Category Archives: Genetics

Brittany Bychkovsky, MD, MSc

As recent guideline updates contribute to the further elucidation of the logistics of screening, the role of genetic testing continues to be parsed out, with Brittany Bychkovsky, MD, MSc, noting that findings ways to identify women at high-risk of developing breast cancer is crucial.

For providers, theres a need within every health care system to develop a system to identify patients who are at high risk for [developing breast cancer]; we should not be relying on a primary care doctor, surgeon, or an oncologist to recognize that a patient is high risk and refer them to genetics. There needs to be a way from a systematic perspective to identify these patients, counsel them appropriately that they are going to be referred for genetic testing, and have the referrals placed, Bychkovsky, an assistant professor of medicine at Harvard Medical School and senior physician at Dana-Farber Cancer Institute, in Boston, Massachusetts, said.

Guidelines published by ASCO and the Society of Surgical Oncology (SSO) in January 2024 noted that testing for breast cancer susceptibility genes beyond BRCA1/2 should be offered to those with newly diagnosed breast cancer and breast cancer survivors as it informs medical therapy, influences surgical decision making, refines risk estimates of second primary cancers, and affects the care of family members.1

ASCO and SSO also provided several recommendations regarding BRCA1/2 testing noting that they now recommend testing for all patients with recurrent breast cancer who are candidates for PARP inhibitors regardless of family history; who develop a second primary cancer in the ipsilateral or contralateral breast; and those with newly diagnosed breast cancer aged 65 years or younger and select patients over the age of 65 based on personal history, family history, ancestry, or eligibility for PARP inhibitors. Additionally, for patients with a prior history of breast cancer and without active disease, testing should be offered to those aged 65 years or younger when diagnosed and selectively in patients diagnosed after 65 years if it informs personal and/or family risk.

In an interview with OncLive, Bychkovsky and Lydia Pace, MD, MPH, a primary care physician (PCP) and associate physician in the Divisions of Womens Health and General Internal Medicine at Brigham and Womens Hospital, in Boston Massachusetts, as well as an associate professor of Medicine at Harvard Medical School, explained approaches to genetic testing for breast cancer. In an additional article, Pace and Bychkovsky highlighted approaches to screening and detailed considerations with the final United States Preventive Services Task Force (USPSTF) screening recommendations published in April 2024; this is an update to the previous 2016 guidelines.2

Bychkovsky: The average lifetime risk of [developing] breast cancer in the general population is approximately 12% to 13%. If a patient has a greater than 20% lifetime risk, theyre considered high risk, but not everyone is managed the same [as] patients with a BRCA mutation or a TP53 mutation who have a greater than 60% lifetime risk of [developing] breast cancer. The moderate-risk genes include ATM, CHEK2, RAD51C, and RAD51D.

Its important to identify patients who are at a high risk for breast cancer between the ages of 25 and 35. Thats the target age where if someone is perceived to be at a high risk, we would want them to be referred for genetic testing. I dont want patients to have an extensive family history of breast cancer and be referred for the first time later in lifewhen this happens, it reflects as shortcoming of our systems and tells me that we are not performing risk assessments in a timely way.

Pace: We PCPs try to use guidelines and the USPSTF is often our go-to, [but] sometimes guidelines are discordant and that can be tricky for us. We usually refer [patients for testing] so were typically not testing ourselves which is another frontier. Should we be testing more to increase access to patients? What benefits or challenges would that have? Thats a whole other health services area.

Right now, at my practice, we are incredibly fortunate to be able to refer to Dr Bychkovskys group which provides our patients with high-quality counselingpretest counseling, posttest counseling, and clear guidance on how to manage results. Not every primary care clinician has that [type of] access for their patients and thats another area where the US and the world have to move forward in order to realize the benefit of precision medicine and figure out how we get patients who receive care elsewhere the same quality of care.

Bychkovsky: What typically happens is a patient is sent a series of questions about their personal and family history of cancer, and then they meet with a genetic counselor who confirms that history and builds a pedigree. We also ask questions about their current age, how many pregnancies have they had, how many children have they had, and any personal risk factors in regard to breast density on imaging.

We ask questions about alcohol use, exercise level, diet, [and other] lifestyle factors. The lifestyle factors are more part of the breast cancer risk assessment [and] thats not considered as criteria to have genetic testing.

For genetic testing, we emphasize the family pedigree. On the family pedigree theres a few things that stand out for me: any pre-menopausal breast cancer diagnoses in paternal relatives, pre-menopausal breast cancer diagnosis in first degree relatives on the maternal side, cancer diagnoses that are at younger ages are significant, [and] ovarian or pancreatic cancer diagnoses. Those types of [factors] allow patients to be eligible for cancer genetic testing. Every case is a bit different, but Im emphasizing the pedigrees that we would see for a patient who has a risk for a hereditary breast cancer gene.

If theres a family history of colorectal, endometrial, or ovarian cancer, thats a scenario where we would want to do genetic testing for Lynch syndrome. We tend to do broad panel testing with 40 to over 100 genes and that is a current standard and has shifted through the years. Prior to 2013 when patients had genetic testing, they were primarily having genetic testing for BRCA1/2, but now were doing large gene panels.

At Dana-Farber, we started [having] anyone with a cancer diagnosis meet with a genetic counselor only to have genetic testing. This has enhanced access to cancer genetic testing, as opposed to meeting with both a genetic counselor and a physician, such as a medical oncologist or a geneticist. That is something within cancer institutions that needs to be explored because if a patient has a preexisting cancer diagnosis, they already have a medical oncologist who has a lot of background and training in cancer genetics, and theres not a need for them to see another geneticist or another physician for genetic testing. There needs to be some thoughtfulness about how we can build systems within whatever network providers are working in to enhance access to cancer genetic testing.

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Enhancing the Referral Process for Genetic Testing Represents Key Next Step in Breast Cancer - OncLive

$1M TRAP award to support preclinical safety study for gene therapy vector targeting rhodopsin- RHO-adRP

Additional project and operational funding to support MERTK gene therapy IND-enabling studies

RESEARCH TRIANGLE PARK, N.C., June 13, 2024 (GLOBE NEWSWIRE) -- Opus Genetics, a patient-first, clinical-stage gene therapy company developing treatments for inherited retinal diseases, today announced it has received $1.7 million in project-based funding from the Foundation Fighting Blindness to help advance two preclinical candidate programs.

Opus is immensely grateful for the generous support from the Foundation Fighting Blindness, which will catalyze our efforts in pioneering treatments for inherited retinal diseases. This $1.7 million funding infusion makes a significant impact to help accelerate the development of these two preclinical candidates, said Ben Yerxa, Ph.D., chief executive officer of Opus. Together, we strive toward a future where therapies to help treat patients with inherited retinal diseases are readily available.

Opus received a $1M Translational Research Acceleration Program (TRAP) award to conduct a preclinical safety study for a gene therapy vector designed to target rhodopsin-mediated autosomal dominant retinitis pigmentosa (RHO-adRP). The safety study will be conducted in the established canine animal model at the University of Pennsylvania School of Veterinary Medicine (Penn Vet). The Company anticipates this is the last preclinical study required before the gene therapy will enter clinical trials. RHO-adRP is one of the most common IRDs, estimated to affect approximately one in 51,000 people, or more than 6,000 people, in the United States alone.

Additionally, Opus received approximately $700,000 in project-based and operational funding to support the preclinical development of a novel viral vector for treating retinitis pigmentosa due to mutations in the proto-oncogene tyrosine-protein kinase MER (MERTK) gene. The Company is collaborating with the Foundation to begin IND-enabling studies for a newly designed adeno-associated virus (AAV) viral vector to replace mutated MERTK genes in the retinal pigmented epithelial (RPE) cells of the retina. The initial funding will provide the resources for testing the vector in an established animal model of the disease and to conduct early safety assessments in larger animals. MERTK mutations cause a rod-cone dystrophy with early macular atrophy, and retinitis pigmentosa is the most common retinal phenotype.

We're excited to announce our funding commitment to Opus, a trailblazer in inherited retinal disease therapeutics and a company created based on our mission of ultimately curing blindness caused by retinal degenerative diseases. This investment highlights our steadfast dedication to hastening innovative solutions for those combating inherited retinal diseases, said Jason Menzo, chief executive officer of the Foundation Fighting Blindness. In collaboration with Opus, we're propelling forward promising clinical candidate programs with the potential to revolutionize the lives of those affected by these challenging conditions.

About Foundation Fighting Blindness Established in 1971, the Foundation Fighting Blindness is the world's leading private funding source for retinal degenerative disease research. The Foundation has raised more than $816 million toward its mission of accelerating research for preventing, treating, and curing blindness caused by the entire spectrum of blinding retinal diseases including:retinitis pigmentosa, macular degeneration, and Usher syndrome. VisitFightingBlindness.orgfor more information.

About Opus Genetics Opus Genetics is a clinical-stage gene therapy company for inherited retinal diseases with a unique model and purpose. Backed by Foundation Fighting Blindness venture arm, the RD Fund, Opus combines unparalleled insight and commitment to patient need with wholly owned programs in numerous orphan retinal diseases. Its AAV-based gene therapy portfolio, including a derisked LCA5 lead program currently in a Phase 1/2 clinical trial, tackles some of the most neglected forms of inherited blindness while creating novel orphan manufacturing scale and efficiencies. Based in Research Triangle Park, N.C., the company leverages knowledge of the best science and the expertise of pioneers in ocular gene therapy to transparently drive transformative treatments to patients. For more information, visit http://www.opusgenetics.com.

Media Contact: Gina Mangiaracina 6 Degrees gmangiaracina@6degreesPR.com

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Opus Genetics Announces $1.7 Million in Project-based Funding from the Foundation Fighting Blindness to Support ... - GlobeNewswire

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New study sheds light on the origin and distribution of a specific variant of the CARD9 gene in East Asia. By comparing the CARD9 variants found in a group of Korean and Japanese patients with CARD9 deficiency with those reported in Chinese patients, researchers from Japan revealed that this particular variant stems from a common ancestor that lived less than 4,000 years ago.

Credit: Department of Child Health and Development, TMDU

Researchers from Japan uncover the genetic diversity and regional patterns of CARD9 deficiency in patients susceptible to fungal diseases

Tokyo, Japan Fungal infections pose life-threatening risks, especially when vital organs or the central nervous system are affected. Individuals harboring variants in the CARD9 gene are particularly susceptible to invasive fungal infections, given that the protein coded by this gene serves as a critical regulator of the immune system. A recent discovery by Tokyo Medical and Dental University (TMDU) researchers suggests that a specific variant of CARD9 prevalent across northern China, Korea, and Japan may have originated from a common ancestor.

In their study published on 17 May 2024 in the Journal of Clinical Immunology, the researchers from TMDU conducted genetic analyses on Japanese and Korean patients who suffered from severe or recurring fungal infections. Their goal was to shed light on the genetic and clinical traits of individuals affected by CARD9 deficiency in East Asia.

The study included a total of five patients who were deficient for CARD9. Among them, two Japanese patients were newly identified as carriers of biallelic variants of CARD9 via DNA sequencing conducted by the research team, prompted by their medical history of fungal infections. Notably, both of these patients, along with three other patients who had previously been investigated, two Korean and one Japanese, were identified as carriers of a CARD9 variant called c.820dup.

The global distribution of CARD9 deficiency is biased, with high incidence in North Africa, the Middle East, and China. Notably, the distribution of CARD9 variants is also biased, with the c.820dup variant being relatively common in China, explains Prof. Hirokazu Kanegane, the lead researcher of the study.

The fact that all five patients shared the same variant caught the researchers attention. They hypothesized that this scenario could be explained by the founder effect, where a variant becomes common in a population that originated from a small group of ancestors. To verify their hypothesis, the researchers performed haplotype analyses. Put simply, they examined groups of genes that are inherited together from a parent (haplotypes) to determine whether these genes were identical among the five patients and matched previously sequenced haplotypes from Chinese CARD9-deficient patients.

Interestingly, they found strong evidence suggesting that all haplotypes containing the c.820dup variant were exactly the same. With further statistical genetic analyses, the researchers estimated the age of the c.820dup variant itself, which turned out to be between 2,000 and 4,000 years. Remarkably, the estimated variants age and its distribution in Japan, Korea, and China are perfectly in line with the history of the East Asia region. Modern Japanese and Koreans are believed to have a genetic background originating from northern China. During the late Neolithic to the Bronze Age, the migration of people from northern China to Korea and Japan spread rice and language. The origins of the variant identified in this study are consistent with this historical period, remarks Prof. Kanegane. We thus conclude that this variant originates from a common ancestor, estimated to have lived less than 4,000 years ago.

Additionally, although the variant observed was the same, the clinical presentation of patients from Japan and Korea differed from that of Chinese patients according to medical records. More specifically, Chinese patients often suffered from black mold infections caused by the genus Phialophora, whereas none of the five patients from Japan and Korea exhibited such infections. The researchers ascribed this discrepancy to environmental factors, possibly related to the more rural lifestyle in northern China.

Together, the findings of this interdisciplinary study make important contributions to our knowledge of anthropology, genetics, and medicine, and shed light on how genetic variants can propagate across different regions and through generations.

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The article, Inherited CARD9 Deficiency Due to a Founder Effect in East Asia, was published in the Journal of Clinical Immunology at DOI: 10.1007/s10875-024-01724-7

Journal of Clinical Immunology

Inherited CARD9 Deficiency Due to a Founder Effect in East Asia

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.

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Shedding light on the origin of a genetic variant underlying fungal infections - EurekAlert

An off-campus Public Health Genetics and Genomics Laboratory will be available for use by faculty and students from Texas A&M University-San Antonio this fall and will be accessible to faculty and students on-campus by 2027.

Chairs of the department are authorized to utilize the laboratory, alongside TAMUSA students who have mentor approval.

Requests to use the facility will be screened by the Public Health Genetics and Genomics Group (PHGGG), as space is limited and resources are fixed.

A major PHGGG activity is to serve the students interested in genetics and genomics of the diseases that are important to the south Texas community and beyond, including Type Two diabetes and obesity and their complications in adults and children, said Ravindranath Duggirala, a professor of Public Health Genomics at A&M-San Antonio and member of the PHGGG.

Stephanie Delostrinos, Business Administrator for the Research and Health Science department, said the lab is currently open and being worked in, but resides at an off-campus location.

Currently, the PHGGG occupies suites 212, 215 and 251 at the San Antonio Technology Center, located in the Medical Center area.

Once the new Public Health and Education Building is completed on campus, the labs will relocate to their home at A&M-San Antonio.

Due to the space limitations, our labs are temporarily located off campus, said Vijay Golla, Vice Provost for Research and Health Sciences at A&M-San Antonio. The labs will be relocated to the campus upon completion of the new Public Health and Education Building which broke ground on April 4, 2024. It is expected to be completed within three years.

Golla said having this facility will act as an important breakthrough for the Southside of San Antonio.

This lab lays the foundation for health science programs at TAMUSA, Golla said.

The genomics lab will be the first of its kind at A&M-San Antonio and will be focused on genetic epidemiology, molecular genetics, translational science and community engaged research.

Some of the important research this facility wants to focus on is the environmental factors influencing conditions suchas obesity, Type Two diabetes and the complications following these conditions.

We believe that some of our students will be interested in the research areas regarding the genetic/genomic and environmental determinants of complex diseases such as Type Two diabetes and obesity and their complications in Mexican-Americans, said Rector Arya, assistant professor of Public Health Genomics and member of the PHGGG. Our team has expertise working with the San Antonio community for over 25 years focusing on large Mexican-American families, and it is important to have the labs on campus for students to have hands-on experience related to the diseases of utmost concern to our community.

The PHGGG Faculty is made up of four Public Health Genomics faculty members Donna M. Lehman, Srinivas Mummidi, Rector Arya and Ravindranath Duggirala.

For additional information regarding the new Genomics lab, contact Ravindranath Duggirala at rduggirala@tamusa.edu.

Amber Esparza and Spring De La Garza contributed to this story.

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Off-campus genomics lab to open this fall, relocate to A&M-San Antonio in 2027 - The Mesquite

Myriad Genetics, Inc. (MYGN Quick QuoteMYGN - Free Report) recently announced a collaboration with GSK plc (GSK Quick QuoteGSK - Free Report) to advance in the field of genetic testing. The latest development is intended to improve access to homologous recombination deficiency (HRD) diagnostic testing for high-grade ovarian cancer (HGSOC) patients.

With this alliance, Myriad's MyChoice HRD Plus and MyChoice CDx Plus Tests, collectively known as Myriad's MyChoice Tests, are now part of a new sponsored testing program that is accessible in Argentina, Brazil, Chile, Colombia, Egypt, Netherlands, Saudi Arabia, Singapore, and the United Arab Emirates.

Per a report by the American Cancer Society, ovarian cancer is one of the leading causes of cancer deaths among women. Approximately 1 in 87 women may develop ovarian cancer in their lifetime. About 1 in 130 people may die from ovarian cancer in her lifetime. Most women with ovarian cancer are diagnosed at 63 years or above.

For patients with ovarian cancer, HRD testing is a crucial prognostic and predictive biomarker. Myriads MyChoice Tests determine HRD status in women with ovarian cancer. Clinicians can order this test through their local pathology labs, and samples are sent to Myriad Genetics.

This partnership with GSK satisfies a common need for patients who might not otherwise have access to testing and fulfills the commitments of both companies to enhance care for patients with advanced ovarian cancer by providing access to genetic testing.

The most detailed tumor test for assessing HRD status is Myriad's MyChoice test, which uses its unique algorithm to examine genomic changes in genes like BRCA1 and BRCA2 as well as the status of the Genomic Instability Score. It makes it possible for medical practitioners to determine which patients have advanced ovarian cancer and who will benefit most from focused therapy.

Per a report by Grand View Research, the global ovarian cancer diagnostics market was estimated to be $1.2 billion in 2018 and is expected to witness a CAGR of 6.2% from 2019 to 2026.

Given the market potential, the collaboration between Myriad Genetics and GSK is likely to benefit both companies to generate additional revenues.

In June, Myriad Genetics announced the addition of a new Universal Plus Panel to itsForesight Carrier Screen. The panel includes 39 conditions and screens up to 272 genes associated with severe inherited conditions.

In May, MYGN and QIAGEN announced their collaboration for developing a globally distributable kit-based test for analyzing HRD status. The next-generation sequencing test aims to support research into personalized medicine in multiple solid tumor types, including ovarian cancer. It is expected to enhance decentralized testing capacities once a regulated product is developed with pharmaceutical partners.

For the past six months, MYGNs shares have gained 18% compared with the industrys rise of 0.6%. The S&P 500 increased 10% in the same time frame.

Image Source: Zacks Investment Research

MYGN carries a Zacks Rank #3 (Hold) at present.

A couple of better-ranked stocks in the broader medical space that have announced quarterly results are DaVita(DVA Quick QuoteDVA - Free Report) andBoston Scientific Corporation(BSX Quick QuoteBSX - Free Report) .

DaVita, carrying a Zacks Rank #2 (Buy) at present, has an estimated long-term growth rate of 13.6%. DVAs earnings surpassed estimates in each of the trailing four quarters, with the average surprise being 29.4%. You can seethe complete list of todays Zacks #1 Rank (Strong Buy) stocks here.

DaVitas shares have gained 44% compared with theindustrys 20.4% rise in the past year.

Boston Scientific reported first-quarter 2024 adjusted earnings per share of 56 cents, which beat the Zacks Consensus Estimate by 9.8%. Revenues of $3.86 billion surpassed the Zacks Consensus Estimate by 4.9%. It currently carries a Zacks Rank #2.

Boston Scientific has a long-term estimated growth rate of 12.5%. BSXs earnings surpassed estimates in the trailing four quarters, the average surprise being 7.5%.

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Myriad Genetics (MYGN) and GSK Unite to Boost HRD Testing - Zacks Investment Research

Raha Kapoor's blue eyes remind fans of her great-grandfather, Raj Kapoor; here's what genetics says  IndiaTimes

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Raha Kapoor's blue eyes remind fans of her great-grandfather, Raj Kapoor; here's what genetics says - IndiaTimes

Cells are the bodys building blocks. Many different types of cells have different functions. They make up all of your bodys organs and tissues. Nearly every cell in a persons body has the same deoxyribonucleic acid, or DNA. DNA is the hereditary material in humans and almost all other organisms. Most DNA is located in the cell nucleus (where it is called nuclear DNA), but a small amount of DNA can also be found in the mitochondria (where it is called mitochondrial DNA).

DNA contains the code for building and maintaining an organism. The code is spelled out in the order, or sequence, of four chemical basesadenine (A), cytosine (C), guanine (G), and thymine (T)in the same way that letters of the alphabet come together to form words, sentences, and paragraphs. Human DNA consists of about three billion bases, and more than 99 percent of those bases are the same in all people.

DNA bases pair with each otherA with T, C with Gto form units called base pairs. Each base is attached to a sugar molecule and a phosphate molecule. Together, base, sugar, and phosphate are called a nucleotide. Nucleotides are arranged in two long strands that form a spiral called a double helix. The structure of the double helix is like a ladder, with base pairs running through the middle like rungs and sugar and phosphate molecules along the outside.

Genes are small sections of the long chain of DNA. They are the basic physical and functional units of heredity. In humans, genes vary in size from a few hundred DNA bases to more than two million bases. The Human Genome Project has estimated that humans have between 20,000 and 25,000 genes. Every person has two copies of each gene, one inherited from each parent. Most genes are the same in all people, but a small number of genes (less than one percent of the total) are slightly different between people. Alleles are forms of the same gene with small differences in their sequence of DNA bases. These small differences contribute to each persons unique features.

Genes act as instructions to make molecules called proteins. To function correctly, each cell depends on thousands of proteins to do their jobs in the right places at the right times. Sometimes changes in a gene, called mutations, prevent one or more of these proteins from working properly. This may cause cells or organs to change or lose their function, which can lead to a disease. Mutations, rather than genes themselves, cause disease. For example, when people say that someone has the cystic fibrosis gene, they are usually referring to a mutated version of the CFTR gene, which causes the disease. All people, including those without cystic fibrosis, have a version of the CFTR gene.

Sections of DNA form genes, and many genes together form chromosomes. People inherit two sets of chromosomes (one from each parent), which is why every person has two copies of each gene. Humans have 23 pairs of chromosomes.

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BASIC GENETICS INFORMATION - Understanding Genetics - NCBI Bookshelf

What is psoriasis and how do you get it?

Psoriasis is a skin condition characterized by itchy scales, inflammation, and redness. It usually occurs on the scalp, knees, elbows, hands, and feet.

According to one study, about 7.4 million people in the United States were living with psoriasis in 2013.

Psoriasis is an autoimmune disease. Immune cells in your blood mistakenly recognize newly produced skin cells as foreign invaders and attack them. This can cause the overproduction of new skin cells beneath the surface of your skin.

These new cells migrate to the surface and force out existing skin cells. That causes the scales, itching, and inflammation of psoriasis.

Genetics almost certainly plays a role. Read on to learn more about the role of genetics in the development of psoriasis.

Psoriasis usually appears between the ages of 15 and 35, according to the National Psoriasis Foundation (NPF). However, it may occur at any age. For example, about 20,000 children under the age of 10 are diagnosed with psoriasis every year.

Psoriasis can occur in people with no family history of the disease. Having a family member with the disease increases your risk.

Scientists working on the genetic causes of psoriasis start by assuming that the condition results from a problem with the immune system. Research on psoriatic skin shows that it contains large numbers of immune cells that produce inflammatory molecules known as cytokines.

Psoriatic skin also contains gene mutations known as alleles.

Early research in the 1980s led to the belief that one specific allele might be responsible for passing on the disease through families.

Researchers later discovered that the presence of this allele, HLA-Cw6, wasnt sufficient to cause a person to develop the disease. More recent studies show that more research is still needed to better understand the relationship between HLA-Cw6 and psoriasis.

Use of more advanced techniques has led to the identification of about 25 different regions in human genetic material (the genome) that may be associated with psoriasis.

As a result, genetic studies can now give us an indication of a persons risk of developing psoriasis. The link between the genes that are associated with psoriasis and the condition itself isnt yet fully understood.

Psoriasis involves an interaction between your immune system and your skin. That means its hard to know whats the cause and whats the effect.

The new findings in genetic research have provided important insights, but we still dont clearly understand what causes a psoriasis outbreak. The precise method by which psoriasis is passed from parent to child is also not fully understood.

Most people with psoriasis have periodic outbreaks or flare-ups followed by periods of remission. About 30 percent of people with psoriasis also experience inflammation of the joints that resembles arthritis. This is called psoriatic arthritis.

Environmental factors that may trigger a psoriasis onset or flare-up include:

Injury or trauma to a portion of your skin may sometimes become the site of a psoriasis flare-up. Infection may also be a trigger. The NPF notes that infection, especially strep throat in young people, is reported as a trigger for psoriasis onset.

Some diseases are more likely in people with psoriasis than in the general population. In one study of women with psoriasis, about 10 percent of the participants had also developed an inflammatory bowel disease like Crohns disease or ulcerative colitis.

People with psoriasis have an increased incidence of:

Gene therapy isnt currently available as a treatment, but theres an expansion of research into the genetic causes of psoriasis. In one of the many promising discoveries, researchers found a rare gene mutation thats linked to psoriasis.

The gene mutation is known as CARD14. When exposed to an environmental trigger, such as an infection, this mutation produces plaque psoriasis. Plaque psoriasis is the most common form of the disease. This discovery helped establish the connection of the CARD14 mutation to psoriasis.

These same researchers also found the CARD14 mutation present in two large families that had many family members with plaque psoriasis and psoriatic arthritis.

This is one of a number of recent discoveries that hold promise that some form of gene therapy may one day be able to help people living with psoriasis or psoriatic arthritis.

For mild to moderate cases, dermatologists usually recommend topical treatments such as creams or ointments. These can include:

If you have a more severe case of psoriasis, your doctor may prescribe phototherapy and more advanced systemic or biologic medications, taken orally or by injection.

Researchers have established a link between psoriasis and genetics. Having a family history of the condition also increases your risk. More research is needed to fully understand the inheritance of psoriasis.

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Psoriasis: Whats the Genetic Link? - Healthline

Defined, toned abs commonly called a six-pack are an often sought-after goal in the gym. But not all toned abs look the same. Some people sport a four-pack, while others may have an eight-pack.

Lets take a look at the difference between ab types as well as the diet, exercise, and lifestyle tips that can help you achieve the strongest abs your genetics will allow.

The difference between ab types lies in the structure of your abdominal muscles.

Your abdomen contains four muscle groups. To get toned abs, youll need to do exercises that strengthen all four muscle groups. These muscle groups are:

Once toned, the rectus abdominis becomes your four-, six-, or eight-pack. It comprises two connected muscle bands that run parallel to each other, down either side of the abdomen.

The linea alba is the fibrous band that separates the rectus abdominis. It forms the line that runs down the middle of the abdomen.

The rectus abdominis also helps:

The transverse abdominis is located deep within the abdomen. It extends from the front of your abdomen to the sides of your body. It helps provide stability and strength to your entire core, back, and pelvis.

If your transverse abdominis isnt being worked, your rectus abdominis wont become defined.

The internal and external obliques help control the twisting and turning movements of your body. Along with the transverse abdominis, they provide a stabilizing girdle for your back and pelvis.

The external obliques are a large muscle group located at the sides of the rectus abdominis. The internal obliques are located just underneath, inside your hip joints. Working your obliques adds definition and tone to your abs.

Being able to achieve a 10-pack is possible for some people.

You need to be born with a rectus abdominis that contains five bands of connective tissue running horizontally across it. You also need to regularly work out these muscles and follow a healthy diet.

Of course, what you eat and how you exercise also play large roles in how your abs ultimately look.

The rectus abdominis muscle has bands of connective tissue (fascia) crossing it horizontally. These bands give the appearance of multiple packs stacked on top of each other on either side of your abdomen.

Youre born with a set number of these connective tissue bands. You cant build additional ones. Your genetics also determine their symmetry, length, and size.

A person with an eight-pack has four bands. A person with a six-pack has three bands. A person with a four-pack has two bands.

Many peoples rectus abdominis has three intersections. This means that if most people worked at it, they could achieve a six-pack.

But just because you have more or less doesnt mean youre stronger or weaker. Its just your genes.

Some of the fittest people around cant achieve six- or eight-pack abs. One of these people is Arnold Schwarzenegger, who, even during his bodybuilding days, sported a four-pack.

Of course, what you eat and how you exercise also play large roles in how your abs ultimately look.

Both sexes have a genetic predetermination for the number of packs they can achieve. However, women require more body fat than men. This essential body fat is needed for:

Because of this, it may be more difficult for women to lose enough abdominal fat to define their abs while staying healthy. Having too little body fat for your body type can lead to various complications in women, like:

Men have around 61 percent more muscle mass than women due to their higher testosterone levels. Men require less body fat for optimum health, too. So, they can more readily lose enough fat to show their toned rectus abdominis muscles underneath.

While your genetics help determine how your abs look, you can still build a strong core. A strong core protects your back and spine, preventing injury.

These exercises can help strengthen your abs and build muscle mass. If you want to have visible abs, youll have to spend time toning them at least every other day and follow a healthy diet.

This highly effective exercise works your entire core, as well as your glutes and hamstrings. It also improves balance and stability.

You can also try harder modifications, like side planks and knee touches.

The dead bug works your obliques, rectus abdominis, and transverse abdominis muscles. It also improves core stability and helps correct excessive anterior pelvic tilt.

If your lower back doesnt touch the floor, roll up a small towel and place it in the small of your back to stay stable during the exercise. This isnt an easier or modified version, and it wont diminish the exercises intensity. Itll protect your lower back from injury.

Looking for a challenge? Check out these dead bug variations.

This exercise focuses directly and intensely on the rectus abdominis muscle. Its excellent for balance and full-body stability. Its also effective whether its done quickly or slowly.

For many people, getting sculpted abs requires time and dedication. These tips can help you get started.

Cardio exercise has been linked to reductions in belly fat. Less belly fat will help make your abs more visible. Cardio examples include:

Try to build cardio into your day-to-day life. Walk or ride a bike instead of driving. Take a run or swim before or after work. Hate running? Here are nine cardio alternatives to try.

Aim for a minimum of 20 to 40 minutes of cardio at least four times a week.

Exercises that require you to move your body against resistance help build muscle strength, tone, and endurance.

Exercise machines and enhancements, such as weights and body bands, all provide resistance. So do many water exercises.

HIIT refers to short, one- to two-minute bursts of high-intensity cardio followed by a rest period of equal time. To be effective, each burst of cardio must be done at your very top capacity.

Because your body is working at its highest capacity, HIIT sessions burn lots of calories both during workouts and for several hours afterward.

A high-protein diet will help you build and repair muscle. Itll also help you feel fuller longer. Opt for lean protein sources, such as:

Your ability to achieve a visible pack of abs whether a four-, six-, or eight-pack is largely determined by genetics.

However, healthy lifestyle choices, like losing belly fat and exercising, can provide anyone with a fit and toned abdomen. A strong core also helps with overall strength and balance.

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Deep Dive Ties Together Dog Genetics, Brain Physiology and Behavior to Explain Why Collies Are Different from Terriers - Scientific American