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olaparib (myChoice CDx)

✓ Approved

Myriad Genetics, Inc. · Companion diagnostic · Companion diagnostic

What is olaparib?

olaparib is a companion diagnostic developed by Myriad Genetics, Inc.. It is approved for therapeutic indications via others.

Drug Profile

Brand NamesmyChoice CDx
CompanyMyriad Genetics, Inc.
Drug ClassCompanion diagnostic
RouteOthers
StatusApproved
Sources: ClinicalTrials.gov, Myriad Genetics, Inc.

Therapeutic Indications

olaparib is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Uterine cancer✓ Approved

Related Research Articles

PubMedDocumenta ophthalmologica. Advances in ophthalmology2026-07-25

Clinical and genetic spectrum of genetic eye diseases seen in two newly developed ophthalmic genetics clinics: two-year experience.

Tawfik Caroline Atef CA, Roshdy Maged Maher MM

Genetic eye diseases (GED) are among the top ten leading causes of global blindness. Ophthalmic genetics has emerged as a dedicated subspecialty, integrating clinical and genetic diagnosis with genetic counseling. We conducted an electronic and physical medical records search for the patients attending the clinics. Clinical data included patient demographics, presenting complaint, physical exam findings, best-corrected visual acuity (BCVA), available ophthalmic and diagnostic radiology imaging, and genetic testing results. Electronic medical records of 499 patients were examined; 472 patients were diagnosed with GED. The mean age was 22.7 years. Males represented 57.1% of the patients. The most common diagnosis was isolated retinitis pigmentosa (32.2%), followed by Stargardt disease (11.0%), early-onset severe retinal dystrophy (10.3%), cone dystrophy (7.1%), cone-rod dystrophy (4.7%), autosomal recessive bestrophinopathy (3.6%), and enhanced S-cone syndrome (3.1%). The mean BCVA was 6/48, where 42% exhibited moderate to severe visual impairment, and 24% were classified as blind. Genetic tests were done for 28.8% of the GED patients with a molecular solving rate of 87.5%. Positive cases encompassed 47 genes; the most common were ABCA4 (11.8%), CRB1 (10.1%), BEST1 (8.4%), and NR2E3 (5.9%). Systemic associations were reported by 12.7%. Within this group hearing loss was the most common association encountered (45%), followed by intellectual disability (16.7%), and polydactyly (15%). This study provides a comprehensive overview of the encountered GEDs spectrum. The data are valuable for refining clinical diagnoses, establishing accurate inheritance patterns, informing family planning, and assessing patient eligibility for emerging gene-targeted therapies.

PMID 42498820
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PubMedFrontiers in systems biology2026-07-25

The interaction of biological network topology and mutation effects in complex trait evolution.

Gouy Alexandre A

The genetic architecture of complex traits can be described through three complementary frameworks: the additive genetic variance-covariance matrix G (quantitative genetics), summarizing the genetic architecture of a set of traits; the distributions of phenotypic and fitness effects of new mutations (population genetics), which together with allele frequency dynamics determine which variants segregate; and the regulatory network topology that conditions both (systems biology). This review synthesizes how the evolutionary genetics of complex traits and the systems biology perspective are related: network topology constrains the distributions of phenotypic and fitness effects of new mutations, influencing the genotype-phenotype map. Then, over evolutionary time, stabilizing selection can reshape topology for increased robustness. Empirical support for these processes is reviewed: genome-scale perturbation experiments, network simulations, and evidence that stabilizing selection progressively sculpts regulatory networks toward additivity. Perspectives and future research directions are discussed.

PMID 42500042
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PubMedVeterinary medicine and science2026-07-25

Green Tea Extract, Keratin Hydrolysate and Vitamin C Exert Anti-Ageing Effects Through the Hippo Signalling Pathway in Feline and Canine Mammary Gland Cells.

Gao Yi Y, Sun Xue X, Ma Yan Y, Li Jiaxi J et al.

Ageing is a progressive decline in organ function and tissue integrity caused by genetic, environmental and physiological factors. With the increasing lifespan of companion animals, effective anti-ageing interventions for elderly felines and canines have attracted growing attention in veterinary medicine. This study aimed to investigate the anti-ageing effects of green tea extract, keratin hydrolysate and vitamin C in feline and canine mammary gland cells and to explore the underlying molecular mechanisms. Feline and canine mammary gland cells were treated with green tea extract, keratin hydrolysate and vitamin C in vitro. Cell proliferation, oxidative stress responses and ageing-associated protein expression induced by actinomycin D were evaluated. The involvement of the Hippo signalling pathway was further analysed to determine the molecular mechanisms underlying the anti-ageing effects. Green tea extract, keratin hydrolysate and vitamin C significantly promoted the proliferation of feline and canine mammary gland cells. These treatments effectively restored the abnormal expression of ageing-related proteins induced by actinomycin D and exhibited protective effects against oxidative damage. Mechanistically, the anti-ageing effects were associated with regulation of the Hippo signalling pathway. Green tea extract, keratin hydrolysate and vitamin C exhibit significant anti-ageing effects in feline and canine mammary gland cells through modulation of the Hippo pathway. These findings suggest their potential as safe and effective anti-ageing interventions for improving health and alleviating geriatric syndromes in ageing companion animals.

PMID 42499304
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PubMedInternational journal of immunogenetics2026-07-25

Wildlife Trade and Genetic Basis of Disease Susceptibility: A Review.

Coker Oluwakayode Michael OM, Fagbenro Olukunle Silas OS, Coker Motunrayo Mojoyin MM

The surge in the trade of wildlife and wildlife products drives several species to extinction while coinciding with the increase in several zoonotic diseases. It is therefore essential to explore the roles of wildlife trade in disease transmission, and how the knowledge of genetics and immunogenetics can help in alleviating the attending challenges. Pathogen-driven selection plays a fundamental role in maintaining immune gene diversity, as individuals with alleles conferring resistance to endemic diseases have higher survival rate. However, anthropogenic disturbances, such as wildlife exploitation, can disrupt these evolutionary processes, leading to reduced genetic diversity and increased disease vulnerability. Advanced genomic tools, such as next-generation sequencing (NGS), whole-genome sequencing (WGS), CRISPR-Cas9 gene editing, genome-wide association studies (GWAS), epigenetics and transcriptomic analysis, can help identify immune gene variations and predict disease susceptibility in both wild and captive populations. Massive research targeting wildlife markets and the interface between the wild and the market players is necessary. It would be interesting to understand dynamics of pathogens and disease susceptibility, through the application of genetics and immunogenetics, thereby enhancing efforts to address the challenges posed by wildlife trade and zoonotic disease emergence.

PMID 42499296
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PubMedJournal of medical genetics2026-07-25

Potential advantage of clinical exome sequencing in BRCA1/2-negative families: a retrospective study of a cohort of 500 patients at a high-risk for hereditary cancers.

Dell'Elice Anastasia A, Palmarini Claudia C, Anaclerio Federico F, Pilenzi Lucrezia L et al.

Hereditary cancer syndromes (HCSs) account for approximately 5-10% of all cancers and are frequently associated with pathogenic variants (PVs) in genes such as BRCA1 and BRCA2. Nevertheless, a substantial proportion of individuals with strong familial cancer aggregation remain genetically unexplained after standard multigene panel testing. Clinical exome sequencing (CES) may overcome this limitation by enabling a broader exploration of cancer susceptibility genes. This retrospective study included 500 high-risk patients who previously tested negative for BRCA1/2 PVs. All samples were analysed using next-generation sequencing technology. Initially, a 60-gene filtered panel recommended by the American Society of Clinical Oncology (ASCO) guidelines was applied, followed by a 102-gene filtered panel derived from CES to identify additional PVs or likely PVs (LPVs) beyond current diagnostic panels. Variant classification was performed according to the American College of Medical Genetics and Genomics/Association for Molecular Pathology guidelines, incorporating ClinGen and gene-specific expert curation recommendations when available. Within the ASCO panel, PV/LPVs were identified in 9% of patients while 35% carried variants of uncertain significance. CES identified additional PVs/LPVs in 5% of patients in genes not currently included in ASCO-recommended surveillance panels, such as RAD50, BLM, WRN, PMS1 and FANCA. These variants may represent candidate susceptibility loci requiring further clinical and functional validation. CES may provide additional exploratory genomic information in selected high-risk BRCA1/2-negative patients, particularly when standard panel testing is uninformative. Although many of the additional findings identified are not yet clinically actionable, CES represents a valuable resource for future reinterpretation as gene-disease evidence evolves. Overall, our findings support the use of CES as a second-tier exploratory approach in carefully selected high-risk cases, while emphasising the need for cautious interpretation and continued gene-disease curation.

PMID 42498519
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PubMedPediatric investigation2026-07-25

Monogenic and syndromic obesity in children: Clinical recognition, genetics, and precision management.

Khalil Hadel H, Feigin Eugene E, Zaitoon Hussein H

Obesity is increasingly being recognized as a heterogeneous condition with strong genetic underpinnings. Monogenic obesity, caused by single-gene mutations, primarily affects the leptin-melanocortin pathway, which regulates hunger and satiety. Mutations in genes, such as LEP, LEPR, POMC, PCSK1, and MC4R, lead to hyperphagia, early onset severe obesity, and metabolic dysregulation. LEP and LEPR mutations impair leptin signaling, resulting in defective appetite suppression, whereas POMC and PCSK1 deficiencies disrupt prohormone processing. MC4R mutations, the most common cause of monogenic obesity, impair satiety signaling and are linked to rapid weight gain. Syndromic obesity, including the Bardet-Biedl and Alström syndromes, involves ciliary dysfunction, leading to developmental abnormalities alongside obesity. Other genes such as SH2B1, SIM1, and BDNF play crucial roles in hypothalamic development and energy regulation. Advances in genomic sequencing have improved the recognition of genetic etiologies; however, many patients remain undiagnosed due to limited testing availability and a lack of clinician awareness. Precision therapies, including set-melanotide for specific melanocortin pathway defects, demonstrate the promise of targeted treatments. However, management must extend beyond pharmacology; lifestyle interventions, psychosocial support, and family-centered care remain essential, especially when intellectual disability or behavioral challenges complicate adherence. Ethical considerations surrounding access and equity are critical, as high-cost therapies and the limited availability of genetic testing risk widening disparities between health systems. Polygenic risk scores and multi-omics approaches may expand precision medicine beyond rare genetic syndromes to common obesity, highlighting the importance of integrating genetics, psychosocial care, and policy advocacy in the management of pediatric obesity.

PMID 42499770
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