SALT LAKE CITY, Aug. 13, 2020 (GLOBE NEWSWIRE) -- Myriad Genetics, Inc. (NASDAQ: MYGN, Myriad or the Company), a global leader in molecular diagnostics and precision medicine, today announced the appointment ofPaul J. Diazas President and Chief Executive Officer, effective August 13, 2020. He will also serve on the Companys Board of Directors. Mr. Diaz brings toMyriad Geneticsmore than three decades of executive leadership and business transformation experience in healthcare across a variety of healthcare segments.

Paul is an exceptional leader and executive with extraordinary passion, vision, experience, and operational skills, saidS. Louise Phanstiel, Chair of Myriads Board of Directors. His focus on building high performing teams, and instilling a culture that empowers people to deliver high quality patient care, distinctive customer service and innovation, will be important to supporting Myriads mission and growth. We are excited to have Paul assume the leadership of Myriad Genetics and chart the course to realize the Companys full potential. We look forward to officially introducing Paul during our fourth quarter earnings call. Myriad is dedicated to providing vital information to physicians, patients and their families that enables them to make better decisions about their health and treatment planning. Pauls personal dedication, throughout his career, to patients and their care will be critical in advancing Myriads vision of being a trusted advisor transforming patients lives worldwide with pioneering molecular diagnostics.

I am very excited to join the talented management team and Board of Directors of Myriad Genetics, an organization dedicated to helping patients and physicians identify the risk of developing disease and accurately diagnosing disease and disease progression, commented Paul. Our goal is to empower patients, as consumers, and their physicians and our payer partners with the information and data to help guide their treatment decisions, to improve clinical outcomes and lower healthcare costs.I am equally excited about Myriads potential for innovation and growth.The Company has a tremendous opportunity to transform its business, and strategically position itself for sustainable, profitable growth. We will look to leverage the companys culture of innovation and revitalize our approach to the commercializing of its products and customer service levels.

Mr. Diaz served as the President and Chief Executive Officer and Executive Director and Director of Kindred Healthcare, Inc. for over ten years, where he led the growth, revitalization and diversification of the business that positioned Kindred as the largest provider of post-acute health care services in the United States. Most recently, Mr. Diaz was a Partner at Cressey & Company LP, a private equity firm focusing on healthcare services and HCIT companies. Mr. Diaz is an experienced director and operating executive, having served as an executive and board member of multiple public and private companies. He currently serves on the board of DaVita, Inc. (NYSE: DVA) and is a member of the Board of Trustees of Johns Hopkins Medicine. Mr. Diaz graduated from The American University with a B.S. in Business Administration and with a J.D. from The Georgetown University Law Center.

Heidrick & Struggles led the search process for Myriad.

About Myriad GeneticsMyriad Genetics Inc., is a leading personalized medicine company dedicated to being a trusted advisor transforming patient lives worldwide with pioneering molecular diagnostics. Myriad discovers and commercializes molecular diagnostic tests that: determine the risk of developing disease, accurately diagnose disease, assess the risk of disease progression, and guide treatment decisions across six major medical specialties where molecular diagnostics can significantly improve patient care and lower healthcare costs. Myriad is focused on three strategic imperatives: transitioning and expanding its hereditary cancer testing markets, diversifying its product portfolio through the introduction of new products and increasing the revenue contribution from international markets. For more information on how Myriad is making a difference, please visit the Company's website: http://www.myriad.com.

Myriad, the Myriad logo, BART, BRACAnalysis, Colaris, Colaris AP, myPath, myRisk, Myriad myRisk, myRisk Hereditary Cancer, myChoice, myPlan, BRACAnalysis CDx, Tumor BRACAnalysis CDx, myChoice CDx, Vectra, Prequel, Foresight, GeneSight, riskScore and Prolaris are trademarks or registered trademarks of Myriad Genetics, Inc. or its wholly owned subsidiaries in the United States and foreign countries. MYGN-F, MYGN-G.

Safe Harbor StatementThis press release contains "forward-looking statements" within the meaning of the Private Securities Litigation Reform Act of 1995, including statements related to realizing the Companys full potential; officially introducing Paul during the Companys fourth quarter earnings call; advancing Myriads vision of being a trusted advisor transforming patients lives worldwide with pioneering molecular diagnostics; the Companys potential for innovation and growth; the Companys tremendous opportunity to transform its business, and strategically position itself for sustainable, profitable growth; and the Companys strategic directives under the caption "About Myriad Genetics." These "forward-looking statements" are based on management's current expectations of future events and are subject to a number of risks and uncertainties that could cause actual results to differ materially and adversely from those set forth in or implied by forward-looking statements. These risks and uncertainties include, but are not limited to: uncertainties associated with COVID-19, including its possible effects on our operations and the demand for our products and services; our ability to efficiently and flexibly manage our business amid uncertainties related to COVID-19; the risk that sales and profit margins of our molecular diagnostic tests and pharmaceutical and clinical services may decline; risks related to our ability to transition from our existing product portfolio to our new tests, including unexpected costs and delays; risks related to decisions or changes in governmental or private insurers reimbursement levels for our tests or our ability to obtain reimbursement for our new tests at comparable levels to our existing tests; risks related to increased competition and the development of new competing tests and services; the risk that we may be unable to develop or achieve commercial success for additional molecular diagnostic tests and pharmaceutical and clinical services in a timely manner, or at all; the risk that we may not successfully develop new markets for our molecular diagnostic tests and pharmaceutical and clinical services, including our ability to successfully generate revenue outside the United States; the risk that licenses to the technology underlying our molecular diagnostic tests and pharmaceutical and clinical services and any future tests and services are terminated or cannot be maintained on satisfactory terms; risks related to delays or other problems with operating our laboratory testing facilities and our healthcare clinic; risks related to public concern over genetic testing in general or our tests in particular; risks related to regulatory requirements or enforcement in the United States and foreign countries and changes in the structure of the healthcare system or healthcare payment systems; risks related to our ability to obtain new corporate collaborations or licenses and acquire new technologies or businesses on satisfactory terms, if at all; risks related to our ability to successfully integrate and derive benefits from any technologies or businesses that we license or acquire; risks related to our projections about our business, results of operations and financial condition; risks related to the potential market opportunity for our products and services; the risk that we or our licensors may be unable to protect or that third parties will infringe the proprietary technologies underlying our tests; the risk of patent-infringement claims or challenges to the validity of our patents or other intellectual property; risks related to changes in intellectual property laws covering our molecular diagnostic tests and pharmaceutical and clinical services and patents or enforcement in the United States and foreign countries, such as the Supreme Court decisions in Mayo Collab. Servs. v. Prometheus Labs., Inc., 566 U.S. 66 (2012), Assn for Molecular Pathology v. Myriad Genetics, Inc., 569 U.S. 576 (2013), and Alice Corp. v. CLS Bank Intl, 573 U.S. 208 (2014); risks of new, changing and competitive technologies and regulations in the United States and internationally; the risk that we may be unable to comply with financial operating covenants under our credit or lending agreements; the risk that we will be unable to pay, when due, amounts due under our credit or lending agreements; and other factors discussed under the heading "Risk Factors" contained in Item 1A of our most recent Annual Report on Form 10-K for the fiscal year ended June 30, 2020, which has been filed with the Securities and Exchange Commission, as well as any updates to those risk factors filed from time to time in our Quarterly Reports on Form 10-Q or Current Reports on Form 8-K. All information in this press release is as of the date of the release, and Myriad undertakes no duty to update this information unless required by law.

Excerpt from:
Myriad Genetics Appoints Paul J. Diaz as President and Chief Executive Officer and a Member of the Board of Directors - GlobeNewswire

A UO-led team of researchers spanning physics, neuroscience, molecular biology, ecology and evolution will use a new $325,000 grant to examine aquatic symbioses the interactions between different animal species living together.

The project is funded by a 30-month award from the Gordon and Betty Moore Foundation and involves the study of zebrafish in controlled ecosystems.

The team will leverage decades worth of pioneering research at the UO involving zebrafish and explorations of the gut microbiome, in which vast numbers of microbes contribute to both health and disease in their hosts. UO has been a leader in zebrafish research since the 1960s, when the late biologist George Streisinger established zebrafish as an ideal model for studying human development and disease.

We aim to develop new tools for studying these symbioses throughout the entire lifespan of zebrafish, which serves as a model aquatic animal and a model for phenomena relevant to all vertebrates, including humans, said Raghuveer Parthasarathy, an Alec and Kay Keith Professor in the Department of Physics, a member of the UOs Institute of Molecular Biology and Materials Science Institute, and the principal investigator on the award.

The project builds on the successes of the zebrafish group here at the UO and it pushes it to the next frontier of trying to capture the whole lifespan of the animal and its ecosystem, Parthasarathy said.

Along with Parthasarathy, the team includes Karen Guillemin, Judith Eisen and Brendan Bohannan, all professors in the Department of Biology. Guillemin is a Philip H. Knight Chair and a member of the Institute of Molecular Biology. Eisen is a member of the Institute of Neuroscience. Bohannan, the James F. and Shirley K. Rippey Chair in Liberal Arts and Sciences, is a member of the Institute of Ecology and Evolution.

The team also includes John Rawls, a professor of molecular genetics and microbiology at Duke University and the director of the Duke Microbiome Center.

Part of the Moore Foundations Symbiosis in Aquatic Systems Initiative, the project will contribute to a larger effort to equip the scientific community with new genetic tools, cultivation methods and other infrastructure to improve experimental capabilities in aquatic symbiosis research over the coming decade. Increasingly, researchers are recognizing that symbiotic bacteria are critical components in the processes that sculpt the evolution, ecology, development and physiology of animals, yet remarkably little is known about exactly how those processes play out.

The four UO researchers have worked together on previous projects as part of the UOs interdisciplinary Microbial Ecology and Theory of Animals, a National Institutes of Health-funded Center of Excellence in Systems Biology. The center is funded by a $7.6 million grant and seeks to better understand the bacteria and other microorganisms that reside in the animal gut and influence many biological functions.

Building on their earlier work studying individual biological processes, the new research will explore the entire ecosystem and lifespan of zebrafish and consider food chains, population densities and other attributes. The project will serve as a bridge between more traditional model system research and field studies, opening up new frontiers in zebrafish research, Parthasarathy said.

The project involves three main areas. Investigators will:

Were hoping to learn how can we both predict and control ecosystem constituents, things like food and bacteria and how can that give us healthy organisms throughout their lifespan, Parthasarathy said. Our approach focuses especially on better understanding nutrition and on engineering new aquatic habitats that allow controlled investigation of symbiotic interactions. We want to watch and learn from the entire process.

The UO team will be building on a strong foundation of zebrafish research. That includes groundbreaking work by Eisen examining interactions between the nervous system, immune system and bacteria in the gut, and Guillemins innovative development of specialized sterile zebrafish that allow scientists to better determine the role microbes play as animals grow.

Bohannan has conducted important research on zebrafish, tracking them throughout their life cycle to see how diet, genetics and immune response affect their microbial diversity. And Parthasarathy has employed physics to better understand how gut microbes move and interact with each other, producing stunning, high-resolution, three-dimensional images and videos of gut bacteria in zebrafish using a technique known as light sheet microscopy.

Rawls, the biologist from Duke University, studies gut bacteria in zebrafish and their role in regulating digestive physiology, innate immunity and gut-brain communication.

I think (this research) may open up a lot of ecological questions, Parthasarathy said. If we succeed, we can expand our methods to other species such as plants and algae and explore their interactions. I think there is lots of potential for growth.

The project is the latest in a string of awards to UO researchers from the Moore Foundation. Earlier this year Eisen received a $2 million grant through the same symbiosis initiative to probe the relationship between symbiotic bacteria and neural development, using zebrafish as a model organism. In January, UO biologist Kelly Sutherland received a $1.1 million grant from the foundation funding her research examining the swimming mechanisms of gelatinous marine organisms.

These awards are a testament to the exceptional research being conducted at the University of Oregon, said Provost and Senior Vice President Patrick Phillips. We are grateful to the Gordon and Betty Moore Foundation for their generous support of our researchers and their investment in these innovative and impactful projects, which support the foundations critical mission of fostering pathbreaking scientific discovery and further the UOs commitment to enriching the human condition through creative inquiry and scientific discovery.

By Lewis Taylor, University Communications

Read this article:
UO team will use zebrafish in new study of aquatic symbioses - AroundtheO

Once known as a paradigm changing class of precision oncology, or targeted, drugs,1 Bruton tyrosine kinase (BTK) inhibitors are now well established as treatment for several hematological malignancies. They are named for Lt Col Ogden C. Bruton, MD, chief of pediatrics at Walter Reed Army Medical Center in the 1950s, who in 1951 discovered the first host immunodeficiency in humans, X-linked agammaglobulinemia.2,3

The BTK protein is essential to helping B cells develop and mature into functional and specialized white blood cells; these are part of the adaptive immune response in producing antibodies, or immunoglobulins.4 But mutations in the BTK gene, more than 600 of which have been identified, can lead to a sizeable reduction in the number of circulating B cells, along with reduced ability to fight infection, absence of the BTK protein, production of abnormal BTK protein, or cancer cell growth.5,6

Mutated immunoglobulins essentially malfunction in their roles as antigen receptors on the surfaces of B cells, especially in the cancer space, by not recognizing antigens as damaging or by not sending the correct signals to destroy the malignant cells.

This is where BTK inhibitors come in: They help to trigger cell death by blocking the B-cell receptor signaling that leukemias and lymphomas use to grow and survive.7 The first-generation BTK inhibitor ibrutinib (Imbruvica) came to market in 2013, when it was approved by the FDA to treat adult patients with mantle cell lymphoma. A targeted treatment, it stops cancer cells from surviving and multiplying by blocking abnormal protein signaling.8 Other indications, as monotherapy or in combination, have been approved for chronic lymphocytic leukemia, Waldenstrm macroglobulinemia, small lymphocytic lymphoma, relapsed/refractory marginal zone lymphoma, and chronic graft-versus-host disease.9 Ibrutinib is a once-daily oral agent and can be used in the frontline and relapsed settings.10

Despite its many benefits and indications, however, ibrutinib as BTK inhibition is also associated with numerous adverse effects (AEs) on nonmalignant cells, which range from common to uncommon and from mild to severe, making ibrutinibs toxicity profile notorious.7

Among the most severe AEs are hemorrhage; high blood pressure; heart rhythm irregularities, including ventricular arrhythmias, atrial fibrillation, and atrial flutter; second primary cancers (eg, skin, other organs); and tumor lysis syndrome.11 Some of the most common AEs, occurring in more than 30% of patients, are hematological (eg, decreased platelets, neutrophils, and hemoglobin), musculoskeletal, and respiratory in nature.

Additional possible AEs include diarrhea, constipation, vomiting, skin infections, dizziness, dehydration, petechiae, arthralgia, stomatitis, rash, and fatigue.12 Ibrutinib carries warnings for use among those with bleeding problems, liver problems, and for those who are planning surgery or recently had surgery; women who are pregnant or thinking of becoming pregnant; women who breastfeed or plan to do so; and men with female partners capable of pregnancy.

Second-generation BTK inhibitors seek to improve upon first-generation agents like ibrutinib by having less cardiotoxicity, fewer AEs that result in stopping treatment, and fewer off-target effects. For example, ibrutinib inhibits the activity of 3 major off-targets: epidermal growth factor, which can result in severe skin toxicities13; interleukin-2 inducible kinase, which impairs natural killer cells cytotoxic abilities14; and the Tec family of kinases, decreasing their ability to aid in phosphorylation.15

In updated results of the ASPEN trial presented at this years virtual American Society of Clinical Oncology (ASCO) 2020 Annual Meeting, zanubrutinib (Brukinsa), the most recent second-generation BTK inhibitor to hit the US market, was shown to have a survival advantage over ibrutinib in patients with Waldenstrm macroglobulinemia who lacked the MYD88 mutation typically associated with successful treatment.16

ASPEN first compared zanubrutinib with ibrutinib in patients with Waldenstrm macroglobulinemia who have the MYD88 mutation, and zanubrutinib was shown in December 2019 to increase the incidence of complete response (CR) or very good partial response (VGPR) by close to 46% compared with ibrutinib28.9% vs 19.8%, respectivelyin patients with relapsed or refractory disease.17

The updated results, from 5 additional months of data, widened this gap, showing a 30.4% CR plus VGPR rate for zanubrutinib compared with 18.2% for ibrutinib, as well as less occurrence of atrial fibrillation/flutter of any grade, bleeding of any grade, major hemorrhage, diarrhea, and hypertension. In addition, patients without the MYD88 mutation had an overall response rate of 80.8%, which included a 50.0% major response ratewhich itself included a VGPR rate of 26.9%and 12-month progression-free survival of 72.4%.18

Lead investigator, Constantine Tam, MBBS, MD, a clinical hematologist and professor at the Peter MacCallum Cancer Centre in Victoria, Australia, noted of zanubrutinib, Those patients who potentially have a history of hypertension or have a history of atrial fibrillationor have an abnormal ECG or abnormal echocardiogrammaybe theyre the ones who would be better off on [zanubrutinib] compared with ibrutinib. We think its how clean the targeting is.19

Zanubrutinib is associated with less incidence of muscle spasm, peripheral edema, pneumonitis, and pneumonia. In essence, fewer overall AEs with second-generation BTK inhibitors means less of a need to reduce dosing and a greater likelihood of being able to stay on treatment longer. Tam noted that most AEs happen with zanubrutinib during the first year on treatment, before their incidence plateaus, whereas prolonged treatment with ibrutinib has a greater chance of inflicting cumulative damage to the vascular system.20 Compared with first-generation BTK inhibitors, the second-generation drugs are associated with fewer concerns about primary and acquired drug resistance. For example, ibrutinib use among patients with relapsed/refractory mantle cell lymphoma has been shown to both have no effect on the disease and have a negative impact on additional therapies.21

These resistance mechanisms of action are 2-fold. They are molecular, in that they involve sustained distal B-cell receptor signaling through PIK3-AKT (protein kinase B) pathway activation, NFkB pathway activation, and cell cycle progression. They also are therapeutic, in that lines of therapy administered after BTK inhibitors do not produce prolonged responses or exceptional overall survival.21

Less Cardiotoxicity in Second Generation

Some of the strongest gains in this newer generation of BTK inhibitors, however, can be seen in the cardiovascular space, when compared with the toxicities of the first-generation inhibitors

that often lead to treatment discontinuation, especially among older, sicker patients who have a history of cardiac disease. In fact, most BTK inhibitors are prescribed for older patients, because the class of drugs is used primarily to treat chronic lymphocytic leukemia, for which the average age of onset is older than 60 years.22

I think its that a lot of the toxicities are related to off-target effects, meaning the binding of the BTK inhibitor drug to receptors or molecules that are not the ones that that theyre supposed to be treating the cancer for, said Michael Kolodziej, MD, FACP, vice president and chief innovation officer, ADVI Health, in an interview with Evidence-Based Oncology.

The big ones that were identified with the first-generation inhibitors were cardiovascular, or hypertension and atrial arrhythmias, atrial fibrillation. And they were not rare side effects.

Kolodziej explained that the second-generation drugs have fewer off-target effectsless cardiovascular toxicity, atrial arrhythmias, and hypertensionbecause of their improved toxicity profile, largely because the drugs are just better at being BTK inhibitors. Its not any more complicated than that.

The chief challenge of the first-generation BTK inhibitors is that the AEs cause clinicians and patients to stop treatment with them, Kolodziej noted. The cancer does not become resistant, but the toxicities become unbearable and the patients become intolerant, he emphasized.

The thinking is that the reduced cardiovascular side effects, the reduced bleeding, are going to allow a better persistence on the second-generation drugs, he explained.

Tolerability and Payers

Indeed, in a pooled analysis of clinical trials of the second-generation BTK inhibitor acalabrutinib (Calquence), also presented in May at ASCO, lead author Richard R. Furman, MD, of Weill Cornell Medicine in New York, found that at a median follow-up of 26.4 months, 65% of patients were still on treatment. Of the 34% of patients who stopped acalabrutinib, half (17%) did so because their disease progressed; only 9% stopped due to treatment-related AEs.23

Tolerability, especially as patients define it, is increasingly important to payers, starting with Medicare. The Center for Medicare and Medicaid Innovation has announced that it will incorporate patient-reported outcomes (PROs) into the Oncology Care First model, the proposed successor to the Oncology Care Model.24 Advocates for including PROs in payment models are encouraging drug developers to broaden definitions of tolerability, to include quality-of-life data in trial designs.25

Its a straightforward idea: When patients can tolerate treatment, it improves their chances of survival. This is important, Tam said during ASCO. The longer you take the drug, the better your responses become.19

Author Information

Maggie L. Shaw is associate editor, The American Journal of Managed Care.

References

1. Erba HP. BTK inhibition in B-cell lymphomas: an overview of Bruton tyrosine kinase inhibition. Targeted Oncology. June 21, 2019. Accessed July 18, 2020. https://www.targetedonc.com/view/btk-lymphoma

2. Wyckoff AS. Dr. Brutons discovery set the stage for modern clinical immunology. American Academy of Pediatrics News. May 31, 2018. Accessed July 18, 2020. https://www.aappublications.org/news/2018/05/31/dyk053118

3. Buckley RH. [Commentary:] agammaglobulinemia, by Col. Ogden C. Bruton, MC, USA, Pediatrics, 1952;9:722-728. Pediatrics. 1998;102(suppl 1):213-215. https://pediatrics.aappublications.org/content/102/Supplement_1/213

4. Deane P. B cells: the antibody factories of the immune system. Life Extension Advocacy Foundation. August 22, 2017. Accessed July 18, 2020. https://www.lifespan.io/news/b-cells/

5. BTK gene: Bruton tyrosine kinase. US National Library of Medicine/Genetics Home Reference. Updated July 7, 2020. Accessed July 18, 2020. https://ghr.nlm.nih.gov/gene/BTK#

6. Bruton tyrosine kinase inhibitor. Science Direct. Accessed July 18, 2020. https://www.sciencedirect.com/topics/medicine-and-dentistry/bruton-tyrosine-kinase-inhibitor

7. BTK inhibitors. Drugs.com. Updated January 7, 2020. Accessed July 18, 2020. https://www.drugs.com/drug-class/btk-inhibitors.html

8. Ibrutinib. MedlinePlus. Updated May 15, 2019. Accessed July 19, 2020. https://medlineplus.gov/druginfo/meds/a614007.html

9. Imbruvica approval history. Drugs.com. Updated 2020. Accessed July 19, 2020. https://www.drugs.com/history/imbruvica.html

10. Berger JA. The evolving role of BTK inhibitors in treating chronic lymphocytic leukemia BTK inhibition: disease state effectiveness. Targeted Oncology. April 16, 2020. Accessed July 19, 2020. https://www.targetedonc.com/view/evolving-btk-cll?seriesVid=2

11. How does Imbruvica work? Imbruvica (ibrutinib). April 20, 2020. Accessed July 19, 2020. https://imbruvica.com/cll/how-does-imbruvica-work

12. Imbruvica. Chemocare. Accessed July 19, 2020. chemocare.com/chemotherapy/drug-info/imbruvica.aspx

13. Ghasoub R, Albattah A, Elazzazy S, et al. Ibrutinib-associated sever[e] skin toxicity: a case of multiple inflamed skin lesions and cellulitis in a 68-year-old male patient with relapsed chronic lymphocytic leukemia case report and literature review. J Oncol Pharm Pract. 2020;26(2):487-491. doi:10.1177/1078155219856422

14. Bennett C. Ibrutinib may impair natural killer cell cytotoxic activity, study suggests. Cancer Therapy Advisor. June 19, 2019. Accessed July 19, 2020. https://www.cancertherapyadvisor.com/home/cancer-topics/lymphoma/ibrutinib-for-mantle-lymphoma-mcl-may-impair-naturalcyto-toxic-activity/

15. Patel V, Balakrishnan K, Bibikova E, et al. Comparison of acalabrutinib, a selective Bruton tyrosine kinase inhibitor, with ibrutinib in chronic lymphocytic leukemia cells. Clin Cancer Res. 2017;23(14):3734-3743. doi:10.1158/1078-0432.CCR-16-1446

16. Garcia-Sanz R, Dimopoulos MA, Lee H-P, et al. Updated results of the ASPEN trial from a cohort of patients with MYD88 wild-type (MYD88WT) Waldenstrm macroglobulinemia (WM). J Clin Oncol. 2020;38(15 suppl; abstr e20056). doi:10.1200/JCO.2020.38.15_suppl.e20056

17. Tam CSL, Opat S, DSa S, et al. ASPEN: results of a phase III randomized trial of zanubrutinib versus ibrutinib for patients with Waldenstrm macroglobulinemia (WM). J Clin Oncol. 2020;38(15 suppl; abstr 8007). doi:10.1200/JCO.2020.38.15_suppl.8007

18. BeiGene presents updated head to head results from phase 3 trial of zanubrutinib vs. ibrutinib in patients with Waldenstrms macroglobulinemia at the 2020 American Society of Clinical Oncology (ASCO) Virtual Scientific Program. News release. BeiGene; May 29, 2020. Accessed August 3, 2020. https://www.globenewswire.com/news-release/2020/05/29/2040883/0/en/BeiGene-Presents-Updated-Head-to-Head-Results-from-Phase-3-Trial-of-Zanubrutinibvs-Ibrutinib-in-Patients-with-Waldenstrm-s-acroglobulinemiaat-the-2020-American-Society-of-Clini.html

19. Caffrey M. Zanubrutinib pulls away from ibrutinib in update, shows durable responses in Waldenstrom patients lacking key mutation. The American Journal of Managed Care. May 30, 2020. Accessed July 21, 2020. https://www.ajmc.com/conferences/asco-2020/zanubrutinib-pulls-away-from-ibrutinib-in-update-shows-durable-responses-in-waldenstrom-patients-lacking-key-mutation

20. Dr Constantine Tam discusses the benefits of zanubrutinib on cardiac effects. The American Journal of Managed Care. May 31, 2020. Accessed July 22, 2020. https://www.ajmc.com/conferences/asco-2020/dr-constantine-tam-discusses-the-benefits-of-zanubrutinib-on-cardiac-effects

21. Hershkovitz-Rokah O, Pulver D, Lenz G, Shpilberg O. Ibrutinib resistance in mantle cell lymphoma: clinical, molecular and treatment aspects. Br J Haematol. 2018;181(3):306-319. doi:10.1111/bjh.15108

22. Chronic lymphocytic leukemia. CancerWall. Accessed July 24, 2020. https://cancerwall.com/chronic-lymphocytic-leukemia-lifeexpectancy-symptoms/

23. Furman RR, Byrd JC, Own RG, et al. Safety of acalabrutinib (acala) monotherapy in hematologic malignancies: pooled analysis from clinical trials. J Clin Oncol. 2020;38(suppl 15; abstr 8064). doi:10.1200/JCO.2020.38.15_suppl.8064

24. Bekele B, Macher D, Ferguson S, et al. Emerging trends in oncology management. Avalere Health. June 2, 2020. Accessed July 31, 2020. https://avalere.com/insights/emerging-trends-in-oncology-management

25. Basch E, Campbell A, Hudgens S, et al. A Friends of Cancer research white paper: broadening the definition of tolerability in cancer clinical trials to better measure the patient experience. Friends of Cancer Research. October 24, 2018. Accessed July 31, 2020. https://www.focr.org/sites/default/files/Comparative%20Tolerability%20Whitepaper_FINAL.pdf

Excerpt from:
Second-Generation BTK Inhibitors Hit the Treatment Bullseye With Fewer Off-Target Effects - AJMC.com Managed Markets Network

This story was originally published on Newsroom.co.nz and is republished with permission

With investigations into a coolstore and freight as a potential pathway for the latest outbreak of Covid-19, what does science say about surfaces and refrigeration?

Surfaces at a Mount Wellington coolstore are being tested for Covid-19 in an effort to uncover the route of the virus back into the community.

Ryan Anderson/Stuff

Americold in Mount Wellington, Auckland, where a south Auckland man with coronavirus works.

A worker at the coolstore has tested positive for the disease. How he caught it is still a mystery. The possibility it could have come in on overseas freight arriving at the coolstore is being investigated.

Were not ruling that out, said Director-General of Health Ashley Bloomfield, We want to get to the bottom of that.

READ MORE:* Coronavirus: Extension to Covid-19 lockdown likely, says disease modelling expert* Coronavirus: Rapid 'cluster busting' to find Covid-19 outbreak source could nip other clusters in the bud* Coronavirus: Auckland cool storage facility tested over concern Covid-19 entered NZ via freight* Coronavirus: Aucklanders should be wearing masks, experts say

The coolstore environment has been swabbed and test results are expected back today.

Yesterday, three other workers from the coolstore returned positive tests for Covid-19.

It's possible the workers were either infected by contaminated goods, or the virus was brought into the workplace after it was caught elsewhere, possibly by the man who was first diagnosed.

Two branches of the coolstore have been closed. One in Mount Wellington, where the man worked, and another close to Auckland Airport.

Genomic sequencing is still underway, but as of yesterday afternoon there hasnt been a link between genome patterns of cases in border quarantine and the genome pattern of the coolstore-related cases.

University of Auckland professor Shaun Hendy said the fact the source of the outbreak hadnt been identified yet was concerning.

MYTCHALL BRANSGROVE/STUFF

Tests are still ongoing to trace the pandemics source.

To date, the genomic information suggests this cluster is not linked to a managed isolation and quarantine facility. The business itself is linked to international freight, air and sea, which does suggest that this is a possible entry route, whether via packaging, or more likely, via person-to-person.

Like many things Covid-19 related, the science of transmission isnt clear-cut; what studies have been done are often laboratory-based.

Surface transmission is considered a lower risk for virus transmission than person-to-person contact but cold environments, such as meat works, have been at the centre of overseas clusters.

Cant touch this

New Zealands news came as China has again claimed it has found the virus on the outer packaging of frozen prawns imported from Ecuador.

Chinas state television said it was found during a routine inspection of a restaurant in Wuhu city.

Its not the first report of this in China. Since July, several other Chinese cities have also reported cases, including the port cities of Xiamen and Dalian leading to imports from three suppliers being suspended.

After nucleic acid sequence analysis and expert judgment, the test results suggested that the container environment and the outer packaging of the goods of the three companies were at risk of contamination by the new coronavirus, and the companies food safety management system was not in order, the General Administration of Customs said in a statement.

The director of the organisation, Bi Kexi, told reporters: "Experts believe that the results do not mean they are contagious but that the companies' food safety management systems are not well implemented," Bi Kexin, director General Administration of Customs said.

For international packaging to be the cause of this outbreak, a chain of events would need to have taken place. Enough of the virus landing - on packaging - perhaps through a person coughing droplets onto a surface - would be the first step. The droplets would need to remain viable throughout the journey to the New Zealand coolstore.

Then the virus on the packaging would need to find a pathway to a person, possibly through someone touching the package and then touching their face.

Studies have been done on how long the virus survives on different surfaces. Traces of the virus were detected on plastic and steel up to three days after contamination and on cardboard for up to one day.

In chilled conditions, the virus can survive longer. One study looking at the survival time of the virus in a test tube found at 4C, the virus survived for 14 days. At 37C it lasted just one day.

The other factor is the amount of virus on a surface. A recent letter published in The Lancet suggests the risk of surface transmission has been exaggerated.

None of these studies present scenarios akin to real life situations, the letter said.

The Rutgers University professor of microbiology, biochemistry and molecular genetics Emanuel Goldmans issue was that in real life the amount of virus would likely be several orders of magnitude smaller.

While saying he believed in erring on the side of caution, he thought the risk was low.

In my opinion, the chance of transmission through inanimate surfaces is very small, and only in instances where an infected person coughs or sneezes on the surface, and someone else touches that surface soon after the cough or sneeze (within one - two hours).

While the risk is considered low, its still a possibility.

In a Chinese mall, several people caught the virus in January despite not being in direct contact with the one person at the mall who was known to have it. A restroom and elevator buttons were considered to be places where these people may have touched contaminated surfaces.

Covid and chill

Cold work environments have been at the centre of outbreaks. The exact reasons why arent clear, although theres plenty of speculation.

In the US 17,358 cases of coronavirus were recorded from meat and poultry factory workers.

An abattoir in Germany was closed after 1500 workers were infected and in Melbourne at least three abattoirs were closed after outbreaks occurred. Abattoir-related outbreaks have also occurred in the United Kingdom, France, Brazil, Denmark and the Netherlands.

There are a few factors likely to be at play and theyre not related to dead animals.

Physical distancing on a production line can be hard as often people work shoulder-to-shoulder. Shifts are long, and casualised employment can make people less likely to stay home when ill because they cant afford time off.

Background noise can mean shouting is needed to communicate, increasing the risk of droplet spread. Air filtration systems push air around, potentially spreading droplets further.

No sunlight and cold conditions extend the life of the virus.

The conditions at the New Zealand coolstore where cases have emerged may not be identical to overseas abattoirs, but there's a chance cold may play a role in giving any virus in the environment a chance to live longer.

This story was originally published on Newsroom.co.nz and is republished with permission

Read this article:
Coronavirus: Cold temperatures are where Covid-19 thrives - Stuff.co.nz

Teachers have every right to be optimistic and enthusiastic about their students achievements.

But that does not mean that they should be allowed, as they have in Scotland, to inflate predicted A Level and GCSE grades when there is no evidence to suggest there has been a dramatic improvement in academic standards.

According to recent analysis by the exams regulator Ofqual, teachers in England have bumped-up predicted A Level marks by 12 per cent on average and GCSE marks by 9 per cent.

No doubt this is borne of good intentions and pride for pupils abilities. But if grades are not adjusted to bring them into line with previous years results, there will be a whole range of unintended consequences.

Most obviously it would discriminate against children who sat exams last year and earlier, who would have performed the same as this years cohort but received worse grades.

But it would also be extremely unfair to students who will sit exams next year when, hopefully, schools will have returned to normal.

They would be doubly penalised, as they already face the disadvantage of having lost months of classroom teaching because of the disruption caused by coronavirus.

It is understandable if the U turn by Nicola Sturgeon brings joy to students whose predicted grades had been marked down. But what about the Scottish students who sat these exams last year?

Relatively speaking they have now all been marked down. The same will apply to Scots students who take these exams next year. Unless Miss Sturgeon artificially inflates their exam grades they will have right to feel equally aggrieved.

This decision may bring Miss Sturgeon short term popularity I suspect it is no coincidence she faces an election next year.

As is often the case with political decisions that bring short term popularity it may not be a good idea in the long term. I hope Boris Johnson does not fall into the same trap.

Crucially, there is no evidence to suggest that controlling grade inflation will increase the attainment gap between children from poorer backgrounds and those who are more fortunate, or that bright children from poor performing schools will be adversely affected.

In fact the reverse is true: the Government has already made major strides in addressing this problem through a wide range of interventions starting from the age of three.

And where there is genuine evidence that grades have been marked down for pupils at a school where standards have increased in the last year because of improved teaching, or it has recently become an academy, this will be taken into account in appeals.

Meanwhile claims that many pupils will see A Level results drastically downgraded as much as from A grade to D are wide of the mark.

Invariably, the adjusted results will be only dropped one grade where the teachers have ranked them towards the bottom of the higher grade range.

Of course, children who fall short of the grades they needed for university are bound to be disappointed but they need not lose hope.

A big drop in overseas students caused by the pandemic means that there will be more places available than usual through the clearing process.

(I might add university Vice-Chancellors need all the 9,000 a year tuition fees they can get to bolster their astronomic salaries.)

And it should be remembered there is nothing new about students falling short of the grades they need. My own daughter had to resit her Maths A Level to get into her molecular genetics course.

We have now offered schools free resits in the Autumn and also given the school the possibility of appealing a students grad on the basis of the mock exam.

Ultimately, the Governments overriding objective has been to ensure that students receive qualifications this summer which have the same value as in any other year and which will enable them to move on successfully to the next stage of their lives be that college, university or an apprenticeship in the workplace.

This process will deliver that.

The rest is here:
It would be unfair to adjust A Level and GCSE grades, says Scarborough and Whitby MP Robert Goodwill - Whitby Gazette

Covid-19

With investigations into a coolstore and freight as a potential pathway for the latest outbreak of Covid-19, whatdoes science say about surfaces and refrigeration?

Surfaces at a Mount Wellington coolstore are being tested for Covid-19 in an effort to uncover the route of the virus back into the community.

A worker at the coolstore has tested positive for the disease. How he caught it is still a mystery. The possibility it could have come in on overseas freight arriving at the coolstore is being investigated.

Were not ruling that out, said Director-General of Health Ashley Bloomfield, We want to get to the bottom of that.

The coolstore environment has been swabbed and test results are expected back today.

Yesterday, three other workers from the coolstore returned positive tests for Covid-19.

It's possible the workers were either infected by contaminated goods, or the virus was brought into the workplace after it was caught elsewhere, possibly by the man who was first diagnosed.

Two branches of the coolstore have been closed. One in Mount Wellington, where the man worked, and another close to Auckland Airport.

Genomic sequencing is still underway, but as of yesterday afternoon there hasnt been a link between genome patterns of cases in border quarantine and the genome pattern of the coolstore-related cases.

University of Auckland professor Shaun Hendy said the fact the source of the outbreak hadnt been identified yet wasconcerning.

To date, the genomic information suggests this cluster is not linked to a managed isolation and quarantine facility. The business itself is linked to international freight, air and sea, which does suggest that this is a possible entry route, whether via packaging, or more likely, via person-to-person.

Like many things Covid-19 related, the science of transmission isnt clear-cut;what studies have been done are often laboratory-based.

Surface transmission is considered a lower risk for virus transmission than person-to-person contact but cold environments, such as meat works, have been at the centre of overseas clusters.

Cant touch this

New Zealands news came as China has again claimed it has found the virus on the outer packaging of frozen prawns imported from Ecuador.

Chinas state television said it was found during a routine inspection of a restaurant in Wuhu city.

Its not the first report of this in China. Since July, several other Chinese cities have also reported cases, including the port cities of Xiamen and Dalian leading to imports from three suppliers being suspended.

After nucleic acid sequence analysis and expert judgment, the test results suggested that the container environment and the outer packaging of the goods of the three companies were at risk of contamination by the new coronavirus, and the companies food safety management system was not in order, the General Administration of Customs said in a statement.

The director of the organisation, Bi Kexi, told reporters: "Experts believe that the results do not mean they are contagious but that the companies' food safety management systems are not well implemented," Bi Kexin, director General Administration of Customs said.

For international packaging to be the cause of this outbreak, a chain of events would need to have taken place. Enough of the virus landing - on packaging - perhaps through a person coughing droplets onto a surface - would be the first step. The droplets would need to remain viable throughout the journey to the New Zealand coolstore.

Then the virus on the packaging would need to find a pathway to a person, possibly through someone touching the package and then touching their face.

Studies have been done on how long the virus survives on different surfaces. Traces of the virus were detected on plastic and steel up to three days after contamination and on cardboard for up to one day.

In chilled conditions, the virus can survive longer. One study looking at the survival time of the virus in a test tube found at 4C, the virus survived for 14 days. At 37Cit lasted just one day.

The other factor is the amount of virus on a surface. A recent letter published in The Lancet suggests the risk of surface transmission has been exaggerated.

None of these studies present scenarios akin to real life situations, the letter said. The Rutgers University professor of microbiology, biochemistry and molecular genetics Emanuel Goldmans issue was that in real life the amount of virus would likely be several orders of magnitude smaller.

While saying he believed in erring on the side of caution, he thought the risk was low.

In my opinion, the chance of transmission through inanimate surfaces is very small, and only in instances where an infected person coughs or sneezes on the surface, and someone else touches that surface soon after the cough or sneeze (within one -two hours).

While the risk is considered low, its still a possibility.

In a Chinese mall, several people caught the virus in January despite not being in direct contact with the one person at the mall who was known to have it. A restroom and elevator buttons were considered to be places where these people may have touched contaminated surfaces.

Covid and chill

Cold work environments have been at the centre of outbreaks. The exact reasons why arent clear, although theres plenty of speculation.

In the US 17,358 cases of coronavirus were recorded from meat and poultry factory workers.

An abattoir in Germany was closed after 1500 workers were infected and in Melbourne at least three abattoirs were closed after outbreaks occurred. Abattoir-related outbreaks have also occurred in the United Kingdom, France, Brazil, Denmark and the Netherlands.

There are a few factors likely to be at play and theyre not related to dead animals.

Physical distancing on a production line can be hard as often people work shoulder-to-shoulder.Shifts are long, and casualised employment can make people less likely to stay home when ill because they cant afford time off.

Background noise can mean shouting is needed to communicate, increasing the risk of droplet spread. Air filtration systems push air around, potentially spreading droplets further.

No sunlight and cold conditions extend the life of the virus.

The conditions at the New Zealand coolstore where cases have emerged may not be identical to overseas abattoirs, but there's a chance cold may play a role in giving any virus in the environment a chance to live longer.

Follow this link:
Cold temperatures are where Covid thrives - Newsroom