Impact of the CYP2C19*17 allele on outcomes in patients receiving genotype-guided antiplatelet therapy after percutaneous coronary intervention.

Clin Pharmacol Ther. 2020 Sep 08;:

Authors: Lee CR, Thomas CD, Beitelshees AL, Tuteja S, Empey PE, Lee JC, Limdi NA, Duarte JD, Skaar TC, Chen Y, Cook KJ, Coons JC, Dillon C, Franchi F, Giri J, Gong Y, Kreutz RP, McDonough CW, Stevenson JM, Weck KE, Angiolillo DJ, Johnson JA, Stouffer GA, Cavallari LH, IGNITE Network Pharmacogenetics Working Group

Abstract
Genotyping for CYP2C19 no function alleles to guide antiplatelet therapy after percutaneous coronary intervention (PCI) improves clinical outcomes. Although results for the increased function CYP2C19*17 allele are also reported, its clinical relevance in this setting remains unclear. A collaboration across nine sites examined antiplatelet therapy prescribing and clinical outcomes in 3,342 patients after implementation of CYP2C19-guided antiplatelet therapy. Risk of major atherothrombotic and bleeding events over 12 months after PCI were compared across CYP2C19 metabolizer phenotype and antiplatelet therapy groups by proportional hazards regression. Clopidogrel was prescribed to a similar proportion of CYP2C19 normal (84.5%), rapid (82.9%) and ultrarapid metabolizers (80.6%) (P=0.360). Clopidogrel-treated normal metabolizers (20.4 events/100 patient-years; adjusted hazard ratio [HR] 1.00, 95% confidence interval [CI] 0.75-1.33, P=0.993) and clopidogrel-treated rapid or ultrarapid metabolizers (19.1 events/100 patient-years; adjusted HR 0.95, 95% CI 0.69-1.30, P=0.734) exhibited no difference in major atherothrombotic events compared to patients treated with prasugrel or ticagrelor (17.6 events/100 patient-years). In contrast, clopidogrel-treated intermediate and poor metabolizers exhibited significantly higher atherothrombotic event risk compared to prasugrel/ticagrelor-treated patients (adjusted HR 1.56, 95% CI 1.12-2.16, P=0.008). When comparing clopidogrel-treated rapid or ultrarapid metabolizers to normal metabolizers, no difference in atherothrombotic (adjusted HR 0.97, 95% CI 0.73-1.29, P=0.808) or bleeding events (adjusted HR 1.34, 95% CI 0.83-2.17, P=0.224) were observed. In a real-world setting of genotype-guided antiplatelet therapy, the CYP2C19*17 allele did not significantly impact post-PCI prescribing decisions or clinical outcomes. These results suggest the CYP2C19 *1/*17 and *17/*17 genotypes have limited clinical utility to guide antiplatelet therapy after PCI.

PMID: 32897581 [PubMed - as supplied by publisher]

The future of research into genetics and the precision dosing of tacrolimus: what do we need to know?

Pharmacogenomics. 2020 Sep 08;:

Authors: Zhu J, Pasternak AL, Crona DJ

PMID: 32896220 [PubMed - as supplied by publisher]

Gene expression profiling in allopurinol-induced severe cutaneous adverse reactions in Vietnamese.

Pharmacogenomics. 2020 Sep 08;:

Authors: Nguyen DV, Chu HC, Vidal C, Anderson J, Nguyen NN, Quynh Do NT, Tran TL, Nguyen TN, Thu Nguyen HT, Fulton RB, Nunen SV, Fernando S

Abstract
Aim: To examine gene expression in different clinical phenotypes of allopurinol-induced severe cutaneous adverse reactions (SCARs). Materials & methods: Gene expression profiling was performed using microarray on 11 RNA samples (four controls, three hypersensitivity syndrome/drug rash with eosinophilia and systemic symptoms, four Stevens-Johnson syndrome/toxic epidermal necrolysis) followed by quantitative real-time PCR in a total of 11 SCARs patients and 11 controls. Results: The biological pathways which were significantly enriched in differentially expressed genes in Stevens-Johnson syndrome/toxic epidermal necrolysis compared with hypersensitivity syndrome/drug rash with eosinophilia and systemic symptoms patients included; cell surface interactions at the vascular wall, immunoregulatory interactions at the immunological synapse and MyD88 signaling pathways. Overexpression of miR146a occurred in allopurinol-tolerant HLA-B*58:01 carriers. Conclusion: Biological pathways are identified which appear to be implicated in determining clinical phenotypes in allopurinol-induced SCARs. Overexpression of miR146a is potentially important for allopurinol tolerance in HLA-B*58:01 carriers.

PMID: 32896208 [PubMed - as supplied by publisher]

Predictive values of colon microbiota in the treatment response to colorectal cancer.

Pharmacogenomics. 2020 Sep 08;:

Authors: Galan-Ros J, Ramos-Arenas V, Conesa-Zamora P

Abstract
The crosstalk between the colon mucosa and the microbiota represents a complex and delicate equilibrium. Gastrointestinal diseases such as inflammatory bowel disease and colorectal cancer (CRC) are associated with a state of altered microbiota composition known as dysbiosis, which seems to play a causative role in some of these illnesses. Recent reports have shown that the colorectal microbiome is responsible for the response and safety to treatments against CRC, especially immunotherapy, hence opening the possibility to use bacteria as a predictive marker and also as a therapeutic agent. The review objective is to summarize updated reports about the the implication of the colorectal microbiome in the development of CRC, in treatment response and its potential as a therapeutic approach.

PMID: 32896201 [PubMed - as supplied by publisher]

[Pharmacogenomic Research in Direct Oral Anticoagulants].

Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 2020 Aug 30;42(4):562-565

Authors: Liu XM, DU LP, Liu B

Abstract
Oral anticoagulants play an important role in the prevention and treatment of thromboembolic diseases.Warfarin,a traditional oral anticoagulant,is limited in clinical use due to its limitations such as narrow therapeutic window and requirements on frequent monitoring and dose adjustment.Direct oral anticoagulants(DOACs)such as dabigatran,rivaroxaban,apixaban,and edoxaban are increasingly used to prevent and treat venous thrombosis or thrombus formation.However,recent studies have documented inter-individual variability in plasma drug levels of DOACs.This article summarizes the recent advances in the pharmacogenomics of DOACs.

PMID: 32895112 [PubMed - in process]

Pharmacogenetic score predicts overall survival, progression-free survival and platinum sensitivity in ovarian cancer.

Pharmacogenomics. 2020 Sep 08;:

Authors: Gagno S, Bartoletti M, Romualdi C, Poletto E, Scalone S, Sorio R, Zanchetta M, Mattia E, Roncato R, Cecchin E, Giorda G, Toffoli G

Abstract
Aim: To define the impact of polymorphisms in genes involved in platinum-taxane and estrogen activity in the outcome of platinum-based treated ovarian cancer patients (OCP). Patients & Methods: Two hundred and thirty OCP were analyzed for 124 germ-line polymorphisms to generate a prognostic score for overall survival (OS), progression-free survival (PFS) and platinum-free interval (PFI). Results: ABCG2 rs3219191D>I, UGT1A rs10929302G>A and UGT1A rs2741045T>C polymorphisms were significantly associated with all three parameters (OS, PFS and PFI) and were used to generate a score. Patients in high-risk group had a poorer OS (hazard ratio [HR]: 1.8; 95% CI: 1.3-2.7; p = 0.0019), PFS (HR: 2.0; 95% CI: 1.4-2.9; p < 0.0001) and PFI (HR: 1.9; 95% CI: 1.4-2.8; p = 0.0002) compared with those in low-risk group. Conclusion: The prognostic-score including polymorphisms involved in drug and estrogen pathways stratifies OCP according to OS, PFS and PFI.

PMID: 32894980 [PubMed - as supplied by publisher]

The clinical consequences of heterogeneity within and between different diabetes types.

Diabetologia. 2020 Oct;63(10):2040-2048

Authors: Redondo MJ, Hagopian WA, Oram R, Steck AK, Vehik K, Weedon M, Balasubramanyam A, Dabelea D

Abstract
Advances in molecular methods and the ability to share large population-based datasets are uncovering heterogeneity within diabetes types, and some commonalities between types. Within type 1 diabetes, endotypes have been discovered based on demographic (e.g. age at diagnosis, race/ethnicity), genetic, immunological, histopathological, metabolic and/or clinical course characteristics, with implications for disease prediction, prevention, diagnosis and treatment. In type 2 diabetes, the relative contributions of insulin resistance and beta cell dysfunction are heterogeneous and relate to demographics, genetics and clinical characteristics, with substantial interaction from environmental exposures. Investigators have proposed approaches that vary from simple to complex in combining these data to identify type 2 diabetes clusters relevant to prognosis and treatment. Advances in pharmacogenetics and pharmacodynamics are also improving treatment. Monogenic diabetes is a prime example of how understanding heterogeneity within diabetes types can lead to precision medicine, since phenotype and treatment are affected by which gene is mutated. Heterogeneity also blurs the classic distinctions between diabetes types, and has led to the definition of additional categories, such as latent autoimmune diabetes in adults, type 1.5 diabetes and ketosis-prone diabetes. Furthermore, monogenic diabetes shares many features with type 1 and type 2 diabetes, which make diagnosis difficult. These challenges to the current classification framework in adult and paediatric diabetes require new approaches. The 'palette model' and the 'threshold hypothesis' can be combined to help explain the heterogeneity within and between diabetes types. Leveraging such approaches for therapeutic benefit will be an important next step for precision medicine in diabetes. Graphical abstract.

PMID: 32894314 [PubMed - as supplied by publisher]

Extremely low dose of 6-mercaptopurine in a Chinese child with acute lymphoblastic leukaemia and multiple pharmacogenetic mutations.

J Clin Pharm Ther. 2020 Sep 07;:

Authors: Zhai XY, Zhou Y, Dong L, Nie AQ, Zhi LJ, Jacqz-Aigrain E, Wang TY, Wang L, Zhao W

Abstract
WHAT IS KNOWN AND OBJECTIVES: Thiopurines are cornerstone drugs in the treatment of acute lymphoblastic leukaemia (ALL), but their use can be complicated by the incidence of life-threatening leucopenia.
CASE DESCRIPTION: We describe a case of a 6-year-old Chinese boy with B-ALL receiving extremely low dose of 6-mercaptopurine (only 4% of recommended dose) during the ALL maintenance therapy phase.
WHAT IS NEW AND CONCLUSION: Complex pharmacogenetic tests and TDM should be recommended in children with complicated ALL to highlight the large individual variability in the responses to 6-MP exposure and the associated adverse effects.

PMID: 32893890 [PubMed - as supplied by publisher]

Induced pluripotent stem cells to model adverse drug reactions in pediatric patients.

Pharmacogenomics. 2020 Sep 07;:

Authors: Genova E, Stocco G, Decorti G

PMID: 32893744 [PubMed - as supplied by publisher]

Genetics and immunological recovery with antiretroviral treatment for HIV.

Pharmacogenomics. 2020 Sep 07;:

Authors: Veloso Carvalho-Silva WH, Andrade-Santos JL, Dos Santos Guedes MC, Guimarães RL

PMID: 32893739 [PubMed - as supplied by publisher]

The role of pharmacogenomics in personalization of the Parkinson's disease treatment.

Pharmacogenomics. 2020 Sep 07;:

Authors: Redenšek S, Dolžan V

Abstract
Parkinson's disease (PD) related phenotypes can vary among patients substantially, including response to dopaminergic treatment in terms of efficacy and occurrence of adverse events. Many pharmacogenetic studies have already been conducted to find genetic markers of response to dopaminergic treatment. Integration of genetic and clinical data has already resulted in construction of clinical pharmacogenetic models for prediction of adverse events. However, the results of pharmacogenetic studies are inconsistent. More comprehensive genome-wide approaches are needed to find genetic biomarkers of PD-related phenotypes to better explain the variability in response to treatment. These genetic markers should be integrated with clinical, environmental, imaging, and other omics data to build clinically useful algorithms for personalization of PD management.

PMID: 32893736 [PubMed - as supplied by publisher]

Effects of rare CYP2C9 alleles on stable warfarin doses in Chinese Han patients with atrial fibrillation.

Pharmacogenomics. 2020 Sep 07;:

Authors: Wang D, Dai DP, Wu H, Chong J, Lü Y, Yin R, Zhao X, Zhao A, Yang J, Chen H

Abstract
Aim: Gene polymorphisms are critical in warfarin dosing variation. Here, the role of rare CYP2C9 alleles on warfarin doses in Chinese Han patients was investigated. Methods: A retrospective study recruited 681 warfarin treated atrial fibrillation patients. The genetic and clinical data were collected. Dose-related variables were selected by univariate analyses and the warfarin-dosing algorithm was derived by multivariate regression analysis. Results: Three rare CYP2C9 alleles (CYP2C9*13, *16 and *60) were associated with lower stable doses. Inclusion of the rare CYP2C9 alleles in the prediction model added an extra 3.7% warfarin dose predictive power. Conclusion: CYP2C9*13, *16 and *60 was associated with lower stable warfarin doses in Chinese patients. The algorithm including rare CYP2C9 alleles tends to more accurately predict stable warfarin doses.

PMID: 32893731 [PubMed - as supplied by publisher]

Investigation of the impact of an ADCY2 polymorphism as a predictive biomarker in bipolar disorder, suicide tendency and response to lithium carbonate therapy: the first report from Iran.

Pharmacogenomics. 2020 Sep 07;:

Authors: Aghabozorg Afjeh SS, Shams J, Hamednia S, Boshehri B, Olfat A, Omrani MD

Abstract
High rates of mortality due to both suicide and medical comorbidities in bipolar patients can be decreased through the administration of lithium, which affects the cerebral endothelium as well as neurons. To investigate the role of ADCY2 in risk of bipolar disorder, we genotyped the ADCY2 rs2290910 in bipolar patients and healthy controls using amplification refractory mutation system PCR. This polymorphism was associated with risk of bipolar disorder (odds ratio [OR]: 0.430, 95% CI: 0.296-0.624; p = 0.001). The C allele was more frequent in suicide ideation group compared other groups (OR: 2.7, 95% CI: 1.386-5.302; p = 0.004). The T allele was more frequent in suicide attempt group compared with suicide ideation group (OR: 0.238, 95% CI: 0.111-0.509; p = 0.001).

PMID: 32893730 [PubMed - as supplied by publisher]

Combining competitive sequestration with nonlinear hybridization chain reaction amplification: an ultra-specific and highly sensitive sensing strategy for single-nucleotide variants.

Anal Chim Acta. 2020 Sep 15;1130:107-116

Authors: Zhao Y, Feng Y, Zhang Y, Xia P, Xiao Z, Wang Z, Yan H

Abstract
Highly specific and sensitive detection of single-nucleotide variants (SNVs) is of central importance in disease diagnosis and pharmacogenomics. However, it remains a great challenge to successfully detect very low amounts of mutant SNV sequences in real samples in which a SNV sequence may be surrounded by high levels of closely related wild-type sequences. Herein, we propose an ultra-specific and highly sensitive SNV sensing strategy by combining the competitive sequestration with the nonlinear hybridization chain reaction (HCR) amplification. The rationally designed sequestration hairpin can effectively sequester the large amount of wild-type sequence and thus dramatically improve the hybridization specificity in recognizing SNVs. To improve the detection sensitivity, a new fluorescent signal probe is fabricated by intercalating SYBR Green I dye into the nonlinear HCR based DNA dendrimer to further bind with SNVs for signal amplification. The hyperbranched DNA dendrimer possesses large numbers of DNA duplexes for dye intercalation, thus the signal probe shows strong fluorescence intensity, leading to large fluorescence signal amplification. Taking advantage of the improved hybridization specificity of the competitive sequestration and the enhanced fluorescence response of the nonlinear HCR amplification, the developed sensing strategy enables ultra-specific and highly sensitive detection of SNVs. Taking human pancreatic cancers and colorectal carcinomas related KRAS gene mutations as models, the developed strategy shows remarkably high specificity against 17 SNVs (discrimination factors ranged from 126 to 1001 with a median of 310), and achieves high sensitivity for 6 KRAS mutations (the best resultant detection limit reached 15 pM for KRAS G13D (c.38G > A)). Notably, combined with PCR amplification, our SNV sensing strategy could detect KRAS G12D (c.35G > A) from extracted human genomic DNA samples at abundance as low as 0.05%. This work expands the rule set of designing specific and sensitive SNV sensing strategies and shows promising potential application in clinical diagnosis.

PMID: 32892930 [PubMed - in process]

Functional consequences of pravastatin isomerization on OATP1B1 mediated transport.

Drug Metab Dispos. 2020 Sep 05;:

Authors: Wagner JB, Ruggiero M, Leeder JS, Hagenbuch B

Abstract
Pravastatin (PVA) can be isomerized to its inactive metabolite 3'α-iso-pravastatin acid (3αPVA) under acidic pH conditions. Previous studies reported inter-individual differences in circulating concentrations of PVA and 3αPVA. This study investigated the functional consequences of PVA isomerization on OATP1B1-mediated transport. We characterized 3αPVA inhibition of OATP1B1-mediated PVA uptake into HEK293 cells expressing the four different OATP1B1 proteins (*1a, *1b, *5 and *15). 3αPVA inhibited OATP1B1-mediated PVA uptake in all four OATP1B1 gene products but with lower IC50/Ki values for OATP1B1*5 and *15 than for the reference proteins (*1a and *1b). PVA and 3αPVA were transported by all four OATP1B1 proteins. Kinetic experiments revealed that maximal transport rates (Vmax values) for OATP1B1 variants *5 and *15 were lower than for *1a and *1b for both substrates. Apparent affinities for 3αPVA transport were similar for all four variants. However, the apparent affinity of OATP1B1*5 for 3αPVA was higher (lower Km value) than for PVA. These data confirm that PVA conversion to 3αPVA can have functional consequences on PVA uptake and impacts OATP1B1 variants more than the reference protein, thus highlighting another source variation that must be taken into consideration when optimizing the PVA dose-exposure relationship for patients. Significance Statement 3'α-iso-pravastatin acid inhibits pravastatin uptake for all OATP1B1 protein types, however, the IC50 values were significantly lower in OATP1B1*5 and *15 transfected cells. This suggests that a lower concentration of 3'α-iso-pravastatin is needed to disrupt OATP1B1-mediated pravastatin uptake, secondary to decreased cell surface expression of functional OATP1B1 in variant expressing cells. These data will refine previous pharmacokinetic models that are utilized to characterize pravastatin inter-individual variability with an ultimate goal of maximizing efficacy at the lowest possible risk for toxicity.

PMID: 32892153 [PubMed - as supplied by publisher]

Genetic mutations associated with susceptibility to perioperative complications in a longitudinal biorepository with integrated genomic and electronic health records.

Br J Anaesth. 2020 Sep 02;:

Authors: Douville NJ, Kheterpal S, Engoren M, Mathis M, Mashour GA, Hornsby WE, Willer CJ, Douville CB

Abstract
BACKGROUND: Existing genetic information can be leveraged to identify patients with susceptibilities to conditions that might impact their perioperative care, but clinicians generally have limited exposure and are not trained to contextualise this information. We identified patients with genetic susceptibilities to anaesthetic complications using a perioperative biorepository and characterised the concordance with existing diagnoses.
METHODS: Adult patients undergoing surgery within Michigan Medicine from 2012 to 2017 were consented for genotyping. Genotypes were integrated with the electronic health record (EHR). We retrospectively characterised frequencies of variants associated with butyrylcholinesterase deficiency, factor V Leiden, and malignant hyperthermia, three pharmacogenetic factors with perioperative implications. We calculated the percentage homozygous and heterozygous for each that had been diagnosed previously and searched for EHR findings consistent with a predisposition.
RESULTS: Analysis of genetic data revealed that 25 out of 40 769 (0.1%) patients were homozygous and 1918 (4.7%) were heterozygous for mutations associated with butyrylcholinesterase deficiency. Of the homozygous individuals, 14 (56%) carried a pre-existing diagnosis. For factor V Leiden, 29 (0.1%) were homozygous and 2153 (5.3%) heterozygous. Of the homozygous individuals, three (10%) were diagnosed by EHR-derived phenotype and six (21%) by clinician review. Malignant hyperthermia was assessed in a subset of patients. We detected two patients with associated mutations. Neither carried clinical diagnoses.
CONCLUSIONS: We identified patients with genetic susceptibility to perioperative complications using an open source script designed for clinician use. We validated this application in a retrospective analysis for three conditions with well-characterised inheritance, and showed that not all genetic susceptibilities were documented in the EHR.

PMID: 32891412 [PubMed - as supplied by publisher]

Genome-wide Study Identifies Association between HLA-B∗55:01 and Self-Reported Penicillin Allergy.

Am J Hum Genet. 2020 Aug 26;:

Authors: Krebs K, Bovijn J, Zheng N, Lepamets M, Censin JC, Jürgenson T, Särg D, Abner E, Laisk T, Luo Y, Skotte L, Geller F, Feenstra B, Wang W, Auton A, 23andMe Research Team, Raychaudhuri S, Esko T, Metspalu A, Laur S, Roden DM, Wei WQ, Holmes MV, Lindgren CM, Phillips EJ, Mägi R, Milani L, Fadista J

Abstract
Hypersensitivity reactions to drugs are often unpredictable and can be life threatening, underscoring a need for understanding their underlying mechanisms and risk factors. The extent to which germline genetic variation influences the risk of commonly reported drug allergies such as penicillin allergy remains largely unknown. We extracted data from the electronic health records of more than 600,000 participants from the UK, Estonian, and Vanderbilt University Medical Center's BioVU biobanks to study the role of genetic variation in the occurrence of self-reported penicillin hypersensitivity reactions. We used imputed SNP to HLA typing data from these cohorts to further fine map the human leukocyte antigen (HLA) association and replicated our results in 23andMe's research cohort involving a total of 1.12 million individuals. Genome-wide meta-analysis of penicillin allergy revealed two loci, including one located in the HLA region on chromosome 6. This signal was further fine-mapped to the HLA-B∗55:01 allele (OR 1.41 95% CI 1.33-1.49, p value 2.04 × 10-31) and confirmed by independent replication in 23andMe's research cohort (OR 1.30 95% CI 1.25-1.34, p value 1.00 × 10-47). The lead SNP was also associated with lower lymphocyte counts and in silico follow-up suggests a potential effect on T-lymphocytes at HLA-B∗55:01. We also observed a significant hit in PTPN22 and the GWAS results correlated with the genetics of rheumatoid arthritis and psoriasis. We present robust evidence for the role of an allele of the major histocompatibility complex (MHC) I gene HLA-B in the occurrence of penicillin allergy.

PMID: 32888428 [PubMed - as supplied by publisher]

Folate Insufficiency Due to MTHFR Deficiency Is Bypassed by 5-Methyltetrahydrofolate.

J Clin Med. 2020 Sep 02;9(9):

Authors: Vidmar Golja M, Šmid A, Karas Kuželički N, Trontelj J, Geršak K, Mlinarič-Raščan I

Abstract
Adequate levels of folates are essential for homeostasis of the organism, prevention of congenital malformations, and the salvage of predisposed disease states. They depend on genetic predisposition, and therefore, a pharmacogenetic approach to individualized supplementation or therapeutic intervention is necessary for an optimal outcome. The role of folates in vital cell processes was investigated by translational pharmacogenetics employing lymphoblastoid cell lines (LCLs). Depriving cells of folates led to reversible S-phase arrest. Since 5,10-methylenetetrahydrofolate reductase (MTHFR) is the key enzyme in the biosynthesis of an active folate form, we evaluated the relevance of polymorphisms in the MTHFR gene on intracellular levels of bioactive metabolite, the 5-methyltetrahydrofolate (5-Me-THF). LCLs (n = 35) were divided into low- and normal-MTHFR activity groups based on their genotype. They were cultured in the presence of folic acid (FA) or 5-Me-THF. Based on the cells' metabolic activity and intracellular 5-Me-THF levels, we conclude supplementation of FA is sufficient to maintain adequate folate level in the normal MTHFR activity group, while low MTHFR activity cells require 5-Me-THF to overcome the metabolic defects caused by polymorphisms in their MTHFR genes. This finding was supported by the determination of intracellular levels of 5-Me-THF in cell lysates by LC-MS/MS. FA supplementation resulted in a 2.5-fold increase in 5-Me-THF in cells with normal MTHFR activity, but there was no increase after FA supplementation in low MTHFR activity cells. However, when LCLs were exposed to 5-Me-THF, a 10-fold increase in intracellular levels of this metabolite was determined. These findings indicate that patients undergoing folate supplementation to counteract anti-folate therapies, or patients with increased folate demand, would benefit from pharmacogenetics-based therapy choices.

PMID: 32887268 [PubMed - as supplied by publisher]

Author Correction: A co-clinical approach identifies mechanisms and potential therapies for androgen deprivation resistance in prostate cancer.

Nat Genet. 2020 Sep 03;:

Authors: Lunardi A, Ala U, Epping MT, Salmena L, Clohessy JG, Webster KA, Wang G, Mazzucchelli R, Bianconi M, Stack EC, Lis R, Patnaik A, Cantley LC, Bubley G, Cordon-Cardo C, Gerald WL, Montironi R, Signoretti S, Loda M, Nardella C, Pandolfi PP

Abstract
An amendment to this paper has been published and can be accessed via a link at the top of the paper.

PMID: 32884149 [PubMed - as supplied by publisher]

Correction: Pharmacogenomics cascade testing (PhaCT): a novel approacre econd screench for preemptive pharmacogenomics testing to optimize medication therapy.

Pharmacogenomics J. 2020 Sep 03;:

Authors: Roosan D, Hwang A, Roosan MR

Abstract
An amendment to this paper has been published and can be accessed via a link at the top of the paper.

PMID: 32884089 [PubMed - as supplied by publisher]