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Oncotarget episodes
- Epigenetics and Immunotherapy Combined Fights Rare LymphomaListen to a blog summary of a recent research paper published by Oncotarget, entitled, "Combined epigenetic and immunotherapy for blastic and classical mantle cell lymphoma."__________________________________________Mantle cell lymphoma (MCL) is a type of non-Hodgkin’s lymphoma (NHL) that is aggressive, difficult to treat and typically affects older adults. Recurrence and mortality rates among patients with MCL have remained high, despite recent therapeutic advances. Blastic mantle cell lymphoma (bMCL) is a rare subtype of MCL associated with a worse disease trajectory.“Despite recent advances, MCL is incurable except with allogeneic stem cell transplant. Blastic mantle cell lymphoma (bMCL) is a rarer subtype of cMCL associated with an aggressive clinical course and poor treatment response, frequent relapse and poor outcomes.”In previous studies, researchers reported that a combination of epigenetic and immunotherapy treatments may have synergistic activity and offer better outcomes in patients with MCL. In the current study, Francis R. LeBlanc, Zainul S. Hasanali, August Stuart, Sara Shimko, Kamal Sharma, Violetta V. Leshchenko, Samir Parekh, Haiqing Fu, Ya Zhang, Melvenia M. Martin, Mark Kester, Todd Fox, Jiangang Liao, Thomas P. Loughran, Juanita Evans, Jeffrey J. Pu, Stephen E. Spurgeon, Mirit I. Aladjem, and Elliot M. Epner from Pennsylvania State University College of Medicine, Penn State Hershey Cancer Institute, Winter Haven Hospital Cassidy Cancer Center, Icahn School of Medicine at Mount Sinai, National Cancer Institute, University of Virginia, UVA Cancer Center, University of Arizona College of Medicine, Oregon Health and Science University, and Beverly Hills Cancer Center used samples from a previous trial to perform correlative studies focused on clinical results in patients with blastic MCL. On August 16, 2022, their research paper was published in Volume 13 of Oncotarget, entitled, “Combined epigenetic and immunotherapy for blastic and classical mantle cell lymphoma.”Full blog - https://www.oncotarget.org/2022/08/24/epigenetics-and-immunotherapy-combined-fights-rare-lymphoma/DOI - https://www.oncotarget.com/article/28258/text/Correspondence to - Francis R. LeBlanc - [email protected]Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28258Keywords - epigenetics, blastic mantle cell lymphoma, cladribineAbout 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.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/OncotargetYouTubeLinkedIn - https://www.linkedin.com/company/oncotargetPinterest - https://www.pinterest.com/oncotarget/Reddit - https://www.reddit.com/user/Oncotarget/Media Contact180092209578 min
- Press Release: Kinase Activity in RCC, Renal Tissue and in Response to TKIA new research paper was published in Oncotarget on August 4, 2022, entitled, “Kinase activity profiling in renal cell carcinoma, benign renal tissue and in response to four different tyrosine kinase inhibitors.”Kinase activity is frequently altered in renal cell carcinoma (RCC), and tyrosine kinase inhibitors (TKIs) are part of the standard treatment strategy in patients with metastatic disease. However, there are still no established biomarkers to predict clinical benefits of a specific TKI.“Despite a number of new treatment options improving RCC patients’ disease control rates and survival, the lack of useful biomarkers remains a major clinical concern.”In the current study, researchers Andliena Tahiri, Katarina Puco, Faris Naji, Vessela N. Kristensen, Glenny Cecilie Alfsen, Lorant Farkas, Frode S. Nilsen, Stig Müller, Jan Oldenburg, and Jürgen Geisler, from University of Oslo, Oslo University Hospital, Akershus University Hospital, and Pamgene International BV, performed protein tyrosine kinase (PTK) profiling using PamChip® technology.“The aim of this study was to identify differences in PTK activity between normal and malignant kidney tissue obtained from the same patient, and to investigate the inhibitory effects of TKIs frequently used in the clinics: sunitinib, pazopanib, cabozantinib and tivozanib.”The results showed that 36 kinase substrates differ (FDR < 0.05) between normal and cancer kidney tissue, where members of the Src family kinases and the phosphoinositide-3-kinase (PI3K) pathway exhibit high activity in renal cancer.Furthermore, ex vivo treatment of clear cell RCC with TKIs revealed that pathways such as Rap1, Ras and PI3K pathways were strongly inhibited, whereas the neurotrophin pathway had increased activity upon TKI addition. Their assay showed that tivozanib and cabozantinib exhibited greater inhibitory effects on PTK activity compared to sunitinib and pazopanib, implying they might be better suitable as TKIs for selected RCC patients.“The results of our study contribute to better understanding of the changes in kinase activity in RCC tumor cells involved in fundamental oncogenic cellular processes and the ex vivo effect of TKIs. We found tivozanib and cabozantinib to be more potent TKIs in RCC samples than sunitinib or pazopanib. The next step will be to correlate the efficacy and toxicity in individual patients with their respective kinase activity of normal and malignant kidney tissue.”DOI: https://doi.org/10.18632/oncotarget.28257Correspondence to: Jürgen Geisler – Email: [email protected]Keywords: kidney cancer, kinase activity, tyrosine kinase inhibitors, renal cell carcinoma, tyrosine kinaseAbout 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:Twitter – https://twitter.com/OncotargetFacebook – https://www.facebook.com/OncotargetYouTube – www.youtube.com/c/OncotargetYouTubeInstagram – https://www.instagram.com/oncotargetjrnl/LinkedIn – https://www.linkedin.com/company/oncotarget/Pinterest – https://www.pinterest.com/oncotarget/LabTube – https://www.labtube.tv/channel/MTY5OASoundCloud – https://soundcloud.com/oncotargetFor media inquiries, please contact: [email protected].5 min
- Glypican-3 (GPC3) Associated With MCPyV-negative Status and Impaired Outcome in MCCA new research paper was published in Oncotarget on August 3, 2022, entitled, “Glypican-3 (GPC3) is associated with MCPyV-negative status and impaired outcome in Merkel cell carcinoma.”Merkel cell carcinoma (MCC) is an aggressive skin cancer, related to the Merkel Cell Polyomavirus (MCPyV) in 80% of cases. Immune checkpoint inhibitors provide sustained benefit in about 50% of MCC patients with advanced disease.Glypican-3 (GPC3) is an oncofetal tumor antigen that is an attractive target for chimeric antigen receptor T cell therapy due to its highly restricted expression on normal tissue and high prevalence in several solid tumors. GPC3 is known to be expressed in MCC but its association with tumor characteristics or prognosis has not been reported.In this study, researchers (Sujatha Muralidharan, Thibault Kervarrec, Glen J. Weiss, and Mahtab Samimi) from SOTIO Biotech Inc. and the University Hospital of Tours investigated MCC GPC3 expression by immunohistochemistry (IHC) and its association with tumor characteristics, MCPyV status and patient outcome.“The aim of the present study was to complete validation of a GPC3 antibody for use in immunohistochemistry (IHC), investigate the expression of GPC3 in MCC by IHC and to assess its association with tumor characteristics, MCPyV status, and patient outcome.”The GC33 antibody clone was validated for GPC3 IHC staining of tumor specimens in comparison to an established GPC3 IHC antibody. An MCC tissue microarray was stained for GPC3 by IHC using GC33 antibody. Association of GPC3+ IHC with baseline characteristics, MCPyV status (qPCR) and outcome (death from MCC/recurrence) were assessed.Forty-two of 62 samples (67.7%) were GPC3+. GPC3 expression was more frequently observed in females (p = 0.048) and MCPyV-negative tumors (p = 0.021). By multivariate analysis, GPC3 expression was associated with increased death from disease (CSS) (hazard ratio [HR] 4.05, 95% CI 1.06–15.43), together with advanced age (HR 4.85, 95% CI 1.39–16.9) and male gender (HR 4.64, 95% CI 1.31–16.41).GPC3 expression is frequent in MCC tumors, especially MCPyV-negative cases, and is associated with increased risk of death. High prevalence of surface GPC3 makes it a putative drug target.“In this study, we found that GPC3 was expressed in nearly 70% of MCC tumors and up to 90% of MCPyV-negative cases, and was associated with worse prognosis in terms of risk of death from MCC.”DOI: https://doi.org/10.18632/oncotarget.28260Correspondence to: Glen J. Weiss - [email protected], and Mahtab Samimi - [email protected]Keywords: Merkel cell carcinoma, glypican-3, Merkel cell polyomavirus, outcomeAbout 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:Twitter – https://twitter.com/OncotargetFacebook – https://www.facebook.com/OncotargetYouTube – www.youtube.com/c/OncotargetYouTubeInstagram – https://www.instagram.com/oncotargetjrnl/LinkedIn – https://www.linkedin.com/company/oncotarget/Pinterest – https://www.pinterest.com/oncotarget/LabTube – https://www.labtube.tv/channel/MTY5OASoundCloud – https://soundcloud.com/oncotargetFor media inquiries, please contact: [email protected].5 min
- Press Release: Novel Regulatory Mechanism of GLI3 by Toll-like Receptor SignalingA new research paper was published in Oncotarget on August 3, 2022, entitled, “A novel mechanism of regulation of the oncogenic transcription factor GLI3 by toll-like receptor signaling.”The transcription factor GLI3 is a member of the GLI family and has been shown to be regulated by canonical hedgehog (HH) signaling through smoothened (SMO). Little is known about SMO-independent regulation of GLI3.“Hedgehog (HH) signaling is well known for its role in embryonic development, cancer and inflammation [1–4]. At the center of HH signaling are the 2 receptors patched (PTCH1) and smoothened (SMO) along with GLI transcription factors [5]. In the absence of HH ligand, PTCH1 inhibits SMO.”In this study, researchers (Stephan J. Matissek, Mona Karbalivand, Weiguo Han, Ava Boutilier, Estefania Yzar-Garcia, Laura L. Kehoe, Devin Storm Gardner, Adam Hage, Krista Fleck, Vicki Jeffers, Ricardo Rajsbaum, and Sherine F. Elsawa) from the University of New Hampshire and University of Texas Medical Branch identified toll-like receptor (TLR) signaling as a novel pathway regulating GLI3 expression.The researchers showed that GLI3 expression is induced by LPS/TLR4 in human monocyte cell lines and peripheral blood CD14+ cells. Further analysis identified TRIF, but not MyD88, signaling as the adapter used by TLR4 to regulate GLI3. Using pharmacological and genetic tools, they identified IRF3 as the transcription factor regulating GLI3 downstream of TRIF.“Furthermore, using additional TLR ligands that signal through TRIF such as the TLR4 ligand, MPLA and the TLR3 ligand, Poly(I:C), we confirm the role of TRIF-IRF3 in the regulation of GLI3.”They found that IRF3 directly binds to the GLI3 promoter region and this binding was increased upon stimulation of TRIF-IRF3 with Poly(I:C). Using Irf3−/− MEFs, the researchers found that Poly(I:C) stimulation no longer induced GLI3 expression. Finally, using macrophages from mice lacking Gli3 expression in myeloid cells (M-Gli3−/−), they found that in the absence of Gli3, LPS stimulated macrophages secrete less CCL2 and TNF-α compared with macrophages from wild-type (WT) mice.“Taken together, these results identify a novel TLR-TRIF-IRF3 pathway that regulates the expression of GLI3 that regulates inflammatory cytokines and expands our understanding of the non-canonical signaling pathways involved in the regulation of GLI transcription factors.”DOI: https://doi.org/10.18632/oncotarget.28261Correspondence to: Sherine F. Elsawa – Email: [email protected]Keywords: GLI3, inflammation, TLRAbout 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:Twitter – https://twitter.com/OncotargetFacebook – https://www.facebook.com/OncotargetYouTube – www.youtube.com/c/OncotargetYouTubeInstagram – https://www.instagram.com/oncotargetjrnl/LinkedIn – https://www.linkedin.com/company/oncotarget/Pinterest – https://www.pinterest.com/oncotarget/LabTube – https://www.labtube.tv/channel/MTY5OASoundCloud – https://soundcloud.com/oncotargetFor media inquiries, please contact: [email protected].Oncotarget Journal Office6666 East Quaker Str., Suite 1AOrchard Park, NY 14127Phone: 1-800-922-0957 (option 2)5 min
- Does a Mechanism Linking Cellular Aging to Cellular Quiescence Exist?Listen to a blog summary of a trending research paper published by Oncotarget on July 28, 2022, entitled, "Diverse geroprotectors differently affect a mechanism linking cellular aging to cellular quiescence in budding yeast."______________________________________The mechanisms of cellular aging and cellular quiescence have been preserved throughout evolution. Cellular quiescence is a temporary state of cell cycle arrest and low metabolic activity. Importantly, quiescent (Q) cells maintain the ability to quickly activate and re-enter the cell cycle (in response to the appropriate stimuli). Recent research has shown that cellular quiescence may play a role in cellular aging.In a 2020 study, research findings indicated that the rate at which yeast cells age is determined by a complicated program that affects 1) when a state of quiescence is entered, 2) how long quiescence is maintained and 3) when the cell exits quiescence. Researchers found that caloric restriction (CR) (a geroprotective intervention) appears to remodel this program, and this remodeling could be responsible for the CR-dependent delay of yeast chronological aging. Thus, the researchers considered the question: Does a single mechanism exist which links cellular aging to cellular quiescence?“We have introduced a new yeast model for studying mechanisms linking cellular aging to cellular quiescence [109, 110].”In a new study, researchers (Anna Leonov, Rachel Feldman, Amanda Piano, Anthony Arlia-Ciommo, Jennifer Anne Baratang Junio, Emmanuel Orfanos, Tala Tafakori, Vicky Lutchman, Karamat Mohammad, Sarah Elsaser, Sandra Orfali, Harshvardhan Rajen, and Vladimir I. Titorenko) from Concordia University, Montreal, used a new yeast model to test their hypothesis that a mechanism exists linking cellular aging to cellular quiescence. On July 28, 2022, their research paper was published in Oncotarget and entitled, “Diverse geroprotectors differently affect a mechanism linking cellular aging to cellular quiescence in budding yeast.”Full blog - https://www.oncotarget.org/2022/08/05/does-a-mechanism-linking-cellular-aging-to-cellular-quiescence-exist/DOI - https://doi.org/10.18632/oncotarget.28256Correspondence to - Vladimir I. Titorenko - [email protected]Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28256Keywords - cellular aging, cellular quiescence, longevity, gerotargets, geroprotectorsAbout OncotargetOncotarget is a peer-reviewed, open access biomedical journal covering research on all aspects of oncology.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/OncotargetYouTubeLinkedIn - https://www.linkedin.com/company/oncotargetPinterest - https://www.pinterest.com/oncotarget/Reddit - https://www.reddit.com/user/Oncotarget/Media Contact1800922095711 min
- Press Release: Chemoradiation Alters PD-L1, CD8+ TILs and Mucin in Rectal CancerA new research paper was published in Oncotarget on July 28, 2022, entitled, “Chemoradiation-induced alteration of programmed death-ligand 1, CD8+ tumor-infiltrating lymphocytes and mucin expression in rectal cancer.”DNA damage and resulting neoantigen formation is considered a mechanism for synergy between radiotherapy and PD-1/PD-L1 pathway inhibition to induce antitumor immune response.In a new research study, by Marina Baretti, Qingfeng Zhu, Wei Fu, Jeffrey Meyer, Hao Wang, Robert A. Anders, and Nilofer S. Azad from Johns Hopkins University School of Medicine, researchers investigated neoadjuvant chemoradiotherapy (nCRT)-induced changes in CD8+ tumor infiltrating lymphocyte, PD-L1 and mucin expression in rectal cancer patients.“The synergistic effects of CRT and PD-1/PD-L1 immunotherapy has been supported by several retrospective analyses in different cancer types, including esophageal cancer, bladder cancer, and lung cancer also support[ed] [14, 21, 22]. However, the role of nCRT to interact synergistically with immune checkpoint inhibitor treatment to improve tumor control in rectal cancer remains uncertain.”Full press release - https://www.oncotarget.com/news/pr/oncotarget-chemoradiation-induced-alteration-of-programmed-death-ligand-cd-tumor-infiltrating-lymphocytes-and-mucin-expression-in-rectal-cancer/DOI: https://doi.org/10.18632/oncotarget.28255Correspondence to: Marina Baretti – Email: [email protected]Keywords: programmed death ligand 1, tumor-infiltrating lymphocytes, immune checkpoints, colorectal cancer, neoadjuvant chemoradiotherapyAbout 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:Twitter – https://twitter.com/OncotargetFacebook – https://www.facebook.com/OncotargetYouTube – www.youtube.com/c/OncotargetYouTubeInstagram – https://www.instagram.com/oncotargetjrnl/LinkedIn – https://www.linkedin.com/company/oncotarget/Pinterest – https://www.pinterest.com/oncotarget/LabTube – https://www.labtube.tv/channel/MTY5OASoundCloud – https://soundcloud.com/oncotargetFor media inquiries, please contact: [email protected]7 min
- Press Release: CUDC907 Promotes Apoptosis Of NF2 Schwannoma CellsA new research paper was published in Oncotarget on July 19, 2022, entitled, “CUDC907, a dual phosphoinositide-3 kinase/histone deacetylase inhibitor, promotes apoptosis of NF2 Schwannoma cells.”Neurofibromatosis Type 2 (NF2) is a rare tumor disorder caused by pathogenic variants of the merlin tumor suppressor encoded by NF2. Patients develop vestibular schwannomas (VS), peripheral schwannomas, meningiomas, and ependymomas. There are no approved drug therapies for NF2. Previous work identified phosphoinositide-3 kinase (PI3K) as a druggable target.Researchers Julianne Huegel, Christine T. Dinh, Maria Martinelli, Olena Bracho, Rosa Rosario, Haley Hardin, Michael Estivill, Anthony Griswold, Sakir Gultekin, Xue-Zhong Liu, and Cristina Fernandez-Valle, from the University of Central Florida and the University of Miami Miller School of Medicine, conducted an unbiased chemical compound screen of the Library of Pharmacologically Active Compounds (LOPAC) as a pilot high-throughput screen to identify NF2 schwannoma targets for inhibition.“Here we screened PI3K pathway inhibitors for efficacy in reducing viability of human schwannoma cells.”The lead compound, CUDC907, a dual histone deacetylase (HDAC)/PI3K inhibitor, was further evaluated for its effects on isolated and nerve-grafted schwannoma model cells, and primary VS cells. CUDC907 (3 nM IG50) reduced human merlin deficient Schwann cell (MD-SC) viability and was 5–100 fold selective for MD over WT-SCs. CUDC907 (10 nM) promoted cell cycle arrest and caspase-3/7 activation within 24 hours in human MD-SCs. Western blots confirmed a dose-dependent increase in acetylated lysine and decreases in pAKT and YAP.In a 14-day treatment regimen, CUDC907 decreased tumor growth rate by 44%, modulated phospho-target levels, and decreased YAP levels. In five primary VS, CUDC907 decreased viability, induced caspase-3/7 cleavage, and reduced YAP levels. Its efficacy correlated with basal phospho-HDAC2 levels. CUDC907 has cytotoxic activity in NF2 schwannoma models and primary VS cells and is a candidate for clinical trials.“In summary, we demonstrated that CUDC907 reduced the activity of three major signaling pathways in NF2 schwannomas (HDAC, PI3K, and YAP) and consistently reduced viability and induced apoptosis in several schwannoma cell models and in all five genetically unique primary VS studied. These consistent results offer the possibility that CUDC907 will promote schwannoma regression in patients with diverse NF2 mutations and support clinical evaluation of CUDC907 for NF2-associated schwannomas and potentially other cancers driven by NF2 pathogenic variants [45]. Current use of this drug in clinical trials for other indications reveals clinical interest in multi-modal drugs over monotherapies.”DOI: https://doi.org/10.18632/oncotarget.28254Correspondence to: Cristina Fernandez-Valle – Email: [email protected]Keywords: fimepinostat, Schwann cell, vestibular schwanomma, merlin, nerve allograftAbout 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:Twitter – https://twitter.com/OncotargetFacebook – https://www.facebook.com/OncotargetYouTube – www.youtube.com/c/OncotargetYouTubeInstagram – https://www.instagram.com/oncotargetjrnl/LinkedIn – https://www.linkedin.com/company/oncotarget/Pinterest – https://www.pinterest.com/oncotarget/LabTube – https://www.labtube.tv/channel/MTY5OASoundCloud – https://soundcloud.com/oncotargetFor media inquiries, please contact: [email protected].6 min
- Predicting Cancer Immunotherapy Response From Gut Microbiomes Using Machine Learning ModelsListen to the press release about a new research paper published in Volume 13 of Oncotarget, “Predicting cancer immunotherapy response from gut microbiomes using machine learning models.”___________________________________A new research paper was published in Oncotarget on July 19, 2022, entitled, “Predicting cancer immunotherapy response from gut microbiomes using machine learning models.”“In the last decade, the use of cancer immunotherapy targeting immune checkpoint inhibitors (ICIs) to boost T cell mediated cancer cell clearance has significantly improved cancer patient survival [1].”Cancer immunotherapy has significantly improved patient survival. Yet, half of patients do not respond to immunotherapy. Gut microbiomes have been linked to clinical responsiveness of melanoma patients on immunotherapies; however, different taxa have been associated with response status with implicated taxa inconsistent between studies.In this new study, by Hai Liang, Jay-Hyun Jo, Zhiwei Zhang, Margaret A. MacGibeny, Jungmin Han, Diana M. Proctor, Monica E. Taylor, You Che, Paul Juneau, Andrea B. Apolo, John A. McCulloch, Diwakar Davar, Hassane M. Zarour, Amiran K. Dzutsev, Isaac Brownell, Giorgio Trinchieri, James L. Gulley, and Heidi H. Kong from the National Institutes of Health Library, National Cancer Institute, National Human Genome Research Institute, West Virginia University, Zimmerman Associates Inc., and the University of Pittsburgh, researchers used a tumor-agnostic approach to find common gut microbiome features of response among immunotherapy patients with different advanced stage cancers.Full press release - https://www.oncotarget.com/news/pr/oncotarget-predicting-cancer-immunotherapy-response-from-gut-microbiomes-using-machine-learning-models/DOI - https://doi.org/10.18632/oncotarget.28252Correspondence to - Heidi H. Kong - [email protected]Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28252Keywords - gut microbiome, immunotherapy, 16S rRNA, machine learning, metagenomicsAbout OncotargetOncotarget is a peer-reviewed, open access biomedical journal covering research on all aspects of oncology.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/OncotargetYouTubeLinkedIn - https://www.linkedin.com/company/oncotargetPinterest - https://www.pinterest.com/oncotarget/Reddit - https://www.reddit.com/user/Oncotarget/Oncotarget is published by Impact Journals, LLC: https://www.ImpactJournals.comMedia Contact180092209576 min
- How Heartburn Can Turn Into Esophageal Cancer, and a Possible BiomarkerListen to a blog summary of a trending research paper published in Volume 13 of Oncotarget, entitled, "Telomere shortening accelerates tumor initiation in the L2-IL1B mouse model of Barrett esophagus and emerges as a possible biomarker."___________________________________Smokers are significantly more likely than nonsmokers to have acid reflux. In many Western countries, a popular diet—known for its convenience, availability and, frankly, its lack of nutritional value—is also known to cause acid reflux. Some of the affordable foods and beverages easily accessible to Western consumers include fried food, fast foods, pizza, potato chips (and other processed snacks), high-fat meats (bacon, sausage), cheese, alcohol, soda, energy drinks, and etcetera. Unfortunately, this indulgent type of diet is accompanied by consequences beyond oily skin and an expanding waistband.BARRETT’S ESOPHAGUSChronic acid reflux can lead to gastroesophageal reflux disease. Gastroesophageal reflux disease can lead to Barrett’s esophagus (BE). BE is a premalignant condition in which the lining of the esophagus becomes damaged by acid reflux. BE can lead to the onset of a type of cancer called esophageal adenocarcinoma (EAC). Over the past few decades, statistics have reported that the incidence of EAC in Western populations is increasing.“Esophageal adenocarcinoma (EAC) is on the rise in western countries with increased incidence and high mortality [1, 2].”Since the popularity of smoking and a heartburn-inducing diet is likely to continue in the West, the early detection of EAC is critical for improving patient outcomes. If a biomarker could indicate a BE patient’s present risk of EAC, early EAC treatment could curb incidence and mortality rates. However, such a biomarker has yet to be confirmed. On February 14, 2022, researchers from Technische Universität München, Columbia University Irving Medical Center and Universitätsklinikum Freiburg published the research paper, “Telomere shortening accelerates tumor initiation in the L2-IL1B mouse model of Barrett esophagus and emerges as a possible biomarker,” in Oncotarget.“Here we aimed to provide functional evidence for the hypothesis that telomere shortening can directly contribute to tumor initiation, and thus serve as a potential biomarker for BE cancer risk stratification [22, 24].”Full blog - https://www.oncotarget.org/2022/07/15/how-heartburn-can-turn-into-esophageal-cancer-and-a-possible-biomarker/DOI - https://doi.org/10.18632/oncotarget.28198Correspondence to - Michael Quante - [email protected]Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28198Keywords - Barrett's esophagus, telomere shortening, esophageal cancer, risk factor, TERT/TERCAbout OncotargetOncotarget is a peer-reviewed, open access biomedical journal covering research on all aspects of oncology.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/OncotargetYouTubeLinkedIn - https://www.linkedin.com/company/oncotargetPinterest - https://www.pinterest.com/oncotarget/Reddit - https://www.reddit.com/user/Oncotarget/Oncotarget is published by Impact Journals, LLC: https://www.ImpactJournals.comMedia Contact180092209579 min
- Behind the Study: Molecular Characterization of Lung Carcinomas Expressing KK-LC-1Dr. Robert Hsu from the Department of Internal Medicine, Division of Medical Oncology, Norris Comprehensive Cancer Center and Hospital, University of Southern California, describes a recent research paper he co-authored that was published by Oncotarget, entitled, “Molecular characterization of Kita-Kyushu lung cancer antigen (KK-LC-1) expressing carcinomas.”DOI - https://doi.org/10.18632/oncotarget.28132Correspondence to - Jorge J. Nieva - [email protected]AbstractCancer/testis antigens (CTAs) are strongly expressed in some solid tumors but minimally expressed in normal tissue, making them appealing therapeutic targets. KK-LC-1 (CXorf61) has cytoplasmic expression in gastric, breast, and lung cancer. We characterized the molecular subtypes of non-small cell lung cancer (NSCLC) expressing KK-LC-1 to inform rational clinical trials of T-cell receptor therapy (TCR-T) targeting KK-LC-1. 9790 NSCLC tumors that underwent whole transcriptome sequencing (Illumina NovaSeq) and NextGen DNA sequencing (NextSeq, 592 Genes and NovaSEQ, WES) at Caris Life Sciences (Phoenix, AZ) were analyzed. Tumors were split into quartiles based on KK-LC-1 expression and pathological and molecular differences were investigated. Adenocarcinoma had significantly higher KK-LC-1 expression than squamous cell carcinoma (median, 3.25 vs. 1.17 transcripts per million (TPM), p < 0.0001). Tumors with the highest quartile of KK-LC-1 expression had a greater proportion of tumors with high tumor mutation burden (TMB) (≥10 mutations per megabase; 44% vs. 28% in Q1, p < 0.001). Increased KK-LC-1 expression was associated with increased M1 macrophage abundance. Higher levels of KK-LC-1 expression were seen in pan-wild type and KRAS mutated tumors and associated with high TMB. TCR-T therapy directed against KK-LC-1 should be considered in patients whose clinical features reflect these characteristics.Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28132Press release - https://www.oncotarget.com/news/pr/kita-kyushu-lung-cancer-antigen-kk-lc-1-expressing-carcinomas/Keywords - lung cancer, tumor microenvironment, diagnostic biomarkers, biomarkers for immunotherapy, cancer testis antigenAbout OncotargetOncotarget is a peer-reviewed, open access biomedical journal covering research on all aspects of oncology.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/OncotargetYouTubeLinkedIn - https://www.linkedin.com/company/oncotargetPinterest - https://www.pinterest.com/oncotarget/Reddit - https://www.reddit.com/user/Oncotarget/Oncotarget is published by Impact Journals, LLC: https://www.ImpactJournals.comMedia Contact180092209576 min
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