Page 5«..4567..1020..»

Category Archives: Epigenetics

Zenith Epigenetics Triple Negative Breast Cancer Clinical Data Highlighted in an Oral Discussion at the American Society of Clinical Oncology…

Posted: June 22, 2022 at 2:35 am

CALGARY, Alberta, June 21, 2022 (GLOBE NEWSWIRE) -- Zenith Epigenetics Ltd. (Zenith or the Company) announced today that the data from its Phase 2 Metastatic Triple Negative Breast Cancer (mTNBC) clinical trial combining ZEN-3694 + Pfizer Inc.s Talzenna (talazoparib) was highlighted at an oral session Optimizing Targeted Therapies in Advanced Breast Cancer: Building on Past Success. The discussant presented the novel concept of administering ZEN-3694, a bromodomain and extraterminal (BET) inhibitor (BETi), to sensitize resistant mTNBC tumors to talazoparib, a poly (ADP-ribose) polymerase (PARP) inhibitor (PARPi), and the clinically meaningful response rate and manageable safety profile of the combination from the Phase 2 study. Selection of an abstract for an oral discussion is a very competitive process with only 24 of the more than 125 accepted abstracts selected for this presentation format. The poster can be viewed on Zenith Epigenetics website (Poster) and the discussion can be viewed on the ASCO website (Discussion).

The data from the Phase 2 trial demonstrate that the ZEN-3694 plus talazoparib combination regimen, with a clinically meaningful response rate of 32% in a defined population, has the potential for treating patients whose tumors do not harbor germline mutations in BRCA1/2, said Dr. Philippe Aftimos, a principal investigator and medical oncologist at The Institut Jules Bordet in Brussels, Belgium. This combination is active with a manageable safety profile and warrants continued clinical evaluation. Zenith has expanded the Phase 2 trial to continue to evaluate the combination in an additional 120 mTNBC patients (NCT03901469).

In conjunction with ASCO, Zeniths TNBC poster was also awarded the GRASP Advocate Choice Award and selected to be discussed at theGRASPPoster Walkthroughs. GRASP, which standsfor Guiding Researchers and Advocates for Scientific Partnerships,is a patient-led organization that brings together patients, clinicians, and researchers to exchange ideas and learn from each other to accelerate scientific breakthroughs. GRASP Poster Walkthroughs are small group discussions of selected posters presented at scientific conferences such as ASCO.

We are very pleased that the data from our mTNBC clinical study, conducted in collaboration with Pfizer, was well received and recognized at ASCO, said Don McCaffrey, CEO of Zenith Epigenetics. The combination regimen of ZEN-3694 + talazoparib has shown promising clinical activity in a mTNBC patient population with significant unmet need. We continue to advance this program toward registration and are committed to bring an important therapy to these patients.

About Zenith and ZEN-3694

Zenith Epigenetics Ltd., a wholly-owned subsidiary of Zenith Capital Corp., is a clinical stage biotechnology company focused on the discovery and development of novel therapeutics for the treatment of cancer and other disorders with significant unmet medical need. Zenith Epigenetics is developing various novel combinations of BET inhibitors with other targeted agents. The lead compound, ZEN-3694, is in clinical development for various oncologic indications, specifically:

About Triple Negative Breast Cancer (TNBC)

TNBC is an aggressive form of breast cancer with low survival rates. TNBC accounts for about 10-15%of all breast cancers and it differs from other types of invasive breast cancer in that it tends to grow and spread faster, has fewer treatment options, and tends to have a worse prognosis. The termtriple-negative breast cancerrefers to the fact that the cancer cells have only low or no amount of the receptors ER, PR, and HER2. Approximately 75,000 women in the US, Japan and the major EU countries are diagnosed with TNBC each year.

About ZEN-3694 + Talazoparib Combination

In the United States, talazoparib is currently approved under the brand name TALZENNA, which is a PARP inhibitor indicated for the treatment of adult patients with deleterious or suspected deleterious germline BRCA-mutated (gBRCAm) HER2-negative locally advanced or metastatic breast cancer. ZEN-3694, in combination with talazoparib, is being developed for targeting tumors that do not have a germline BRCA mutation which represent approximately 89% of TNBC tumors. Preclinical and clinical data has shown that BET inhibition may reduce the levels of DNA repair proteins such as BRCA1/2 and RAD51 and thus create synthetic lethality in wildtype BRCA1/2 TNBC tumors when combined with PARP inhibition.

For further information, please contact:

Investor Relations & Communications

Zenith EpigeneticsPhone: 587-390-7865Email: info@zenithepigenetics.comWebsite:www.zenithepigenetics.com

This news release may contain certain forward-looking information as defined under applicable Canadian securities legislation, that are not based on historical fact, including without limitation statements containing the words "believes", "anticipates", "plans", "intends", "will", "should", "expects", "continue", "estimate", "forecasts" and other similar expressions. In particular, this news release includes forward looking information relating to the Companys development activities involving ZEN-3694 in combination with Pfizers PARP inhibitor Talzenna, and other targeted agents used in precision oncology, as well as other planned PARPi based combination therapy clinical trials in other tumor types. Our actual results, events or developments could be materially different from those expressed or implied by these forward-looking statements. We can give no assurance that any of the events or expectations will occur or be realized. By their nature, forward-looking statements are subject to numerous assumptions and risk factors including those discussed in our most recent MD&A which are incorporated herein by reference and are available through SEDAR at http://www.sedar.com. The forward-looking statements contained in this news release are expressly qualified by this cautionary statement and are made as of the date hereof. Zenith disclaims any intention and has no obligation or responsibility, except as required by law, to update or revise any forward-looking statements, whether as a result of new information, future events or otherwise.

Read more:
Zenith Epigenetics Triple Negative Breast Cancer Clinical Data Highlighted in an Oral Discussion at the American Society of Clinical Oncology...

Posted in Epigenetics | Comments Off on Zenith Epigenetics Triple Negative Breast Cancer Clinical Data Highlighted in an Oral Discussion at the American Society of Clinical Oncology…

The relationship between P16INK4A and TP53 promoter methylation and the risk and prognosis in patients with oesophageal cancer in Thailand |…

Posted: June 22, 2022 at 2:35 am

Sung, H. et al. Global cancer statistics 2020: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA Cancer J. Clin. 71(3), 209249 (2021).

PubMed Article Google Scholar

Chao, Y. K. et al. Factors associated with survival in patients with oesophageal cancer who achieve pathological complete response after chemoradiotherapy: A nationwide population-based study. Eur. J. Cardiothorac. Surg. 51(1), 155159 (2017).

PubMed Article Google Scholar

Imsamran, W., Chaiwerawattana, A., Wiangnon, S., Pongnikorn, D., Suwangrungrung, K., Sangrajrang S. & Buasom R. (eds.). Cancer in Thailand, Vol. VIII, 20102012. (Bangkok Medical Publisher, 2015).

Ghobadi, N. et al. A genetic variant in CDKN2A/2B locus was associated with poor prognosis in patients with esophageal squamous cell carcinoma. J. Cell Physiol. 234(4), 50705076 (2019).

CAS PubMed Article Google Scholar

Zhao, R., Choi, B. Y., Lee, M. H., Bode, A. M. & Dong, Z. Implications of genetic and epigenetic alterations of CDKN2A (p16(INK4a)) in cancer. EBioMedicine 8, 3039 (2016).

PubMed PubMed Central Article Google Scholar

Wang, S., Pan, D., Su, M., Huang, G. & Sun, G. Moderately high folate level may offset the effects of aberrant DNA methylation of P16 and P53 genes in esophageal squamous cell carcinoma and precancerous lesions. Genes Nutr. 15(1), 18 (2020).

PubMed PubMed Central Article CAS Google Scholar

Zhou, C. et al. The association and clinical significance of CDKN2A Promoter methylation in head and neck squamous cell carcinoma: a meta-analysis. Cell Physiol. Biochem. 50, 868882 (2018).

CAS PubMed Article Google Scholar

Pan, D. et al. MTHFR C677T genetic polymorphism in combination with serum vitamin B2, B12 and aberrant DNA methylation of P16 and P53 genes in esophageal squamous cell carcinoma and esophageal precancerous lesions: A casecontrol study. Cancer Cell Int. 19, 288 (2019).

PubMed PubMed Central Article CAS Google Scholar

Wang, T. H., Hsia, S. M., Shih, Y. H. & Shieh, T. M. Association of smoking, alcohol use, and betel quid chewing with epigenetic aberrations in cancers. Int. J. Mol. Sci. 18(6), 1210 (2017).

PubMed Central Article CAS Google Scholar

Talukdar, F. R., Ghosh, S. K., Laskar, R. S. & Mondal, R. Epigenetic, genetic and environmental interactions in esophageal squamous cell carcinoma from northeast India. PLoS ONE 8(4), e60996 (2013).

ADS CAS PubMed PubMed Central Article Google Scholar

Li, D. et al. Specific DNA methylation markers in the diagnosis and prognosis of esophageal cancer. Aging 11(23), 1164011658 (2019).

CAS PubMed PubMed Central Article Google Scholar

Ma, K., Cao, B. & Guo, M. The detective, prognostic, and predictive value of DNA methylation in human esophageal squamous cell carcinoma. Clin. Epigenetics 8, 43 (2016).

PubMed PubMed Central Article CAS Google Scholar

Lopes, N., Correia, M. P., Henrique, R. & Jernimo, C. Epigenetic alterations in esophageal cancer: expression and role of the involved enzymes. Int. J. Mol. Sci. 21(10), 3522 (2020).

CAS PubMed Central Article Google Scholar

Lin, L., Cheng, X. & Yin, D. Aberrant DNA methylation in esophageal squamous cell carcinoma: biological and clinical implications. Front. Oncol. 10, 549850 (2020).

PubMed PubMed Central Article Google Scholar

Das, M. et al. P16 hypermethylation: a biomarker for increased esophageal cancer susceptibility in high incidence region of North East India. Tumour Biol. 36(3), 16271642 (2015).

CAS PubMed Article Google Scholar

Jesionek-Kupnicka, D. et al. TP53 promoter methylation in primary glioblastoma: Relationship with TP53 mRNA and protein expression and mutation status. DNA Cell Biol. 33(4), 217226 (2014).

CAS PubMed PubMed Central Article Google Scholar

Kajiura, K. et al. Frequent silencing of the candidate tumor suppressor TRIM58 by promoter methylation in early-stage lung adenocarcinoma. Oncotarget 8(2), 28902905 (2017).

PubMed Article Google Scholar

Zhou, C. et al. DNA methylation biomarkers for head and neck squamous cell carcinoma. Epigenetics 13(4), 398409 (2018).

PubMed PubMed Central Article Google Scholar

Nanok, C., Jearanaikoon, P., Proungvitaya, S. & Limpaiboon, T. Aberrant methylation of HTATIP2 and UCHL1 as a predictive biomarker for cholangiocarcinoma. Mol Med Rep. 17(3), 41454153 (2018).

CAS PubMed Google Scholar

Yatagai, N. et al. TP53 inactivation and expression of methylation-associated proteins in gastric adenocarcinoma with enteroblastic differentiation. Virchows Arch. 474(3), 315324 (2019).

CAS PubMed Article Google Scholar

Chang, H. W., Ling, G. S., Wei, W. I. & Yuen, A. P. Smoking and drinking can induce p15 methylation in the upper aerodigestive tract of healthy individuals and patients with head and neck squamous cell carcinoma. Cancer 101(1), 125132 (2004).

PubMed Article Google Scholar

Ghantous, Y., Schussel, J. L. & Brait, M. Tobacco and alcohol-induced epigenetic changes in oral carcinoma. Curr. Opin. Oncol. 30(3), 152158 (2018).

CAS PubMed PubMed Central Article Google Scholar

Xie, W. et al. Relationship between DLEC1 and PBX3 promoter methylation and the risk and prognosis of gastric cancer in peripheral blood leukocytes. J. Cancer Res. Clin. Oncol. 146(5), 11151124 (2020).

CAS PubMed Article Google Scholar

Takeshima, H. & Ushijima, T. Accumulation of genetic and epigenetic alterations in normal cells and cancer risk. npj Precis. Oncol. https://doi.org/10.1038/s41698-019-0079-0 (2019).

Article PubMed PubMed Central Google Scholar

Shao, Y., Jiang, H., Wu, X., Luo, Y. & Tang, W. P16 promoter hypermethylation is associated with increased risk of nasopharyngeal carcinoma. Mol. Clin. Oncol. https://doi.org/10.3892/mco.2014.396 (2014).

Article PubMed PubMed Central Google Scholar

Das, M. et al. P16 gene silencing along with p53 single-nucleotide polymorphism and risk of esophageal cancer in Northeast India. Tumour Biol. https://doi.org/10.1177/1010428317698384 (2017).

Article PubMed Google Scholar

Guo, M. et al. Accumulation of promoter methylation suggests epigenetic progression in squamous cell carcinoma of the esophagus. Clin. Cancer Res. 12(15), 45154522 (2006).

CAS PubMed Article Google Scholar

Xu, R., Wang, F., Wu, L., Wang, J. & Lu, C. A systematic review of hypermethylation of p16 gene in esophageal cancer. Cancer Biomark. 13(4), 215226 (2013).

PubMed Article CAS Google Scholar

Abbaszadegan, M. R. et al. Aberrant p16 methylation, a possible epigenetic risk factor in familial esophageal squamous cell carcinoma. Int. J. Gastrointest. Cancer 36(1), 4754 (2005).

CAS PubMed Article Google Scholar

Baba, Y., Watanabe, M. & Baba, H. Review of the alterations in DNA methylation in esophageal squamous cell carcinoma. Surg. Today. 43(12), 13551364 (2013).

CAS PubMed Article Google Scholar

Wang, J. et al. Aberrant DNA methylation of P16, MGMT, and hMLH1 genes in combination with MTHFR C677T genetic polymorphism in esophageal squamous cell carcinoma. Cancer Epidemiol. Biomark. Prev. 17(1), 118125 (2008).

CAS Article Google Scholar

Oka, D. et al. The presence of aberrant DNA methylation in noncancerous esophageal mucosae in association with smoking history: A target for risk diagnosis and prevention of esophageal cancers. Cancer 115(15), 34123426 (2009).

CAS PubMed Article Google Scholar

Toh, Y. et al. Alcohol drinking, cigarette smoking, and the development of squamous cell carcinoma of the esophagus: molecular mechanisms of carcinogenesis. Int. J. Clin. Oncol. 15(2), 135144 (2010).

CAS PubMed Article Google Scholar

Fujiwara, S. et al. Hypermethylation of p16 gene promoter correlates with loss of p16 expression that results in poorer prognosis in esophageal squamous cell carcinomas. Dis. Esophagus 21(2), 125131 (2008).

CAS PubMed Article Google Scholar

Limpaiboon, T. et al. P53 status and human papillomavirus infection in Thai women with cervical carcinoma. Southeast Asian J. Trop. Med. Public Health 31(1), 6671 (2000).

CAS PubMed Google Scholar

Abat, D. et al. Genetic alterations of chromosomes, p53 and p16 genes in low- and high-grade bladder cancer. Oncol. Lett. 8(1), 2532 (2014).

PubMed PubMed Central Article Google Scholar

Fagundes, R. B., Mello, C. R. & Tollens, P. P53 protein in esophageal mucosa of individuals at high risk of squamous cell carcinoma of the esophagus. Dis. Esophagus 14, 185190 (2001).

CAS PubMed Article Google Scholar

Lima, E. M. et al. Methylation status of ANAPC1, CDKN2A and TP53 promoter genes in individuals with gastric cancer. Braz. J. Med. Biol. Res. 41(6), 539543 (2008).

CAS PubMed Article Google Scholar

Zhao, L. J. et al. Association of p53 Arg72Pro polymorphism with esophageal cancer: A meta-analysis based on 14 case control studies. Genet. Test. Mol. Biomarkers 17, 721726 (2013).

CAS PubMed Article Google Scholar

Samareh-Fekri, M. et al. Detection of Helicobacter pylori in the bronchoalveolar lavage of patients with lung cancer using real-time PCR. Jundishapur J. Microbiol. 9(11), e32144 (2016).

PubMed PubMed Central Article CAS Google Scholar

Zhou, C., Li, J. & Li, Q. CDKN2A methylation in esophageal cancer: A meta-analysis. Oncotarget 8(30), 5007150083 (2017).

PubMed PubMed Central Article Google Scholar

Huang, Y. et al. Cigarette smoke induces promoter methylation of single-stranded DNA-binding protein 2 in human esophageal squamous cell carcinoma. Int. J. Cancer 128(10), 22612273 (2011).

CAS PubMed PubMed Central Article Google Scholar

Ye, F. & Xu, X. C. Benzo[a]pyrene diol epoxide suppresses retinoic acid receptor-beta2 expression by recruiting DNA (cytosine-5-)-methyltransferase 3A. Mol. Cancer 9, 93 (2010).

PubMed PubMed Central Article CAS Google Scholar

Warnakulasuriya, S. & Straif, K. Carcinogenicity of smokeless tobacco: Evidence from studies in humans & experimental animals. Indian J. Med. Res. 148(6), 681686 (2018).

CAS PubMed PubMed Central Article Google Scholar

Anantharaman, D. et al. Population attributable risk of tobacco and alcohol for upper aerodigestive tract cancer. Oral Oncol. 47(8), 725731 (2011).

PubMed Article Google Scholar

Yang, X. et al. Smoking and alcohol drinking in relation to the risk of esophageal squamous cell carcinoma: A population-based case-control study in China. Sci .Rep. 7(1), 17249 (2017).

ADS PubMed PubMed Central Article CAS Google Scholar

Fan, Y., Yuan, J. M., Wang, R., Gao, Y. T. & Yu, M. C. Alcohol, tobacco, and diet in relation to esophageal cancer: The Shanghai Cohort Study. Nutr. Cancer 60(3), 354363 (2008).

PubMed PubMed Central Article Google Scholar

Da Costa, A. M. et al. HPV infection and p53 and p16 expression in esophageal cancer: are they prognostic factors. Infect. Agent Cancer 12, 54 (2017).

PubMed PubMed Central Article CAS Google Scholar

Aghcheli, K. et al. Prognostic factors for esophageal squamous cell carcinomaa population-based study in Golestan Province, Iran, a high incidence area. PLoS ONE 6(7), e22152 (2011).

ADS CAS PubMed PubMed Central Article Google Scholar

Fujiwara, S. et al. Hypermethylation of p16 gene promoter correlates with loss of p16 expression that results in poorer prognosis in esophageal squamous cell carcinomas. Dis. Esophagus. 21(2), 125131 (2008).

CAS PubMed Article Google Scholar

Li, F. et al. Targeting epigenetic aberrations in esophageal squamous cell carcinoma. Curr. Pharmacol. Rep. 6, 415428 (2020).

Go here to read the rest:
The relationship between P16INK4A and TP53 promoter methylation and the risk and prognosis in patients with oesophageal cancer in Thailand |...

Posted in Epigenetics | Comments Off on The relationship between P16INK4A and TP53 promoter methylation and the risk and prognosis in patients with oesophageal cancer in Thailand |…

Introducing Cantata Bio, Inventive Multimodal Solutions for Accelerating Genome-based R&D – Business Wire

Posted: June 13, 2022 at 2:13 am

CAMBRIDGE, Mass. & SCOTTS VALLEY, Calif.--(BUSINESS WIRE)--Cantata Bio launched today, with the mission of enabling researchers to address the worlds most challenging scientific questions, from human disease to agricultural sustainability, using leading-edge multi-dimensional NGS technologies. The company is a result of the merger between Dovetail Genomics, the industry leader in advanced proximity ligation genomic solutions, and Arc Bio, which develops novel, proprietary metagenomic tools for accurate and sensitive microbial profiling. Committed to delivering the most innovative NGS-based solutions, Cantata Bio comprises three business units, Epigenetics & Genome Structure, Microbial Profiling, and Genetic Analysis Solutions.

The benefits of this merger to both our customers and the companies were clear - accelerated innovation, the potential to aggregate multimodal data to better service our partners, and streamlined operations, said Todd Dickinson, CEO of Cantata Bio. Cantata Bio aims to dramatically accelerate advances in the life sciences industry with key competencies, including integrated metagenomics workflows for understanding the interplay between microbes and disease, and unique NGS sequencing assays that deliver industry-leading long-range data empowering genome assembly, haplotype phasing, chromatin structure and epigenomic applications.

Serving on the Board of Directors for former Dovetail and Arc Bios parent company, EdenRoc Sciences, Todd Dickinson continues in the role of CEO for Cantata Bio. A life sciences executive with more than 20 years of genomics experience, Todd was a founding scientist of Illumina, holding a variety of technical and commercial executive roles both at Illumina and subsequently at Bionano Genomics.

Along with the company launch, Cantata Bio announced today its Dovetail TopoLink Kit, a revolutionary new assay delivering genomic interactions at unparalleled speed. With genomic interactions critical to understanding functional biology, the TopoLink Assay removes the bias introduced from motif-based assays, captures chromatin topology features with a higher rate of discovery, and offers superior accuracy in detecting chromatin loops, all in an unprecedented six hour sample-to-sequencing library workflow - less than half the time of traditional Hi-C approaches.

Cantata Bio has seen early demand for TopoLink, having already allocated the first several kits to members of its First Adopters Circle. These include Chris Mason, Professor of Genomics, Physiology, & Biophysics, and Director of Emerging Genome Technologies at Tempus Labs, David Sinclair, Professor in the Department of Genetics and co-Director of the Paul F. Glenn Center for Biology of Aging Research at Harvard Medical School, Melissa Fullwood, Nanyang Assistant Professor at SBS, NTU and Junior Principal Investigator at CSI Singapore, and Emily Bernstein, Professor, and Dan Hasson, Associate Professor, at the Tisch Cancer Institute of the Icahn School of Medicine at Mount Sinai.

Cantata Bio and its newest product, the Dovetail TopoLink Kit, were announced today at Advances in Genome Biology and Technology (AGBT), where Cantata Bio is an official sponsor. To learn more about the Dovetail TopoLink Kit or Cantata Bio, visit suite 1825 throughout the conference, and join us for our launch party on the evening of June 7th during and after the Passport prizes/CLICK2WIN event. For more information, visit http://www.cantatabio.com.

About Cantata Bio

Cantata Bio is enabling researchers to solve tomorrows most challenging scientific problems through novel, multi-dimensional approaches that unlock access to genomic, epigenomic and metagenomic information at unprecedented levels. Combining proprietary technologies with platform solutions, services, and cutting-edge bioinformatics and software, our unique approaches are solving complex problems, including chromatin topology analysis, small and large structural variant detection, de novo chromosome assembly, haplotype phasing, metagenomics, and microbiome analysis. Our customers are positively impacting the fields of epigenetics, developmental biology, cancer research, evolutionary biology, infectious disease, and more. Cantata Bio is based in Scotts Valley, California and Cambridge, Massachusetts. For more information on Cantata Bio, its technology, and offerings, visit http://www.cantatabio.com.

Read more from the original source:
Introducing Cantata Bio, Inventive Multimodal Solutions for Accelerating Genome-based R&D - Business Wire

Posted in Epigenetics | Comments Off on Introducing Cantata Bio, Inventive Multimodal Solutions for Accelerating Genome-based R&D – Business Wire

Omega Therapeutics (OMGA) Research Analysts’ Weekly Ratings Changes – Defense World

Posted: June 13, 2022 at 2:13 am

A number of firms have modified their ratings and price targets on shares of Omega Therapeutics (NASDAQ: OMGA) recently:

Omega Therapeutics stock opened at $3.70 on Friday. The company has a debt-to-equity ratio of 0.11, a quick ratio of 15.23 and a current ratio of 15.23. The firm has a market capitalization of $177.05 million and a price-to-earnings ratio of -0.77. Omega Therapeutics, Inc. has a fifty-two week low of $1.98 and a fifty-two week high of $31.41. The stocks fifty day moving average is $3.85 and its two-hundred day moving average is $8.97.

Omega Therapeutics (NASDAQ:OMGA Get Rating) last posted its quarterly earnings data on Thursday, March 10th. The company reported ($0.44) EPS for the quarter, beating analysts consensus estimates of ($0.57) by $0.13. The company had revenue of $0.14 million for the quarter. As a group, sell-side analysts forecast that Omega Therapeutics, Inc. will post -2.17 EPS for the current fiscal year.

Omega Therapeutics, Inc operates as a development-stage biopharmaceutical company. Its OMEGA Epigenomic Programming platform is designed to coopt nature's operating system by harnessing the power of epigenetics, the mechanism for gene control and cell differentiation. The company is developing omega epigenomic controller (OEC) candidates to up-regulate the expression of HNF4a, a transcriptional master regulator as a potential way to restore liver-cell function in patients suffering from chronic liver diseases; to control the expression of genes that have been strongly linked to cell-growth inhibition in patients with diabetes and other conditions to restore the capacity for corneal regeneration; to down-regulate expression of the CXCL1, 2, 3, and IL-8 gene cluster; to control expression of genes implicated in patients with idiopathic pulmonary fibrosis to halt or reverse disease progression and improve disease outcomes; to down-regulate the expression of SFRP1, a protein that inhibits hair growth; and to treat non-small cell lung cancer and small cell lung cancer.

Read More

Receive News & Ratings for Omega Therapeutics Inc Daily - Enter your email address below to receive a concise daily summary of the latest news and analysts' ratings for Omega Therapeutics Inc and related companies with MarketBeat.com's FREE daily email newsletter.

Visit link:
Omega Therapeutics (OMGA) Research Analysts' Weekly Ratings Changes - Defense World

Posted in Epigenetics | Comments Off on Omega Therapeutics (OMGA) Research Analysts’ Weekly Ratings Changes – Defense World

Plant biologist nominated for prestigious early career award – University of Georgia

Posted: June 13, 2022 at 2:13 am

UGAs Schmitz named finalist for 2022 Blavatnik National Awards for Young Scientists

University of Georgia faculty member Robert Schmitz was recently chosen as a finalist for a national award for young scientists. The Blavatnik National Awards for Young Scientists is the worlds largest unrestricted prize honoring early career scientists and engineers.

Schmitz is a plant biologist who performs groundbreaking research on plant epigeneticsthe chemical modifications to DNA and associated proteins that alter gene expressionto unlock new methods to increase agricultural sustainability and food security. He found that some plant epigenetic mechanisms differ from those of animals, and that this unique mode of epigenetic modification impacts plant evolution and can inform crop breeding.

His discoveries in the epigenetics of maize offer plant breeders targets in the maize genome to improve crop performance, such as overall yield or resistance to disease. Schmitzs work, as described in the Blavatnik Awards finalists announcement, has set in motion the discovery and creation of new plant biotechnology that could help feed the world.

The honorees were chosen from a highly competitive pool of 309 nominees from 150 leading universities and scientific institutions from 38 states across the United States.

From the announced group of finalists, three winnersin life sciences, chemistry, and physical sciences and engineeringwill be named on June 29, each receiving $250,000 as a Blavatnik National Awards Laureate.

I am thankful for this recognition and grateful to past and present lab members that have advanced our understanding of plant epigenetics, said Schmitz, who holds a UGA Foundation Professorship of Plant Sciences and is the Lars G. Ljungdahl Distinguished Investigator. We are fortunate to work alongside so many great colleagues in the department of genetics at the University of Georgia.

Three independent jurieseach representing one of the award categoriesselected the finalists and will determine the winning laureates. Laureates must be faculty-level scientific researchers, 42 years of age or younger, and are nominated to the competition by their university or research institution.

At his initial hire as an assistant professor, Bob was clearly a rising star in the field of epigenetics, said Nancy Manley, Distinguished Research Professor and head of the Franklin College of Arts and Sciences department of genetics. This award reflects what we know alreadythat his creativity, productivity and leadership while a faculty member at UGA have more than borne out that early promise, and promise even more great things in the future.

This is an extraordinary honor and I would like to acknowledge the Blavatnik National Awards for Young Scientists for recognizing the importance of agricultural research as part of their life sciences portfolio, Schmitz said.

Read more:
Plant biologist nominated for prestigious early career award - University of Georgia

Posted in Epigenetics | Comments Off on Plant biologist nominated for prestigious early career award – University of Georgia

Julee Cruise’s Career: How and where to watch Twin Peaks and all her TV appearances – Bolavip US

Posted: June 13, 2022 at 2:13 am

Julee Cruiseborn on December 1, 1956 in Iowa.Since childhood she has had a special affinity for the world of music. She studied French horn at Drake University and performed as a singer and actress in Minneapolis with the Children's Theatre Company. Her favorite role to play was Jinjur from Lyman Frank Baum's Oz books.

As a singer, songwriter and actress, she has recorded four studio albums: Floating into the Night, The Voice of Love, The Art of Being a Girl and My Secret Life. During the 80's she collaborated with figures such as Angelo Badalamenti (composer of Blue Velvet) and David Lynch (film director). Both have been the producers of his first two albums.

But fame and worldwide recognition came with her participation in the famous mystery series Twin Peaks. With an angelic voice, the singerperformed the song "Falling" in 1990, which became the orchestral theme for the television series. Thanks to its impact, she won Best Pop Instrumental awardat the 33rd Grammy Awards.

With her enveloping and ethereal voice, she was also a collaborator of many soundtracks, programs and television series of high popularity. Some like Scream, Psych in the episode "Dual Spires", Saturday Night Live in the 90's and one of her most remarkable projects, Blue Velvet.

Cruise married Editor-in-Chief and Vice President of Guideposts Publications, Eduard Grinnan. The two lived together, with their golden retriever puppy Grace, in a residence located in Manhattan, New York.

On March 28, 2018, the singer went public on her Facebook page that she had systemic lupus, which caused her considerable pain and affected her ability to walk and stand. "The pain is so bad that I cry. I can hardly walk and now it's hard to stand",she said.

The singer died on Friday, June 10, at the age of 65, after a lifetime of struggling with lupus, a disease she had suffered from since youth.Although the cause of the disease in general is still unknown, but there is concrete evidence of the influence of genetics, epigenetics (changes in chromosomes that affect gene activity), environmental factors, viruses and infections.

For those of you who go back I thought you might want to know that I said goodbye to my wife, Julee Cruise, today. She left this realm on her own terms. No regrets. She is at peace. Having had such a varied music career she often said that the time she spent as a B filling in for Cindy while she was having a family was the happiest time of her performing life. She will be forever grateful to them. When she first stepped up the mic with Fred and Kate she said it was like joining the Beatles.She will love them always and never forget their travels together around the world. I played her Roam during her transition. Now she will roam forever. Rest In Peace, my love, and love to you all, wrote her husband to members of B-52 fan group.

As the husband said his last goodbye, his favorite song was Roam by The B-52's. The song Roam is a party piece by the group, with whom Cruise toured during the 1990s as a replacement for lead singer Cindy Wilson.

The fact that Grinnan decided to break the news to the band's fans first speaks volumes about his love for the group. His release was made on the fan group "the B-52's universe the world's greatest party band".

TV Shows

1. Twin Peaks (1990).Available on Paramount +

2. The Red Shoes (1983).

3. The Marvelous Land of Oz (1981).

4.Industrial Symphony No. 1: The Dream of the Brokenhearted (1990).

5.David Lynch: Don't Look at Me (1989)

6. The Red Shoes (1983).

7.Twin Peaks: Fire Walk with Me (1992).Available on HBO MAX.

8. Blue Velvet (1986). Available on Hulu, Kanopy, Tubi, Hoopla, The Criterion Channel and Paramount +.

9. Alice in Wonderland (1982).

10. Puss in Boots (1982).

Music

1.Floating into the Night (1989).Available on Spotify, Deezer and YouTube Music.

2.Cosmic Thing by The B-52's (1989). Available on Spotify, Deezer and YouTube Music.

3.Dance This Mess Around by The B-52's(1990). Available on Deezer.

4.The Voice of Love (1993). Available on Spotify and YouTube Music.

5.The Art of Being a Girl (2002). Available onSpotify and YouTube Music.

6.Julee Cruise/Nutcracker EP: An American Nightmare Maxi (2003).Available on Deezerand YouTube Music.

7.My Secret Life (2011).Available on Spotify, Deezer and YouTube Music.

Visit link:
Julee Cruise's Career: How and where to watch Twin Peaks and all her TV appearances - Bolavip US

Posted in Epigenetics | Comments Off on Julee Cruise’s Career: How and where to watch Twin Peaks and all her TV appearances – Bolavip US

Hitting the Pro Race Track: Onovi Health Adds Marko Radiic, Professional Race Car Driver & Entrepreneur, as a Brand Ambassador – PR Newswire

Posted: June 13, 2022 at 2:12 am

The high performance telehealth company Onovi believes the collaboration will help race car drivers & entrepreneurs improve performance on and off the track.

BIRMINGHAM, Ala., June 9, 2022 /PRNewswire/ -- Onovi, the leader in performance-driven men's healthcare, today announced a partnership with Marko Radiic of SRQ Motorsports Group. Radiic, an Onovi N1 client, represents Onovi in the SRO GTA America series powered by Amazon Web Services, Inc. Onovi Health is powered by the Gapin Institute for High Performance Medicine.

Just as race teams strategize and look for every tweak to improve the car's performance, Marko Radiic does the same with his personal health and performance. Radiic works with his medical and performance teams at Onovi to make precise adjustments off-track so he can perform better on-track.

"We are proud to partner with Marko Radiic and SRQ Motorsports on the upcoming GT America series," said Onovi CEO Clete Walker. "Marko has embraced the N1 Performance Health Program from Onovi Health and has been a fantastic example of how the program can improve endurance and stamina."

The physical toll of racing is far greater than many realize, and the drivers are required to function at optimal levels. The stressors faced by race car drivers include exposure to high G-force levels, heat stress, and intense muscular effort in addition to mental stress, dehydration, and more. With precision-based prep and recovery, a race car driver will have a competitive advantage to find their way into the winner's circle.

Tracy Gapin, MD, Chief Medical Officer for Onovi and creator of the N1 Performance Health Program said, "N1 is a personalized health program designed to optimize your mind and body for high performance. The program utilizes advanced breakthroughs in science and high performance medicine. N1 combines cutting-edge genetic & epigenetic science with the latest research in physiology, hormones, precision medicine and wearable technology. Whereas our current broken healthcare system only addresses disease, Onovi and the N1 program focus on health optimization."

The N1 Performance Health Program starts with baseline diagnostics and advanced lab testing to determine a precise health strategy. The program includes a medical doctor, functional health coach, nutritionist, fitness trainer, epigenetics specialist, and concierge team to interpret and leverage health data. Onovi also offers subscription services for hormone optimization, testosterone therapy, peptide therapy and at-home lab testing.

"The N1 Program dramatically improved my racing performance. The cutting-edge strategies and wearable tech helped me upgrade my health and training regimen, including my race-day approach. It also improved my personal and professional life, which is why I wanted to get involved with the brand. I'm excited to bring this level of precision to the professional racing circuit," said Radiic.

Radiic, the brand ambassador, is a great example of a high performer. The N1 program gives the 50-year-old race car driver and Guinness World Record holder, the extra edge in his health, training regimen and race day approaches. The data-driven program relies on wearable technology as one component of the systems-based precision approach.

Onovi http://www.onovihealth.com

About Onovi Health

Onovi Health, a high performance health company, provides a personalized, holistic and data-driven approach to provide a complete men's telehealth solution. Led by Urologists and men's health experts, Onovi combines cutting-edge genetic & epigenetic science with physiology, biochemistry, brain/peak performance, hormones and lifestyle for personalized solutions to reach peak performance. Onovi offers personalized men's health programs, telehealth services and at-home lab testing.

Related Links

Gapin Institute http://www.gapininstitute.com

Marko Radiic https://bit.ly/3auJyFY

Media Contact

Leann Spofford(941) 524-4592[emailprotected]

SOURCE Onovi Health

Visit link:
Hitting the Pro Race Track: Onovi Health Adds Marko Radiic, Professional Race Car Driver & Entrepreneur, as a Brand Ambassador - PR Newswire

Posted in Epigenetics | Comments Off on Hitting the Pro Race Track: Onovi Health Adds Marko Radiic, Professional Race Car Driver & Entrepreneur, as a Brand Ambassador – PR Newswire

Epigenetics: Definition & Examples | Live Science

Posted: June 4, 2022 at 2:24 am

Epigenetics literally means "above" or "on top of" genetics. It refers to external modifications to DNA that turn genes "on" or "off." These modifications do not change the DNA sequence, but instead, they affect how cells "read" genes.

Examples of epigenetics

Epigenetic changes alter the physical structure of DNA. One example of an epigenetic change is DNA methylation the addition of a methyl group, or a "chemical cap," to part of the DNA molecule, which prevents certain genes from being expressed.

Another example is histone modification. Histones are proteins that DNA wraps around. (Without histones, DNA would be too long to fit inside cells.) If histones squeeze DNA tightly, the DNA cannot be "read" by the cell. Modifications that relax the histones can make the DNA accessible to proteins that "read" genes.

Epigenetics is the reason why a skin cell looks different from a brain cell or a muscle cell. All three cells contain the same DNA, but their genes are expressed differently (turned "on" or "off"), which creates the different cell types.

Epigenetic inheritance

It may be possible to pass down epigenetic changes to future generations if the changes occur in sperm or egg cells. Most epigenetic changes that occur in sperm and egg cells get erased when the two combine to form a fertilized egg, in a process called "reprogramming." This reprogramming allows the cells of the fetus to "start from scratch" and make their own epigenetic changes. But scientists think some of the epigenetic changes in parents' sperm and egg cells may avoid the reprogramming process, and make it through to the next generation. If this is true, things like the food a person eats before they conceive could affect their future child. However, this has not been proven in people.

Epigenetics and cancer

Scientists now think epigenetics can play a role in the development of some cancers. For instance, an epigenetic change that silences a tumor suppressor gene such as a gene that keeps the growth of the cell in check could lead to uncontrolled cellular growth. Another example might be an epigenetic change that "turns off" genes that help repair damaged DNA, leading to an increase in DNA damage, which in turn, increases cancer risk.

Go here to read the rest:
Epigenetics: Definition & Examples | Live Science

Posted in Epigenetics | Comments Off on Epigenetics: Definition & Examples | Live Science

Genetics and Epigenetics of Addiction DrugFacts | National Institute on …

Posted: June 4, 2022 at 2:24 am

Genetics: The Blueprint of Health and DiseasePurified DNA fluorescing orange under UV light

Why do some people become addicted while others don't? Family studies that include identical twins, fraternal twins, adoptees, and siblings suggest that as much as half of a person's risk of becoming addicted to nicotine, alcohol, or other drugs depends on his or her genetic makeup. Finding the biological basis for this risk is an important avenue of research for scientists trying to solve the problem of drug addiction.

Genetics is the study of genes. Genes are functional units of DNA that make up the human genome. They provide the information that directs a body's basic cellular activities. Research on the human genome has shown that, on average, the DNA sequences of any two people are 99.9 percent the same. However, that 0.1 percent variation is profoundly importantit accounts for three million differences in the nearly three billion base pairs of DNA sequence! These differences contribute to visible variations, like height and hair color, and invisible traits, such as increased risk for or protection from certain diseases such as heart attack, stroke, diabetes, and addiction.

Some diseases, such as sickle cell anemia or cystic fibrosis, are caused by a change, known as a mutation, in a single gene. Some mutations, like the BRCA 1 and 2 mutations that are linked to a much higher risk of breast and ovarian cancer, have become critical medical tools in evaluating a patient's risk for serious diseases. Medical researchers have had striking success at unraveling the genetics of these single-gene disorders, though finding treatments or cures has not been as simple. Most diseases, including addiction, are complex, and variations in many different genes contribute to a person's overall level of risk or protection. The good news is that scientists are actively pursuing many more paths to treatment and prevention of these complex illnesses.

Recent advances in DNA analysis are helping researchers untangle complex genetic interactions by examining a person's entire genome all at once. Technologies such as genome-wide association studies (GWAS), whole genome sequencing, and exome sequencing (looking at just the protein-coding genes) identify subtle variations in DNA sequence called single-nucleotide polymorphisms (SNPs). SNPs are differences in just a single letter of the genetic code from one person to another. If a SNP appears more often in people with a disease than those without, it is thought to either directly affect susceptibility to that disease or be a marker for another variation that does.

GWAS and sequencing are extremely powerful tools because they can find a connection between a known gene or genes and a disorder, and can identify genes that may have been overlooked or were previously unknown.

Through these methods, scientists can gather more evidence from affected families or use animal models and biochemical experiments to verify and understand the link between a gene and the risk of addiction. These findings would then be the basis for developing new treatment and intervention approaches.

It is estimated that 30% of marijuana users have a cannabis use disorder, representing problematic useand in some casesaddiction. The risk for cannabis use disorder has a strong genetic component, but the genetic architecture has been unclear. Scientists recently performed a genome-wide association study11 to try to identify genes that might put people at risk for problematic cannabis use. They studied 2,387 cases and 48,985 controls, and replicated their findings in another large group. They identified a genetic locus on chromosome 8 that controls the levels of the gene CHRNA2 expressed in the brain.Low levels of expression of the gene CHRNA2 in the cerebellum are found to beassociated with cannabis use disorder, including diagnosis at an earlier age. In addition, genetic factors associated with educational attainment were found to be protective against the disorder. The findings suggest that under expression of CHRNA2 in the cerebellum (and probably other brain regions) is involved in cannabis use disorders, and provides a potential target for future prevention strategies, therapies and medications.

That old saying "nature or nurture" might be better phrased "nature and nurture" because research shows that a person's health is the result of dynamic interactions between genes and the environment. For example, both genetics and lifestyle factorssuch as diet, physical activity, and stressaffect high blood pressure risk. NIDA research has led to discoveries about how a person's surroundings affect drug use in particular.

For example, a community that provides healthy after-school activities has been shown to reduce vulnerability to drug addiction, and data show that access to exercise can discourage drug-seeking behavior, an effect that is more pronounced in males than in females.1-3

Studies suggest that an animal's drug use can be affected by that of its cage mate,4, 5 showing that some social influences can enhance risk or protection. In addition, exposure to drugs or stress in a person's social or cultural environment can alter both gene expression and gene function, which, in some cases, may persist throughout a persons life. Research also suggests that genes can play a part in how a person responds to his or her environment, placing some people at higher risk for disease than others.

Scientists doing genetics research have collected millions of data points ("big data") that could be of use to other scientists. However, different software systems and measurement formats have made sharing data sets difficult. NIH has created the Big Data to Knowledge (BD2K) program to support the research and development of innovative and transformative approaches and tools to help scientists use big data and data science in their research(https://commonfund.nih.gov/bd2k). When the data can be combined and harmonized, a process called data integration, the chances of identifying new genetic information that could give rise to new disease insights is amplified.

Epigenetics is the study of functional, and sometimes inherited, changes in the regulation of gene activity and expression that are not dependent on gene sequence.6 "Epi-" itself means "above" or "in addition to." Environmental exposures or choices people make can actually "mark"or remodelthe structure of DNA at the cell level or even at the level of the whole organism. So, although each cell type in the human body effectively contains the same genetic information, epigenetic regulatory systems enable the development of different cell types (e.g., skin, liver, or nerve cells) in response to the environment. These epigenetic marks can affect health and even the expression of the traits passed to children. For example, when a person uses cocaine, it can mark the DNA, increasing the production of proteins common in addiction. Increased levels of these altered proteins correspond with drug-seeking behaviors in animals.

Histones, as another example, are like protein spools that provide an organizational structure for genes. Genes coil around histones, tightening or loosening to control gene expression. Drug exposure can affect specific histones, modifying gene expression in localized brain regions.7 Science has shown that manipulation of histone-modifying enzymes and binding proteins may have promise in treating substance use disorders.8-10

The development of multidimensional data sets that include and integrate genetic and epigenetic information provide unique insights into the molecular genetic processes underlying the causes and consequences of drug addiction. Studying and using these data types to identify biological factors involved in substance misuse is increasingly important because technologic advances have improved the ability of researchers to single out individual genes or brain processes that may inform new prevention and treatment interventions.

An international group of over 100 scientists used a comprehensive database to collect information on smoking and alcohol use behaviors.They measured behaviors such as age when smoking was initiated, age when smoking cessation occurred, number of cigarettes per day, and drinks per week. The scientists then cross-checked those findings with life events (like years of education); physical characteristics (like heart rate or cholesterol level); and diseases suffered (such as mental illnesses, or Type 2 diabetes). The investigators correlated those results with specific genes suspected in various types of substance use. Theyfound12 that there were over 400 locations in the genome and at least 566 variants within these locations that influence smoking or alcohol use, bringing science closer to identifying clusters of genes that could play a part in addiction. The study even identified new genes and functions not expected to be important in addiction.Three of the genetic locations (identified as CUL3, PDE4B, PTGER3) mapped to all of the smoking and alcohol phenotypes measured.

Clinicians often find substantial variability in how individual patients respond to treatment. Part of that variability is due to genetics. Genes influence the numbers and types of receptors in peoples brains, how quickly their bodies metabolize drugs, and how well they respond to different medications. Learning more about the genetic, epigenetic, and neurobiological bases of addiction will eventually advance the science of addiction.

Scientists will be able to translate this knowledge into new treatments directed at specific targets in the brain or to treatment approachescalled pharmacogenomics. This emerging science promises to harness the power of genomic information to improve treatments for addiction by tailoring the treatment to the person's specific genetic makeup. This is called precision medicine. By knowing a person's genomic information, health care providers will be better equipped to match patients with the most suitable treatments and medication dosages, and to avoid or minimize adverse reactions.

The mission of the NIDA's Division of Neuroscience and Behavior (DNB) is to advance the science of drug use and addiction through basic and clinical biomedical neuroscience and behavioral research. The DNB's Genetics, Epigenetics, and Developmental Neuroscience Branch supports research on the genetics, epigenetics, and developmental mechanisms that underlie substance use, misuse, and addiction.

The DNB accomplishes its mission by developing and supporting an extramural research program that provides an understanding of the neurobiological and behavioral mechanisms of drugs of abuse and its consequences. The research supported by DNB provides important fundamental information to prevent and/or intervene in drug use and addiction.

For more information about genetics and drug abuse, visit:

More here:
Genetics and Epigenetics of Addiction DrugFacts | National Institute on ...

Posted in Epigenetics | Comments Off on Genetics and Epigenetics of Addiction DrugFacts | National Institute on …

Epigenetics at the Intersection of COVID-19 Risk and Environmental Chemical Exposures – DocWire News

Posted: June 4, 2022 at 2:23 am

This article was originally published here

Curr Environ Health Rep. 2022 Jun 1. doi: 10.1007/s40572-022-00353-9. Online ahead of print.

ABSTRACT

PURPOSE OF REVIEW: Several environmental contaminants have been implicated as contributors to COVID-19 susceptibility and severity. Immunomodulation and epigenetic regulation have been hypothesized as mediators of this relationship, but the precise underlying molecular mechanisms are not well-characterized. This review examines the evidence for epigenetic modification at the intersection of COVID-19 and environmental chemical exposures.

RECENT FINDINGS: Numerous environmental contaminants including air pollutants, toxic metal(loid)s, per- and polyfluorinated substances, and endocrine disrupting chemicals are hypothesized to increase susceptibility to the SARS-CoV-2 virus and the risk of severe COVID-19, but few studies currently exist. Drawing on evidence that many environmental chemicals alter the epigenetic regulation of key immunity genes and pathways, we discuss how exposures likely perturb host antiviral responses. Specific mechanisms vary by contaminant but include general immunomodulation as well as regulation of viral entry and recognition, inflammation, and immunologic memory pathways, among others. Associations between environmental contaminants and COVID-19 are likely mediated, in part, by epigenetic regulation of key immune pathways involved in the host response to SARS-CoV-2.

PMID:35648356 | DOI:10.1007/s40572-022-00353-9

Link:
Epigenetics at the Intersection of COVID-19 Risk and Environmental Chemical Exposures - DocWire News

Posted in Epigenetics | Comments Off on Epigenetics at the Intersection of COVID-19 Risk and Environmental Chemical Exposures – DocWire News

Page 5«..4567..1020..»