Monthly Archives: April 2022

Margaret McGovern, MD, PhD, has been appointed deputy dean for clinical affairs at Yale School of Medicine and chief executive officer of Yale Medicine, effective July 1, 2022.

McGovern is currently Knapp Professor of Pediatrics and dean for clinical affairs at Renaissance School of Medicine at Stony Brook University and vice president of Stony Brook Medicine (SBM) Health System clinical programs and strategy. Prior to assuming these roles in 2018, she was chair of Pediatrics and physician-in-chief at Stony Brook Childrens Hospital. She led the development and planning of Stony Brook Childrens Hospital and markedly expanded its pediatric clinical research and education programs. McGovern also led the Stony Brook faculty practice plan for six years during her tenure as chair of Pediatrics. In 2019, she led the formation of the SBM Clinically Integrated Network, which is engaged in delivering high-quality, high value care by building a population health platform. She serves as the physician executive leader for the initiative.

She received her PhD in genetics from the Mount Sinai Graduate School of Biomedical Sciences and her MD from Mount Sinai School of Medicine (now called Icahn School of Medicine at Mount Sinai). She completed her residency training in pediatrics and fellowships in clinical and molecular genetics at Mount Sinai Hospital before joining the faculty. At Icahn, she was vice chair of the Department of Genetics and Molecular Medicine and professor of human genetics, and of oncological sciences and obstetrics and gynecology. She was the program director for the NIH-funded General Clinical Research Center (GCRC) and carried out CDC- and NIH-funded research focused primarily on the integration of molecular genetic diagnostic testing into clinical practice and inborn errors of metabolism. She is considered a world authority on sphingolipidoses.

At Yale, McGovern will play an essential role in the development of clinical strategy for the School of Medicine at an important juncture in the relationship between YSM and Yale New Haven Health System. She will provide strategic counsel and otherwise work to realize YSMs vision for its clinical enterprise. As CEO of YM, she will participate actively in the senior leadership group of the medical schools academic health system and play a key role in setting and realizing strategic goals. As deputy dean for clinical affairs, she will serve as the physician leader who represents the clinical mission of the School of Medicine in all venues. In this role, she will work closely with the clinical chairs in the recruitment of clinical faculty, mentor the next generation of clinical leaders, and collaborate with the deputy deans of research and education to balance the needs for enhancing the academic and educational missions of YSM with clinical ambulatory operational efficiencies, quality improvement, and sound clinical finances.

Submitted by Robert Forman on April 05, 2022

Read more:
Margaret McGovern, MD, PhD, Appointed YSM Deputy Dean and CEO of Yale Medicine - Yale School of Medicine

image:The HUSH and NEXT complexes function to control expression of TE transcripts at either the transcriptional or post-transcriptional level, respectively. HUSH is recruited to TE loci decorated with H3K9me3 histone marks and is required for transcriptional (txn) suppression. NEXT is recruited to HUSH-bound loci through a physical connection that requires ZCCHC8 and MPP8 and functions to decay pA- RNAs produced at TE loci view more

Credit: William Garland, Aarhus University

Mammalian genomes have been colonised by transposable elements (TEs), so called genetic parasites, which occupy ~ 50% of genomic DNA and harbour the potential to propagate, resulting in genetic instability. These elements are therefore subjected to tight cellular control. Whilst our understanding of TE regulation has been dominated by transcriptional and epigenetic models, the role of post-transcriptional RNA decay regulation has until now been unexplored.

A Danish team has identified a connection between the mouse orthologous nuclear exosome targeting (NEXT) and the human silencing hub (HUSH) complexes, involved in nuclear RNA decay and epigenetic silencing of TEs respectively. The researchers show that NEXT globally supresses TE RNA levels in mouse embryonic stem (ES) cells, and that this is aided by a recruitment to TE loci via the HUSH complex. This reveals an unprecedented collaborative mechanism of transcriptional and post-transcriptional control to limit the genotoxic activity of TE RNAs.

Previously, the Torben Heick Jensen laboratory identified and characterised the NEXT complex that target non-adenylated (pA-) RNAs to the nuclear exosome complex for decay. Upon depletion of NEXT, cells stabilise and accumulate such RNAs, but a putative role of NEXT in the regulation of TE RNAs had remained unexplored.

To investigate this, the NEXT component ZCCHC8 was knocked out (KO) in ES cells using CRISPR/Cas9 followed by high-throughput RNA sequencing and a focussed analysis of TE RNAs. Interestingly, this showed that TE RNAs were stabilised in NEXT KO conditions.

Upon further examination, it was shown that NEXT physically interact with HUSH via ZCCHC8 and that this connection provides a method of recruitment to target NEXT to DNA to degrade pA- TE RNAs whilst HUSH functions to regulate pA+ TE RNAs. This combinatorial mechanism ensures that TEs remain restricted by the collaborative functions of NEXT and HUSH.

These findings are a result of a collaborative project between the laboratories of Torben Heick Jensen at the Department of Molecular Biology and Genetics, Aarhus University, Kristian Helin at the Center for Epigenetics, Memorial Sloan Kettering Cancer Center and Albin Sandelin at the Biotech Relearch and Innovation Centre (BRIC), Copenhagen University. The studies were spearheaded by postdoc Will Garland from Aarhus University.

This study was published in the internationally recognised journalMolecular Cell.

Chromatin modifier HUSH co-operates with RNA decay factor NEXT to restrict transposable element expression.William Garland, Iris Mller, Mengjun Wu, Manfred Schmid, Katsutoshi Imamura, Leonor Rib, Albin Sandelin, Kristian Helin and Torben Heick Jensen.Molecular Cell(2022) doi:10.1016/j.molcel.2022.03.004.

Assistant ProfessorWill Garland-garland@mbg.au.dkProfessorTorben Heick Jensen-thj@mbg.au.dkDepartment of Molecular Biology and Genetics, Aarhus University, Denmark

Experimental study

Cells

Chromatin modifier HUSH co-operates with RNA decay factor NEXT to restrict transposable element expression

28-Mar-2022

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

More:
Uncovering a cooperation between RNA decay and chromatin regulating complexes that keep transposable element RNAs under control - EurekAlert

Summary: Mutations in the IL18RAP gene reduce inflammation and appear to protect the brain against ALS.

Source: Weizmann Institute of Science

Genetic mutations linked to a disease often spell bad news. Mutations in over 25 genes, for example, are associated with amyotrophic lateral sclerosis, or ALS, and they all increase the risk of developing this incurable disorder.

Now, a research team headed by Prof. Eran Hornstein of the Weizmann Institute of Science has linked a new gene to ALS, but this one contains mutations of a different sort: They seem to play a defensive rather than an offensive role in the disease.

The gene newly linked to ALS is located in the part of our genome once called junk DNA. This DNA makes up over 97 percent of the genome, but because it does not encode proteins, it used to be considered junk.

Today, though this noncoding DNA is still regarded as biological dark matter, its already known to serve as a crucial instruction manual. Among other things, it determines whengeneswithin the coding DNAthe ones that do encode proteinsare turned on and off.

Hornsteins lab in Weizmanns Molecular Neuroscience and Molecular Genetics Departments studies neurodegenerative diseasesthat is, diseases in which neurons degenerate and die. The team is focusing on our noncoding DNA.

This massive, noncoding part of the genome has been overlooked in the search for the genetic origins of neurodegenerative diseases like ALS, Hornstein explains.

This is despite the fact that for most ALS cases, proteins cannot explain the emergence of the disease.

Many people know about ALS thanks to the Ice Bucket Challenge that went viral a few years ago. This rare neurological disease attacks motor neurons, the nerve cells responsible for controlling voluntary muscle movement involved in everything from walking to talking and breathing.

The neurons gradually die off, ultimately causing respiratory failure and death. One of the symptoms of ALS is inflammation in the brain regions connected to the dying neurons, caused by immune mechanisms in the brain.

Our brain has an immune system, explains Dr. Chen Eitan, who led the study in Hornsteins lab together with Aviad Siany. If you have a degenerative disease, your brains immune cells, calledmicroglia, will try to protect you, attacking the cause of the neurodegeneration.

The problem is that in ALS, the neurodegeneration becomes so severe that the chronic microglial activation in the brain rises to extremely high levels, turning toxic. The immune system thus ends up causing damage to thebrainit set out to protect, leading to the death of more motor neurons.

Thats where the new findings, published today inNature Neuroscience, come in. The Weizmann scientists focused on a gene called IL18RAP, long known to affect microglia, and found that it can contain mutations that mitigate the microglias toxic effects. We have identified mutations in this gene that reduce inflammation, Eitan says.

After analyzing the genomes of more than 6,000 ALS patients and of more than 70,000 people who do not have ALS, the researchers concluded that the newly identified mutations reduce the risk of developing ALS nearly fivefold.

It is therefore extremely rare for ALS patients to have these protective mutations, and those rare patients who do harbor them tend to develop the disease roughly six years later, on average, than those without the mutations. In other words, the mutations seem to be linked to a core ALS process, slowing the disease down.

To confirm the findings, the researchers used gene-editing technology to introduce the protective mutations into stem cells from patients with ALS, causing these cells to mature into microglia in a laboratory dish.

They then cultured microglia, with or without the protective mutations, in the same dishes with motor neurons. Microglia harboring the protective mutations were found to be less aggressive towardmotor neuronsthan microglia that did not have themutations.

Motor neurons survived significantly longer when cultured with protective microglia, rather than with regular ones, Siany says.

Eitan notes that the findings have potential implications for ALS research and beyond. Weve found a new neuroprotective pathway, she says.

Future studies can check whether modulating this pathway may have a positive effect on patients. On a more general level, our findings indicate that scientists should not ignore noncoding regions of DNAnot just in ALS research, but in studying other diseases with a genetic component as well.

Author: Press OfficeSource: Weizmann Institute of ScienceContact: Press Office Weizmann Institute of ScienceImage: The image is in the public domain

Original Research: Closed access.Whole-genome sequencing reveals that variants in the Interleukin 18 Receptor Accessory Protein 3UTR protect against ALS by Chen Eitan et al. Nature Neuroscience

Abstract

Whole-genome sequencing reveals that variants in the Interleukin 18 Receptor Accessory Protein 3UTR protect against ALS

The noncoding genome is substantially larger than the protein-coding genome but has been largely unexplored by genetic association studies.

Here, we performed region-based rare variant association analysis of >25,000 variants in untranslated regions of 6,139 amyotrophic lateral sclerosis (ALS) whole genomes and the whole genomes of 70,403 non-ALS controls.

We identified interleukin-18 receptor accessory protein (IL18RAP) 3 untranslated region (3UTR) variants as significantly enriched in non-ALS genomes and associated with a fivefold reduced risk of developing ALS, and this was replicated in an independent cohort. These variants in theIL18RAP3UTR reduce mRNA stability and the binding of double-stranded RNA (dsRNA)-binding proteins.

Finally, the variants of theIL18RAP3UTR confer a survival advantage for motor neurons because they dampen neurotoxicity of human induced pluripotent stem cell (iPSC)-derived microglia bearing an ALS-associated expansion inC9orf72, and this depends on NF-B signaling.

This study reveals genetic variants that protect against ALS by reducing neuroinflammation and emphasizes the importance of noncoding genetic association studies.

Visit link:
Mutations in Noncoding DNA Are Found to Protect the Brain From ALS - Neuroscience News

Summary: Researchers have identified 75 regions of the genome associated with Alzheimers disease, including 42 novel regions. The findings shed new light on the biological mechanisms of Alzheimers and provide a new avenue for the treatment of this neurodegenerative disorder.

Source: INSERM

Identifying genetic risk factors for Alzheimers disease is essential if we are to improve our understanding and treatment of it. Progress in human genome analysis along with genome-wide association studies [1]are now leading to major advances in the field.

Researchers in Europe, the US and Australia have identified 75regions of the genome that are associated with Alzheimers disease. Forty-two of these regions are novel, meaning that they have never before been implicated in the disease.

The findings, published inNature Genetics, bring new knowledge of the biological mechanisms at play and open up new avenues for treatment and diagnosis.

Alzheimers disease is the most common form of dementia, affecting around 1,200,000 people in France. This complex, multifactorial disease, which usually develops after the age of 65, has a strong genetic component. The majority of cases are thought to be caused by the interaction of different genetic predisposition factors with environmental factors.

Although our understanding of the disease continues to improve, there is no cure at this time. The medications available are mainly aimed at slowing cognitive decline and reducing certain behavioral disorders.

In order to better understand the origins of the disease, one of the major challenges of research is to better characterize its genetic risk factors by identifying the pathophysiological processes at play [2], and thereby propose novel therapeutic targets.

As part of an international collaboration, researchers from Inserm, Institut Pasteur de Lille, Lille University Hospital and Universit de Lille conducted a genome-wide association study (GWAS) on the largest Alzheimers patient group set up until now [3], under the coordination of Inserm Research Director Jean-Charles Lambert.

Encouraged by advances in genome analysis, these studies consist of analyzing the entire genome of tens of thousands or hundreds of thousands of individuals, whether healthy or sick, with the aim of identifying genetic risk factors associated with specific aspects of the disease.

Using this method, the scientists were able to identify 75regions (loci) of the genome associated with Alzheimers, 42of which had never previously been implicated in the disease.

Following this major discovery, we characterized these regions in order to give them meaning in relation to our clinical and biological knowledge, and thereby gain a better understanding of the cellular mechanisms and pathological processes at play, explains Lambert.

Highlighting pathological phenomena

In Alzheimers disease, two pathological brain phenomena are already well documented: namely, the accumulation of amyloid-beta peptides and the modification of the protein Tau, aggregates of which are found in the neurons.

Here, the scientists confirmed the importance of these pathological processes. Their analyses of the various genome regions confirm that some are implicated in amyloid peptide production and Tau protein function.

Furthermore, these analyses also reveal that a dysfunction of innate immunity and of the action of the microglia (immune cells present in the central nervous system that play a trash collector role by eliminating toxic substances) is at play in Alzheimers disease.

Finally, this study shows for the first time that the tumor necrosis factor alpha (TNF-alpha)-dependent signaling pathway is involved in disease [4].

These findings confirm and add to our knowledge of the pathological processes involved in the disease and open up new avenues for therapeutic research. For example, they confirm the utility of the following: the conduct of clinical trials of therapies targeting the amyloid precursor protein, the continuation of microglial cell research that was initiated a few years ago, and the targeting of the TNF-alpha signaling pathway.

Risk score

Based on their findings, the researchers also devised a genetic risk score in order to better evaluate which patients with cognitive impairment will, within three years of its clinical manifestation, go on to develop Alzheimers disease.

While this tool is not at all intended for use in clinical practice at present, it could be very useful when setting up therapeutic trials in order to categorize participants according to their risk and improve the evaluation of the medications being tested,explains Lambert.

In order to validate and expand their findings, the team would now like to continue its research in an even broader group. Beyond this exhaustive characterization of the genetic factors of Alzheimers disease, the team is also developing numerous cellular and molecular biology approaches to determine their roles in its development.

Furthermore, with the genetic research having been conducted primarily on Caucasian populations, one of the considerations for the future will be to carry out the same type of studies in other groups in order to determine whether the risk factors are the same from one population to the next, which would reinforce their importance in the pathophysiological process.

Notes

[1]These studies consist of analyzing the entire genome of thousands or tens of thousands of people, whether healthy or sick, to identify genetic risk factors associated with specific aspects of the disease.

[2]All functional problems caused by a particular disease or condition.

[3]Here, the researchers were interested in the genetic data of 111,326 people who were diagnosed with Alzheimers disease or had close relatives with the condition, and 677,663 healthy controls. These data are derived from several large European cohorts grouped within the EuropeanAlzheimer & DementiaBioBank(EADB) consortium.

[4] Tumor necrosis factor alpha is a cytokine: an immune system protein implicated in the inflammation cascade, particularly in tissue lesion mechanisms.

Author: Priscille RiviereSource: INSERMContact: Priscille Riviere INSERMImage: The image is in the public domain

Original Research: Open access.New insights into the genetic etiology of Alzheimers disease and related Dementias by Jean-Charles Lambert et al. Nature Genetics

Abstract

New insights into the genetic etiology of Alzheimers disease and related Dementias

Characterization of the genetic landscape of Alzheimers disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes.

We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/proxy AD cases and 677,663 controls.

We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication.

Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex.

We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia.

The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and theAPOE4 allele.

See the rest here:
Alzheimers Disease: The Identification of 75 Genetic Risk Factors Brings New Insights - Neuroscience News

ROCKVILLE, Md. Apr. 5, 2022 The Association for Molecular Pathology (AMP), the premier global, molecular diagnostic professional society, called on Congress to allow for a thorough evaluation of the Verifying Accurate Leading-edge IVCT Development (VALID) Act of 2021, or any other legislation to change regulations for laboratory developed testing procedures (LDPs). Representatives from AMP, the American Association for Clinical Chemistry (AACC), the American College of Medical Genetics and Genomics (ACMG), and the Association of Pathology Chairs (APC) hosted a congressional briefing yesterday to educate lawmakers about how diagnostic tests are currently regulated and the substantial impact the VALID Act would have on clinical testing laboratories, healthcare providers, and patients throughout the U.S.

The VALID Act is a complex bill proposing dramatic modifications to current oversight mechanisms and a wide range of stakeholders have expressed significant concerns with the current draft. In February, AMP joined a number of other organizations asking that Congress consider the VALID Act separately from the must-pass Medical Device User Fee Agreement (MDUFA V) legislative process. To allow for thorough discussions and appropriate stakeholder engagement, it is important that this legislation goes through regular order with its own independent hearing, mark-up, and scheduled votes. More time and diverse stakeholder agreement are needed to ensure the policy is sound and in the best interest of patients and public health.

Congress needs to consider the lessons learned during the COVID-19 pandemic about how over burdensome and unnecessary regulation of laboratory testing affects testing capacity within the U.S. In February 2020, the U.S. declared a public health emergency and in turn, the U.S. Food and Drug Administration (FDA) began requiring emergency use authorization of all countermeasures used for clinical care. Subsequently, the FDA asserted authority to require regulatory review of COVID-19 tests before they could be offered to patients, halting the development and deployment of these tests, and leaving laboratory professionals paralyzed and unable to provide the care they are trained to do. As a result, this country went weeks without access to these critical public health tools while COVID-19 spread undetected throughout our communities.

AMP remains committed to working with and educating members of Congress and other key stakeholders to create an appropriate LDP oversight framework that modernizes the current regulatory system, demonstrates quality, enhances transparency, and fosters the rapid innovation and promise of new diagnostic technologies and tests, said Mary Steele Williams, AMP Executive Director. The current COVID-19 public health emergency highlights the critical need for laboratories to be allowed to respond quickly, and to continue advancing and offering the tens of thousands of high-quality, validated LDPs that benefit patients each and every day.

ABOUT AMP

The Association for Molecular Pathology (AMP) was founded in 1995 to provide structure and leadership to the emerging field of molecular diagnostics. AMP's 2,500+ members practice various disciplines of molecular diagnostics, including bioinformatics, infectious diseases, inherited conditions, and oncology. Our members are pathologists, clinical laboratory directors, basic and translational scientists, technologists, and trainees that practice in a variety of settings, including academic and community medical centers, government, and industry. Through the efforts of its Board of Directors, Committees, Working Groups, and Members, AMP is the primary resource for expertise, education, and collaboration in one of the fastest growing fields in healthcare. AMP members influence policy and regulation on the national and international levels, ultimately serving to advance innovation in the field and protect patient access to high-quality, appropriate testing. For more information, visit http://www.amp.org and follow AMP on Twitter: @AMPath.

Read more:
Association for Molecular Pathology Hosted a Congressional Briefing to Urge Lawmakers to Consider the VALID Act of 2021 Separately from the Medical...

Multi-Center Study on Track to Commence in Late 2022Initiated Reimbursement Process with The Centers for Medicare and Medicaid Services

BERKELEY, Calif. and MAINZ, Germany, March 31, 2022 (GLOBE NEWSWIRE) -- Mainz Biomed N.V. (NASDAQ:MYNZ) (Mainz Biomed or the Company), a molecular genetics diagnostic company specializing in the early detection of cancer, announced today that it has received supportive feedback from the U.S. Food & Drug Administration (FDA) on the Companys pre-submission package profiling the potential pivotal clinical trial design for ColoAlert, its highly efficacious, and easy-to-use detection test for colorectal cancer (CRC). As Mainz prepares to launch ColoAlerts pivotal clinical trial, the Company is also pleased to announce the formal commencement of its reimbursement process for ColoAlert by scheduling an initial meeting with The Centers for Medicare and Medicaid Services (CMS) in April 2022. The CMS is a federal agency in the U.S. Department of Health and Human Services (HHS) that administers the Medicare program and works in partnership with state governments to administer Medicaid, the Children's Health Insurance Program (CHIP), and health insurance portability standards.

We are encouraged by the FDAs supportive commentary on our proposed pivotal clinical trial design for ColoAlert and will now work with our clinical team to finalize the studys protocols and make the necessary preparations to ensure premier trial execution, commented Guido Baechler, Chief Executive Officer of Mainz Biomed. In concert with final pivotal clinical trial preparations, we are excited to pursue reimbursement for ColoAlert and are looking forward to commencing formal discussions with the CMS.

An integral part of Mainzs clinical execution and medical reimbursement strategies is its partnership with Precision for Medicine, a leading global Clinical Research Organization. Precision for Medicine will continue to work with Mainzs management team to implement the U.S. focused regulatory and market access strategy for ColoAlert by finalizing ColoAlerts clinical development plan to ensure the trial design is cost-effective, robust, and efficient. The Company is planning to integrate CMS guidelines into ColoAlerts pivotal trial design, utilizing currently marketed CRC screening tests as benchmarks to provide the test with an optimal product profile for regulatory approval and success in the marketplace.

Mainz is marketing ColoAlert across Europe through its unique business model of partnering with third-party laboratories for test kit processing versus the traditional methodology of operating a single facility. The Company is also running ColoFuture, an international clinical study evaluating the potential to integrate a portfolio of in-licensed novel mRNA biomarkers into the product which have previously demonstrated the unique ability to identify curable precancerous colonic polyps, as well as treatable early-stage CRC (Herring et al 2021). ColoFuture is evaluating the effectiveness of these biomarkers to enhance ColoAlerts technical profile to extend its capability to include the identification of advanced adenomas (AA), a type of pre-cancerous polyp often attributed to CRC, while increasing ColoAlerts rates of diagnostic sensitivity and specificity. The results of the study will ultimately impact the configuration of ColoAlert prior to commencing the U.S. pivotal study which is on track to begin in late 2022.

About ColoAlert ColoAlert detects colorectal cancer (CRC) via a simple-to-administer test with a sensitivity and specificity nearly as high as the invasive colonoscopy*. The test utilizes proprietary methods to analyze cell DNA for specific tumor markers combined with the fecal immunochemical test (FIT) and is designed to detect tumor DNA and CRC cases in their earliest stages. The product is CE-IVD marked (complying with EU safety, health and environmental requirements) and is transitioning to compliance with IVDR. The product is commercially available in a selection of countries in the European Union. Mainz Biomed currently distributes ColoAlert through a number of clinical affiliates. Once approved in the U.S., the Companys commercial strategy is to establish scalable distribution through a collaborative partner program with regional and national laboratory service providers across the country. * Dollinger MM et al. (2018)

About the ColoFuture Study The ColoFuture study is an international clinical trial evaluating over 600 patients (women or men) in the age range of 40-85 at two participating centers in Norway and two in Germany. Subjects are invited to potentially participate in the trial when referred for a colonoscopy (pre-inclusion) to screen for CRC or an overall diagnostic analysis. Those who agree to provide a stool sample in advance of the procedure will be eligible for participation. Inclusion criteria are based on one of the following diagnostic outcomes: CRC, advanced precancerous lesions in colon, or normal colon. Then, each patient outcome will compare the observations recorded from the colonoscopy to the results from the ColoAlert test that incorporates the novel biomarkers. The primary endpoints of the study are to determine sensitivity and specificity rates for CRC with ColoAlert plus the new mRNA biomarkers. There are multiple secondary endpoints for evaluating the modified ColoAlert test, including, determining sensitivity for AA lesions in colon, specificity for advanced precancerous lesions in colon and, specificity for no colorectal finding (normal colon). The Company is expecting to complete enrollment during the second half of 2022 and is targeting reporting study results in early 2023.

About Colorectal Cancer Colorectal cancer (CRC) is the second most lethal cancer in the U.S. and Europe, but also the most preventable with early detection providing survival rates above 90%. Annual testing costs per patient are minimal, especially when compared to late-stage treatments of CRC which cost patients an average of $38,469 per year. The American Cancer Society estimates that in 2021 there will be approximately 149,500 new cases of colon and rectal cancer in the U.S. with 52,980 resulting in death. Recent FDA decisions suggest that screening with stool DNA tests such as ColoAlert in the US should be conducted once every three years starting at age 45. Currently there are 112 million Americans aged 50+, a total that is expected to increase to 157 million within 10 years. Appropriately testing these US-based 50+ populations every three years as prescribed equates to a US market opportunity of approximately $3.7 Billion per year.

About Mainz Biomed N.V. Mainz Biomed develops market-ready molecular genetic diagnostic solutions for life-threatening conditions. The Companys flagship product is ColoAlert, an accurate, non-invasive, and easy-to-use early detection diagnostic test for colorectal cancer. ColoAlert is currently marketed across Europe with FDA clinical study and submission process intended to be launched in the first half of 2022 for U.S. regulatory approval. Mainz Biomeds product candidate portfolio includes PancAlert, an early-stage pancreatic cancer screening test based on Real-Time Polymerase Chain Reaction-based (PCR) multiplex detection of molecular-genetic biomarkers in stool samples, and the GenoStick technology, a platform being developed to detect pathogens on a molecular genetic basis.

For more information, please visit http://www.mainzbiomed.com

For media enquiries, please contact press@mainzbiomed.com

For investor enquiries, please contact ir@mainzbiomed.com

Forward-Looking Statements Certain statements made in this press release are forward-looking statements within the meaning of the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. Forward-looking statements may be identified by the use of words such as anticipate, believe, expect, estimate, plan, outlook, and project and other similar expressions that predict or indicate future events or trends or that are not statements of historical matters. These forward-looking statements reflect the current analysis of existing information and are subject to various risks and uncertainties. As a result, caution must be exercised in relying on forward-looking statements. Due to known and unknown risks, actual results may differ materially from the Companys expectations or projections. The following factors, among others, could cause actual results to differ materially from those described in these forward-looking statements: (i) the failure to meet projected development and related targets; (ii) changes in applicable laws or regulations; (iii) the effect of the COVID-19 pandemic on the Company and its current or intended markets; and (iv) other risks and uncertainties described herein, as well as those risks and uncertainties discussed from time to time in other reports and other public filings with the Securities and Exchange Commission (the SEC) by the Company. Additional information concerning these and other factors that may impact the Companys expectations and projections can be found in its initial filings with the SEC, including its registration statement on Form F-1 filed on January 21, 2022. The Companys SEC filings are available publicly on the SECs website at http://www.sec.gov. Any forward-looking statement made by us in this press release is based only on information currently available to Mainz Biomed and speaks only as of the date on which it is made. Mainz Biomed undertakes no obligation to publicly update any forward-looking statement, whether written or oral, that may be made from time to time, whether as a result of new information, future developments or otherwise, except as required by law.

Go here to read the rest:
Mainz Biomed Completes Successful Pre-Submission Process with the U.S FDA for ColoAlert's ... - KULR-TV