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1. Fine-mapping of 150 breast cancer risk regions identifies 191 likely target genes

Author

Fachal, L, Aschard, H, Beesley, J, Barnes, DR, Allen, J, Kar, S, Pooley, KA, Dennis, J, Michailidou, K, Turman, C, Soucy, P, Lemaçon, A, Lush, M, Tyrer, JP, Ghoussaini, M, Marjaneh, MM, Jiang, X, Agata, S, Aittomäki, K, Alonso, MR, Andrulis, IL, Anton-Culver, H, Antonenkova, NN, Arason, A, Arndt, V, Aronson, KJ, Arun, BK, Auber, B, Auer, PL, Azzollini, J, Balmaña, J, Barkardottir, RB, Barrowdale, D, Beeghly-Fadiel, A, Benitez, J, Bermisheva, M, Białkowska, K, Blanco, AM, Blomqvist, C, Blot, W, Bogdanova, NV, Bojesen, SE, Bolla, MK, Bonanni, B, Borg, A, Bosse, K, Brauch, H, Brenner, H, Briceno, I, Brock, IW, Brooks-Wilson, A, Brüning, T, Burwinkel, B, Buys, SS, Cai, Q, Caldés, T, Caligo, MA, Camp, NJ, Campbell, I, Canzian, F, Carroll, JS, Carter, BD, Castelao, JE, Chiquette, J, Christiansen, H, Chung, WK, Claes, KBM, Clarke, CL, Mari, V, Berthet, P, Castera, L, Vaur, D, Lallaoui, H, Bignon, YJ, Uhrhammer, N, Bonadona, V, Lasset, C, Révillion, F, Vennin, P, Muller, D, Gomes, DM, Ingster, O, Coupier, I, Pujol, P, Collonge-Rame, MA, Mortemousque, I, Bera, O, Rose, M, Baurand, A, Bertolone, G, Faivre, L, Dreyfus, H, Leroux, D, Venat-Bouvet, L, Bézieau, S, Delnatte, C, Chiesa, J, Gilbert-Dussardier, B, Gesta, P, and Prieur, FP

Subjects
Quantitative Trait Loci, ABCTB Investigators, Breast Neoplasms, Regulatory Sequences, Nucleic Acid, Polymorphism, Single Nucleotide, Medical and Health Sciences, Linkage Disequilibrium, GEMO Study Collaborators, Risk Factors, Breast Cancer, Biomarkers, Tumor, Genetics, Humans, 2.1 Biological and endogenous factors, Genetic Predisposition to Disease, Genetic Testing, Aetiology, Polymorphism, EMBRACE Collaborators, HEBON Investigators, Cancer, Tumor, Nucleic Acid, Prevention, Human Genome, Chromosome Mapping, Bayes Theorem, Single Nucleotide, Biological Sciences, Female, KConFab Investigators, Regulatory Sequences, Biomarkers, Genome-Wide Association Study, Biotechnology, Developmental Biology
Abstract

© 2020, The Author(s), under exclusive licence to Springer Nature America, Inc. Genome-wide association studies have identified breast cancer risk variants in over 150 genomic regions, but the mechanisms underlying risk remain largely unknown. These regions were explored by combining association analysis with in silico genomic feature annotations. We defined 205 independent risk-associated signals with the set of credible causal variants in each one. In parallel, we used a Bayesian approach (PAINTOR) that combines genetic association, linkage disequilibrium and enriched genomic features to determine variants with high posterior probabilities of being causal. Potentially causal variants were significantly over-represented in active gene regulatory regions and transcription factor binding sites. We applied our INQUSIT pipeline for prioritizing genes as targets of those potentially causal variants, using gene expression (expression quantitative trait loci), chromatin interaction and functional annotations. Known cancer drivers, transcription factors and genes in the developmental, apoptosis, immune system and DNA integrity checkpoint gene ontology pathways were over-represented among the highest-confidence target genes.

Published
2020

2. Breast cancer risk variants at 6q25 display different phenotype associations and regulate ESR1, RMND1 and CCDC170

Author

Dunning, AM, Michailidou, K, Kuchenbaecker, KB, Thompson, D, French, JD, Beesley, J, Healey, CS, Kar, S, Pooley, KA, Lopez-Knowles, E, Dicks, E, Barrowdale, D, Sinnott-Armstrong, NA, Sallari, RC, Hillman, KM, Kaufmann, S, Sivakumaran, H, Marjaneh, MM, Lee, JS, Hills, M, Jarosz, M, Drury, S, Canisius, S, KBolla, M, Dennis, J, Wang, Q, LHopper, J, Southey, MC, Broeks, A, Schmidt, MK, Lophatananon, A, Muir, K, Beckmann, MW, Fasching, PA, Dos-Santos-Silva, I, Peto, J, Sawyer, EJ, Tomlinson, I, Burwinkel, B, Marme, F, Guénel, P, Truong, T, Bojesen, SE, Flyger, H, Gonzlez-Neira, A, Perez, JIA, Anton-Culver, H, Eunjung, L, Arndt, V, Brenner, H, Meindl, A, Schmutzler, RK, Brauch, H, Hamann, U, Aittomki, K, Blomqvist, C, Ito, H, Matsuo, K, Bogdanova, N, Dörk, T, Lindblom, A, Margolin, S, Kosma, VM, Mannermaa, A, Tseng, CC, Wu, AH, Lambrechts, D, Wildiers, H, Chang-Claude, J, Rudolph, A, Peterlongo, P, Radice, P, EOlson, J, GGiles, G, and Milne, RL

Abstract

© 2016 Nature America, Inc. We analyzed 3,872 common genetic variants across the ESR1 locus (encoding estrogen receptor α) in 118,816 subjects from three international consortia. We found evidence for at least five independent causal variants, each associated with different phenotype sets, including estrogen receptor (ER + or ER -) and human ERBB2 (HER2 + or HER2 -) tumor subtypes, mammographic density and tumor grade. The best candidate causal variants for ER - tumors lie in four separate enhancer elements, and their risk alleles reduce expression of ESR1, RMND1 and CCDC170, whereas the risk alleles of the strongest candidates for the remaining independent causal variant disrupt a silencer element and putatively increase ESR1 and RMND1 expression.

Published
2016

3. Fine scale mapping of the 17q22 breast cancer locus using dense SNPs, genotyped within the Collaborative Oncological Gene-Environment Study (COGs)

Author

Darabi, H, Beesley, J, Droit, A, Kar, S, Nord, S, Marjaneh, MM, Soucy, P, Michailidou, K, Ghoussaini, M, Wahl, HF, Bolla, MK, Wang, Q, Dennis, J, Alonso, MR, Andrulis, IL, Anton-Culver, H, Arndt, V, Beckmann, MW, Benitez, J, Bogdanova, NV, Bojesen, SE, Brauch, H, Brenner, H, Broeks, A, Bruening, T, Burwinkel, B, Chang-Claude, J, Choi, J-Y, Conroy, DM, Couch, FJ, Cox, A, Cross, SS, Czene, K, Devilee, P, Doerk, T, Easton, DF, Fasching, PA, Figueroa, J, Fletcher, O, Flyger, H, Galle, E, Garcia-Closas, M, Giles, GG, Goldberg, MS, Gonzalez-Neira, A, Guenel, P, Haiman, CA, Hallberg, E, Hamann, U, Hartman, M, Hollestelle, A, Hopper, JL, Ito, H, Jakubowska, A, Johnson, N, Kang, D, Khan, S, Kosma, V-M, Kriege, M, Kristensen, V, Lambrechts, D, Le Marchand, L, Lee, SC, Lindblom, A, Lophatananon, A, Lubinski, J, Mannermaa, A, Manoukian, S, Margolin, S, Matsuo, K, Mayes, R, Mckay, J, Meindl, A, Milne, RL, Muir, K, Neuhausen, SL, Nevanlinna, H, Olswold, C, Orr, N, Peterlongo, P, Pita, G, Pylkaes, K, Rudolph, A, Sangrajrang, S, Sawyer, EJ, Schmidt, MK, Schmutzler, RK, Seynaeve, C, Shah, M, Shen, C-Y, Shu, X-O, Southey, MC, Stram, DO, Surowy, H, Swerdlow, A, Teo, SH, Tessier, DC, Tomlinson, I, Torres, D, Truong, T, Vachon, CM, Vincent, D, Winqvist, R, Wu, AH, Wu, P-E, Yip, CH, Zheng, W, Pharoah, PDP, Hall, P, Edwards, SL, Simard, J, French, JD, Chenevix-Trench, G, Dunning, AM, Darabi, H, Beesley, J, Droit, A, Kar, S, Nord, S, Marjaneh, MM, Soucy, P, Michailidou, K, Ghoussaini, M, Wahl, HF, Bolla, MK, Wang, Q, Dennis, J, Alonso, MR, Andrulis, IL, Anton-Culver, H, Arndt, V, Beckmann, MW, Benitez, J, Bogdanova, NV, Bojesen, SE, Brauch, H, Brenner, H, Broeks, A, Bruening, T, Burwinkel, B, Chang-Claude, J, Choi, J-Y, Conroy, DM, Couch, FJ, Cox, A, Cross, SS, Czene, K, Devilee, P, Doerk, T, Easton, DF, Fasching, PA, Figueroa, J, Fletcher, O, Flyger, H, Galle, E, Garcia-Closas, M, Giles, GG, Goldberg, MS, Gonzalez-Neira, A, Guenel, P, Haiman, CA, Hallberg, E, Hamann, U, Hartman, M, Hollestelle, A, Hopper, JL, Ito, H, Jakubowska, A, Johnson, N, Kang, D, Khan, S, Kosma, V-M, Kriege, M, Kristensen, V, Lambrechts, D, Le Marchand, L, Lee, SC, Lindblom, A, Lophatananon, A, Lubinski, J, Mannermaa, A, Manoukian, S, Margolin, S, Matsuo, K, Mayes, R, Mckay, J, Meindl, A, Milne, RL, Muir, K, Neuhausen, SL, Nevanlinna, H, Olswold, C, Orr, N, Peterlongo, P, Pita, G, Pylkaes, K, Rudolph, A, Sangrajrang, S, Sawyer, EJ, Schmidt, MK, Schmutzler, RK, Seynaeve, C, Shah, M, Shen, C-Y, Shu, X-O, Southey, MC, Stram, DO, Surowy, H, Swerdlow, A, Teo, SH, Tessier, DC, Tomlinson, I, Torres, D, Truong, T, Vachon, CM, Vincent, D, Winqvist, R, Wu, AH, Wu, P-E, Yip, CH, Zheng, W, Pharoah, PDP, Hall, P, Edwards, SL, Simard, J, French, JD, Chenevix-Trench, G, and Dunning, AM

Abstract

Genome-wide association studies have found SNPs at 17q22 to be associated with breast cancer risk. To identify potential causal variants related to breast cancer risk, we performed a high resolution fine-mapping analysis that involved genotyping 517 SNPs using a custom Illumina iSelect array (iCOGS) followed by imputation of genotypes for 3,134 SNPs in more than 89,000 participants of European ancestry from the Breast Cancer Association Consortium (BCAC). We identified 28 highly correlated common variants, in a 53 Kb region spanning two introns of the STXBP4 gene, that are strong candidates for driving breast cancer risk (lead SNP rs2787486 (OR = 0.92; CI 0.90-0.94; P = 8.96 × 10(-15))) and are correlated with two previously reported risk-associated variants at this locus, SNPs rs6504950 (OR = 0.94, P = 2.04 × 10(-09), r(2) = 0.73 with lead SNP) and rs1156287 (OR = 0.93, P = 3.41 × 10(-11), r(2) = 0.83 with lead SNP). Analyses indicate only one causal SNP in the region and several enhancer elements targeting STXBP4 are located within the 53 kb association signal. Expression studies in breast tumor tissues found SNP rs2787486 to be associated with increased STXBP4 expression, suggesting this may be a target gene of this locus.

Published
2016

4. Investigation of association between PFO complicated by cryptogenic stroke and a common variant of the cardiac transcription factor GATA4

Author

Marjaneh, MM, Kirk, EP, Posch, MG, Ozcelik, C, Berger, F, Hetzer, R, Otway, R, Butler, TL, Blue, GM, Griffiths, LR, Fatkin, D, Martinson, JJ, Winlaw, DS, Feneley, MP, Harvey, RP, Marjaneh, MM, Kirk, EP, Posch, MG, Ozcelik, C, Berger, F, Hetzer, R, Otway, R, Butler, TL, Blue, GM, Griffiths, LR, Fatkin, D, Martinson, JJ, Winlaw, DS, Feneley, MP, and Harvey, RP

Abstract

Patent foramen ovale (PFO) is associated with clinical conditions including cryptogenic stroke, migraine and varicose veins. Data from studies in humans and mouse suggest that PFO and the secundum form of atrial septal defect (ASDII) exist in an anatomical continuum of septal dysmorphogenesis with a common genetic basis. Mutations in multiple members of the evolutionarily conserved cardiac transcription factor network, including GATA4, cause or predispose to ASDII and PFO. Here, we assessed whether the most prevalent variant of the GATA4 gene, S377G, was significantly associated with PFO or ASD. Our analysis of world indigenous populations showed that GATA4 S377G was largely Caucasian-specific, and so subjects were restricted to those of Caucasian descent. To select for patients with larger PFO, we limited our analysis to those with cryptogenic stroke in which PFO was a subsequent finding. In an initial study of Australian subjects, we observed a weak association between GATA4 S377G and PFO/Stroke relative to Caucasian controls in whom ASD and PFO had been excluded (OR = 2.16; p = 0.02). However, in a follow up study of German Caucasians no association was found with either PFO or ASD. Analysis of combined Australian and German data confirmed the lack of a significant association. Thus, the common GATA4 variant S377G is likely to be relatively benign in terms of its participation in CHD and PFO/Stroke. © 2011 Moradi Marjaneh et al.

Published
2011

5. Asymptomatic Plasmodium falciparum infection evades triggering a host transcriptomic response.

Author

Prah DA, Dunican C, Amoah LE, Marjaneh MM, Kaforou M, Nordgren A, Jones-Warner W, Aniweh Y, Awandare GA, Cunnington AJ, and Hafalla JC

Subjects
Humans, Plasmodium falciparum genetics, Transcriptome, Asymptomatic Infections, Prevalence, Plasmodium vivax genetics, Malaria, Falciparum, Malaria, Vivax
Abstract

Competing Interests: Declaration of Competing Interest The author declares no competing interests.

Published
2023
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6. Modelling upper respiratory viral load dynamics of SARS-CoV-2.

Author

Challenger JD, Foo CY, Wu Y, Yan AWC, Marjaneh MM, Liew F, Thwaites RS, Okell LC, and Cunnington AJ

Subjects
Antibodies, Viral, Humans, Viral Load, COVID-19, SARS-CoV-2
Abstract

Relationships between viral load, severity of illness, and transmissibility of virus are fundamental to understanding pathogenesis and devising better therapeutic and prevention strategies for COVID-19. Here we present within-host modelling of viral load dynamics observed in the upper respiratory tract (URT), drawing upon 2172 serial measurements from 605 subjects, collected from 17 different studies. We developed a mechanistic model to describe viral load dynamics and host response and contrast this with simpler mixed-effects regression analysis of peak viral load and its subsequent decline. We observed wide variation in URT viral load between individuals, over 5 orders of magnitude, at any given point in time since symptom onset. This variation was not explained by age, sex, or severity of illness, and these variables were not associated with the modelled early or late phases of immune-mediated control of viral load. We explored the application of the mechanistic model to identify measured immune responses associated with the control of the viral load. Neutralising antibodies correlated strongly with modelled immune-mediated control of viral load amongst subjects who produced neutralising antibodies. Our models can be used to identify host and viral factors which control URT viral load dynamics, informing future treatment and transmission blocking interventions., (© 2021. The Author(s).)

Published
2022
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7. The Role of Heat Shock Protein 27 in Carcinogenesis and Treatment of Colorectal Cancer.

Author

Asgharzadeh F, Moradi-Marjaneh R, and Marjaneh MM

Subjects
Humans, Biomarkers, Carcinogenesis, Prognosis, Colorectal Neoplasms drug therapy, Colorectal Neoplasms metabolism, HSP27 Heat-Shock Proteins metabolism
Abstract

The incidence of colorectal cancer (CRC) has significantly increased in recent decades, which has made this disease an important global health issue. Despite many efforts, there is no useful prognostic or diagnostic biomarker for CRC. Heat shock protein 27 (Hsp27) is one of the most studied members of the Hsp family. It has attracted particular attention in CRC pathogenesis since it is involved in fundamental cell functions for cell survival. Evidence shows that Hsp27 plays important role in CRC progression and metastasis. Hsp27 overexpression has been observed in CRC and is suggested to be associated with CRC's poor prognosis. In the present review, we focus on the current knowledge of the role of Hsp27 in CRC carcinogenesis and the underlying mechanisms. In addition, we discuss the value of targeting Hsp27 in CRC treatment., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Published
2022
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8. The Role of Heat Shock Protein 40 in Carcinogenesis and Biology of Colorectal Cancer.

Author

Asgharzadeh F, Moradi-Marjaneh R, and Marjaneh MM

Subjects
Carcinogenesis, HSP40 Heat-Shock Proteins genetics, HSP70 Heat-Shock Proteins metabolism, Humans, Colorectal Neoplasms genetics, Colorectal Neoplasms metabolism, HSP40 Heat-Shock Proteins metabolism
Abstract

Colorectal cancer (CRC) is the third most common cancer worldwide. Despite the enormous amount of effort in the diagnosis and treatment of CRC, the overall survival rate of patients remains low. The precise molecular and cellular basis underlying CRC has not been completely understood yet. Over time, new genes and molecular pathways involved in the pathogenesis of the disease are being identified. The accurate discovery of these genes and signaling pathways are important and urgent missions for the next generation of anticancer therapy research. Chaperone DnaJ, also known as Hsp40 (heat shock protein 40), has been of particular interest in CRC pathogenesis, as it is involved in the fundamental cell activities for maintaining cellular homeostasis. Evidence shows that protein family members of DnaJ/Hsp40 play both roles, enhancing and reducing the growth of CRC cells. In the present review, we focus on the current knowledge of the molecular mechanisms responsible for DnaJ/Hsp40 in CRC carcinogenesis and biology., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Published
2022
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9. Diabetes and COVID-19; a Review of Possible Mechanisms.

Author

Moradi-Marjaneh R, Asgharzadeh F, Khordad E, and Marjaneh MM

Subjects
Humans, SARS-CoV-2, COVID-19, Diabetes Mellitus
Abstract

Coronavirus disease 2019 (SARS-CoV-2) (COVID-19) has recently raised worldwide public health concerns. The available data on COVID-19 in patients with diabetes is limited but generally indicate that there is an increased risk of developing COVID-19 infection in diabetic patients, which ultimately impacts the overall patient's survival. Various aspects might be involved; however, the exact mechanisms and interrelationships between diabetes and the novel COVID-19 have not yet been fully elucidated. This review summarizes the possible mechanisms by which present diabetes predispose individuals to COVID-19 infection, modulates the hostviral interactions and increases the risk of mortality. We hope this review can provide beneficial information for further studies and contribute to improved disease management of diabetic patients with COVID-19., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Published
2021
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10. The Clinical Impact of Quantitative Cell-free DNA, KRAS, and BRAF Mutations on Response to Anti-EGFR Treatment in Patients with Metastatic Colorectal Cancer.

Author

Moradi-Marjaneh R, Asgharzadeh F, Khordad E, and Marjaneh MM

Subjects
Biomarkers, Tumor genetics, Class I Phosphatidylinositol 3-Kinases, Humans, Mutation, Proto-Oncogene Proteins B-raf genetics, Proto-Oncogene Proteins p21(ras) genetics, Cell-Free Nucleic Acids genetics, Colorectal Neoplasms drug therapy, Colorectal Neoplasms genetics
Abstract

Colorectal cancer (CRC) is one of the most common leading causes of cancer death in the world. Although EGFR inhibitors have established efficacy in metastatic colorectal cancer (mCRC), some patients do not respond to this treatment. The EGFR inhibitors' failure and acquired resistance are partly due to KRAS and BRAF mutations. Thus, prognostic biomarkers that help to select eligible patients are highly in demand. To improve patient selection, assessment of mutational status in circulating cell free DNA (cfDNA), which possibly represents the dynamicity of tumor genetic status better than tumor tissue, could be advantageous. This review summarizes the current knowledge of the prognostic value of cfDNA in patients with mCRC treated with EGFR inhibitors with emphasis on the clinical importance of identification of KRAS and BRAF mutations., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Published
2021
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