclusion, we demonstrated that the combination of Nerofe and DOX exerts a synergistic effect during mCRC treatment, which could stem from several independent and complementary mechanisms of action.”DOI - https://doi.org/10.18632/oncotarget.28467Correspondence to - Yoram Devary - [email protected]Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28467Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - Colorectal cancer, KRAS, apoptosis, hormone peptide, endoplasmic reticulum stressAbout 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 Contact180092209574 min
- ERβ as a Mediator of Estrogen Signaling in Inflammatory Breast CancerA new editorial paper was published in Oncotarget's Volume 14 on June 12, 2023, entitled, “ERβ as a mediator of estrogen signaling in inflammatory breast cancer.”In this new editorial, researchers Harika Nagandla and Christoforos Thomas from Houston Methodist Neal Cancer Center discuss inflammatory breast cancer (IBC)—a rare and aggressive form of breast cancer which accounts for 2–4% of all new breast cancer cases detected in the United States. Even with the application of standard multi-modality treatment approach that incorporates neoadjuvant chemotherapy, radiation and surgery, the 5-year survival rate for IBC is only about 40–50%. Breast cancer can be typically stratified into different types based on the presence of molecular drivers such estrogen receptor (ERα), progesterone receptor (PR) or human epidermal growth factor receptor 2 (HER2), which inform the treatment choice.For IBC, there is a substantially higher incidence of ERα negativity compared with other forms of breast cancer that can reach up to 60%. A specific targetable driver signaling pathway has not been identified so far. About one in three patients already have distant metastasis at the time of diagnosis, contributing to the aggressiveness and poor outcomes associated with IBC.Despite the absence of ERα from the majority of IBC tumors, estrogen signaling has been implicated in progression of the disease through ERα-independent pathways. ERβ is a ligand activated transcription factor that mediates effects of estrogen, along with ERα in different tissues during growth and development by regulating transcription of target genes. Tumor suppressive effects of ERβ have been documented in diverse cancer types such as thyroid, kidney, prostate, glioblastoma, ovarian and breast cancer.“The work from our group [6] establishes ERβ as a tumor suppressor in IBC by demonstrating its strong antimetastatic activity in preclinical models of the disease and delineating the mechanism of action.”DOI - https://doi.org/10.18632/oncotarget.28425Correspondence to - Christoforos Thomas - [email protected]Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28425Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/Keywords - inflammatory breast cancer, IBC, ERβ, metastasis, actin based cell migrationAbout 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 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/