Evolving Health Testing and Prognosis
A cooperative-based clinical laboratory using state-of-the-art innovation in Next Generation Sequencing and machine/deep learning
Next Generation Squencing
Genomic Sequencing Revolutionary Methods never used before. Next generation sequencing has changed medicine in the past decade in ways most people couldn’t imagine. It has allowed a rapid evolution to the field of precision medicine with new drugs with being approved regularly.
We work together
A Cooperation Model of Bringing new solutions. Simply put a co-op means we all work together as a team to make things better. In the case of the Genomic Testing Cooperative it means that our lab works with other labs, physicians and patients to improve the communities access to cutting edge healthcare at an affordable price.
AI Machine Learning
Bringing computer science to laboratories
Our AI helps us sort through curate large sets of data so we can quickly make sense of genomic alterations and assess their impact on a patient prognosis, diagnosis and help predict their response to therapy. We use machine learning to review these alterations and track their frequency allowing us to gain new insights about cancer.
Machine/deep Learning meets Next Generation Sequencing
- Who are we? Genomic Testing Cooperative (GTC) is creating a genomic testing lab combining next-gen sequencing (NGS) with AI that will disrupt the current model.
- Why? Genomic testing is expensive and risky for smaller labs because competing with major NGS labs is challenging to get scale and payment.
- How? Using a co-op model to reduce sales and service costs – the biggest impediment to profitability by sharing resources.
- What makes it different? We use the latest advances in NGS combined with AI to compile the latest information to treat patients. The Co-op model produces big data for AI analysis and of value for Pharma and insurance companies.
OFFERING NEXT-GEN TESTS FOR ALL
Available and Affordable for Everyone
FDA Approves* Vitrakvi (larotrectinib), a targeted therapy for patients with solid tumors harboring an NTRK gene fusion, regardless of tumor type
Genomic Testing Cooperative (GTC) offers a comprehensive next-generation sequencing (NGS) Solid Tumor Fusion/ Expression profile specifically testing for fusions in NTRK1, NTRK2, and NTRK3 for $1,500.
Contact us today at (949) 540-9421 to order and learn more about our NGS offering. Get Results in 7 to 10 days.
Features of Our Services
Diagnosis and Classifications
Accurate variant calling using deep learning
Transforming diagnostic testing by adapting AI
Innovative state-of-the-art new tests
Interpreting NGS data using deep learning
Treatment recommendation aided by deep learning
Personalized medicine aided by AI
Increasing efficiency using deep learning
Transforming diagnostic testing by adapting AI
Personalized medicine aided by deep learning
Interpreting NGS data using machine learning
Advanced Genomic Testing
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FEATURED BLOG POSTS AND PUBLICATIONS
Mutations in cell free DNA (cfDNA) or cells in the peripheral blood along with anemia or thrombocytopenia are the whole mark of myelodysplastic syndrome (MDS). The incidence of MDS is 3-4 per 100,000 per year but increases significantly above the age of 50 and it is at 30 per 100,000 per year in patients above the age of 70. The diagnosis of MDS is confirmed when mutations in hematopoietic cells are detected at relatively high levels (>40% of cells). However, mutations at low levels in few cells can be detected in normal individuals. In general, random somatic mutations occur in normal cells, but rarely these cells evolve into viable clone, but with aging, the possibility of a clone to accumulate increases. Clonal hematopoiesis of indeterminate potential (CHIP) is defined by the presence of low-level mutations in the peripheral blood in clinically normal individuals. CHIP is detected in 3-5% of normal individuals above the age of 50 and in approximately 10% of people aged 70 to 80. The most common mutation is on the DNMT3A gene, followed by TET2 and ASXL1. The rate of transformation to a hematological neoplasia is 0.5–1% per year. Clonal cytopenias of undetermined significance (CCUS) is defined by the presence of cytopenia (anemia, low platelets or white cells) along with low level mutations but does not meet World Health Organization (WHO)-defined criteria for MDS and the mutations are detected in <40% of cells. Approximately 25% to 65% of patients with cytopenia will have mutation in one or more genes. These patients with mutations have significantly higher probability of developing MDS or other hematopoietic neoplasms (AML, MPN, lymphoma,…) within 5 years. In addition, recent studies linked mutations in peripheral blood to cardiovascular disease (CVD). Recent data show that patients with CHIP have 4.0-times greater risk of myocardial infarction as compared to individuals without such clone. The prevalence of CHIP in patients with coronary artery disease is reported to be at 18.2%. In contrast, the prevalence of CHIP in centenarians is only at 2.5%. It has been shown that mutations in TET2 gene, which is one of the commonly mutated genes in CHIP, are pro-inflammatory and lead to the development of atherosclerotic plaques. Based on that it has been suggested that anti-inflammatory agents might slow the progression of cardiovascular disease in patients with low level mutations in peripheral blood. Therefore, testing the peripheral blood for the presence of mutations provides information for: Diagnosis of myelodysplastic syndrome (MDS). Detecting the presence of mutations in the presence of cytopenia and confirming the diagnosis of clonal cytopenias of undetermined (CCUS) Detecting the presence of CHIP to monitor the development of hematologic neoplasms, especially MDS Detecting CHIP and predicting increased risk of cardiovascular disease (CVD) Additional studies are needed to determine the clinical relevance of anti-inflammatory agents in reducing CVD or to determine the relationship between duration of the presence of CHIP or level of the mutated clone with progression of CVD or hematologic neoplasms. References: The shadowlands of MDS: idiopathic cytopenias of undetermined significance (ICUS) and clonal hematopoiesis of indeterminate potential (CHIP). Malcovati L, Cazzola M. Hematology Am Soc Hematol Educ Program. 2015;2015:299-307. doi: 10.1182/asheducation-2015.1.299. PMID: Clonal hematopoiesis of indeterminate potential and its distinction from myelodysplastic syndromes. Steensma DP, Bejar R, Jaiswal S, Lindsley RC, Sekeres MA, Hasserjian RP, Ebert BL. 2015 Jul 2;126(1):9-16. doi: 10.1182/blood-2015-03-631747. PMID: 25931582. Deep Sequencing of Cell-Free Peripheral Blood DNA as a Reliable Method for Confirming the Diagnosis of Myelodysplastic Syndrome. Albitar F, Ma W, Diep K, De Dios I, Agersborg S, Thangavelu M, Brodie S, Albitar M. Genet Test Mol Biomarkers. 2016 Jul;20(7):341-5. doi: 10.1089/gtmb.2015.0278. Epub 2016 Jun 1. Age-related clonal hematopoiesis associated with adverse outcomes. Jaiswal S1, Fontanillas P, Flannick J, Manning A, Grauman PV, Mar BG, Lindsley RC, Mermel CH, Burtt N, Chavez A, Higgins JM, Moltchanov V, Kuo FC, Kluk MJ, Henderson B, Kinnunen L, Koistinen HA, Ladenvall C, Getz G, Correa A, Banahan BF, Gabriel S, Kathiresan S, Stringham HM, McCarthy MI, Boehnke M, Tuomilehto J, Haiman C, Groop L, Atzmon G, Wilson JG, Neuberg D, Altshuler D, Ebert BL. N Engl J Med. 2014 Dec 25;371(26):2488-98. doi: 10.1056/NEJMoa1408617. Clonal Hematopoiesis and Its Impact on Cardiovascular Disease. Sano S, Wang Y, Walsh K. Circ J. 2018 Sep 4. doi: 10.1253/circj.CJ-18-0871. PMID: 30185689. Clinical Implications of Clonal Hematopoiesis. Steensma DP. Mayo Clin Proc. 2018 Aug;93(8):1122-1130. doi: 10.1016/j.mayocp.2018. PMID: 30078412. Myeloid cell contributions to cardiovascular health and disease. Nahrendorf M. Nat Med. 2018 Jun;24(6):711-720. doi: 10.1038/s41591-018-0064-0. PMID: 29867229. Atherosclerosis and clonal hematopoyesis: A new risk factor. Páramo Fernández JA. Clin Investig Arterioscler. 2018 May - Jun;30(3):133-136. doi: 10.1016/j.arteri.2018.03.001. Tet2-Mediated Clonal Hematopoiesis Accelerates Heart Failure Through a Mechanism Involving the IL-1β/NLRP3 Inflammasome. Sano S, Oshima K, Wang Y, MacLauchlan S, Katanasaka Y, Sano M, Zuriaga MA, Yoshiyama M, Goukassian D, Cooper MA, Fuster JJ, Walsh K. J Am Coll Cardiol. 2018 Feb 27;71(8):875-886. doi: 10.1016/j.jacc.2017.12.037. Somatic Mutations and Clonal Hematopoiesis: Unexpected Potential New Drivers of Age-Related Cardiovascular Disease. Fuster JJ, Walsh K. Circ Res. 2018 Feb 2;122(3):523-532. doi: 10.1161/CIRCRESAHA.117.312115. Clonal Hematopoiesis and Evolution to Hematopoietic Malignancies. Bowman RL, Busque L, Levine RL. Cell Stem Cell. 2018 Feb 1;22(2):157-170. doi: 10.1016/j.stem.2018.01.011. Risk and timing of cardiovascular death among patients with myelodysplastic syndromes. Brunner AM, Blonquist TM, Hobbs GS, Amrein PC, Neuberg DS, Steensma DP, Abel GA, Fathi AT. Blood Adv. 2017 Oct 18;1(23):2032-2040. doi: 10.1182/bloodadvances.2017010165. eCollection 2017 Oct 24. The maturation of a 'neural-hematopoietic' inflammatory axis in cardiovascular disease. Stiekema LCA, Schnitzler JG, Nahrendorf M, Stroes ESG. Curr Opin Lipidol. 2017 Dec;28(6):507-512. doi: 10.1097/MOL.0000000000000457. Clonal Hematopoiesis and Risk of Atherosclerotic Cardiovascular Disease. Jaiswal S, Natarajan P, Silver AJ, Gibson CJ, Bick AG, Shvartz E, McConkey M, Gupta N, Gabriel S, Ardissino D, Baber U, Mehran R, Fuster V, Danesh J, Frossard P, Saleheen D, Melander O, Sukhova GK, Neuberg D, Libby P, Kathiresan S, Ebert BL. N Engl J Med. 2017 Jul 13;377(2):111-121. doi: 10.1056/NEJMoa1701719. Clonal hematopoiesis associated with TET2 deficiency accelerates atherosclerosis development in mice. Fuster JJ, MacLauchlan S, Zuriaga MA, Polackal MN, Ostriker AC, Chakraborty R, Wu CL, Sano S, Muralidharan S, Rius C, Vuong J, Jacob S, Muralidhar V, Robertson AA, Cooper MA, Andrés V, Hirschi KK, Martin KA, Walsh K. 2017 Feb 24;355(6327):842-847. doi: 10.1126/science.aag1381. Clonal hematopoiesis. Jan M, Ebert BL, Jaiswal S. Semin Hematol. 2017 Jan;54(1):43-50. doi: 10.1053/j.seminhematol.2016.10.002. Epub 2016 Oct 20. Review. Clonal Hematopoiesis Associated With Adverse Outcomes After Autologous Stem-Cell Transplantation for Lymphoma. Gibson CJ, Lindsley RC, Tchekmedyian V, Mar BG, Shi J, Jaiswal S, Bosworth A, Francisco L, He J, Bansal A, Morgan EA, Lacasce AS, Freedman AS, Fisher DC, Jacobsen E, Armand P, Alyea EP, Koreth J, Ho V, Soiffer RJ, Antin JH, Ritz J, Nikiforow S, Forman SJ, Michor F, Neuberg D, Bhatia R, Bhatia S, Ebert BL. J Clin Oncol. 2017 May 10;35(14):1598-1605. doi: 10.1200/JCO.2016.71.6712.
Chronic Lymphocytic Leukemia Prognostic Indicator
Circulating Ki-67 index in plasma as a biomarker and prognostic indicator in chronic lymphocytic leukemia. Ki-67 is a nuclear antigen that is expressed in all stages of the cell cycle, except G(0), and is widely used as a marker of cellular proliferation in human tumors. We recently showed that elevated levels of Ki-67 circulating in plasma (cKi-67) are associated with shorter survival in patients with acute lymphoblastic leukemia. The current study included 194 patients with CLL and 96 healthy control subjects. cKi-67 levels in plasma were determined using an electrochemiluminescent immunoassay. We normalized the cKi-67 level to the absolute number of lymphocytes in the patient's peripheral blood to establish the plasma cKi-67 index. The cKi-67 index showed significant correlation with lymph node involvement and Rai stage (P=0.05). Higher cKi-67 index values were significantly associated with shorter survival. Multivariate Cox proportional hazards regression analysis demonstrated that the association of the cKi-67 index with shorter survival was independent of IgV(H) mutation status. In a multivariate model incorporating the cKi-67 index with B2M and IgV(H), only cKi-67 index and B2M levels remained as independent predictors of survival. The results of this study suggest that the plasma cKi-67 index, along with B2M level, is a strong predictor of clinical behavior in CLL. Links to more resources Full Text Sources Elsevier Science ClinicalKey Europe PubMed Central - Author Manuscript PubMed Central - Author Manuscript Other Literature Sources COS Scholar Universe Medical Chronic Lymphocytic Leukemia - Genetic Alliance Miscellaneous NCI CPTAC Assay Portal
Patients with Myeloproliferative Disorders
MPL mutation profile in JAK2 mutation-negative patients with myeloproliferative disorders. Mutations in the thrombopoietin receptor gene (myeloproliferative leukemia, MPL) have been reported in patients with JAK2 V617F-negative chronic myeloproliferative disorders (MPDs). We evaluated the prevalence of MPL mutations relative to JAK2 mutations in patients with suspected MPDs. A total of 2790 patient samples submitted for JAK2 mutation analysis were tested using real-time polymerase chain reaction and bidirectional sequencing of plasma RNA. JAK2 V617F-negative samples were tested for JAK2 exons 12 to 14 mutations, and those with negative results were then tested for mutations in MPL exons 10 and 11. Of the 2790 patients, 529 (18.96%) had V617F, 12 (0.43%) had small insertions or deletions in exon 12, and 7 (0.25%) had other JAK2 mutations in exons 12 to 14. Of the 2242 JAK2 mutation-negative patients, 68 (3.03%) had MPL mutations. W515L was the predominant MPL mutation (n=46; 68%), and 10 (15%) patients had other W515 variants. The remaining MPL mutations (n=12, 17%) were detected at other locations in exons 10 and 11 and included 3 insertion/deletion mutations. The S505N mutation, associated with familial MPD, was detected in 3 patients. Overall, for every 100 V617F mutations in patients with suspected MPDs, there were 12.9 MPL mutations, 2.3 JAK2 exon 12 mutations, and 1.3 JAK2 exons 13 to 14 mutations. These findings suggest that MPL mutation screening should be performed before JAK2 exons 12 to 14 testing in JAK2 V617F-negative patients with suspected MPDs.