Samir Amin
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About
Titles
Associate Research Scientist
Biography
I work in the comparative genomics field to decode evolutionary history of spontaneous canine and human glioma. My current research is focused on characterizing and targeting evolutionarily constrained (epi-) genetic elements and underlying tissue-specific selection pressures that can drive brain tumor progression and therapy resistance. | About | CV
Appointments
Neurosurgery
Associate Research ScientistPrimary
Other Departments & Organizations
Education & Training
- Postdoctoral Associate
- The Jackson Laboratory for Genomic Medicine
- PhD
- Baylor College of Medicine, Computational Cancer Biology (2017)
- Graduate Research Assistant
- The UT MD Anderson Cancer Center
- Research Trainee
- Dana-Farber Cancer Institute
- Resident Physician / Hospitalist
- Bhailal Amin General Hospital
- MBBS
- The Maharaja Sayajirao University of Baroda
Research
Publications
Featured Publications
Comparative Molecular Life History of Spontaneous Canine and Human Gliomas
Amin S, Anderson K, Boudreau C, Martinez-Ledesma E, Kocakavuk E, Johnson K, Barthel F, Varn F, Kassab C, Ling X, Kim H, Barter M, Lau C, Ngan C, Chapman M, Koehler J, Long J, Miller A, Miller C, Porter B, Rissi D, Mazcko C, LeBlanc A, Dickinson P, Packer R, Taylor A, Rossmeisl J, Woolard K, Heimberger A, Levine J, Verhaak R. Comparative Molecular Life History of Spontaneous Canine and Human Gliomas. Cancer Cell 2020, 37: 243-257.e7. PMID: 32049048, PMCID: PMC7132629, DOI: 10.1016/j.ccell.2020.01.004.Peer-Reviewed Original ResearchConceptsComparative genomic analysisDNA methylation patternsReceptor tyrosine kinasesCell cycle pathwayGenomic analysisMethylation sequencingLife historyMutational processesTyrosine kinaseHigh similarityHuman gliomasTumorigenic mechanismsHost environmentMutational rateSomatic alterationsSporadic gliomasIDH1 R132Canine gliomasMolecular profileGlioma etiologyHuman pediatricPediatric gliomasTranscriptomeKinaseUnique insightsAnalyses of non-coding somatic drivers in 2,658 cancer whole genomes
Rheinbay E, Nielsen MM, Abascal F, Wala JA, Shapira O, Tiao G, Hornshøj H, Hess JM, Juul RI, Lin Z, Feuerbach L, Sabarinathan R, Madsen T, Kim J, Mularoni L, Shuai S, Lanzós A, Herrmann C, Maruvka YE, Shen C, Amin SB, Bandopadhayay P, Bertl J, Boroevich KA, Busanovich J, Carlevaro-Fita J, Chakravarty D, Chan CWY, Craft D, Dhingra P, Diamanti K, Fonseca NA, Gonzalez-Perez A, Guo Q, Hamilton MP, Haradhvala NJ, Hong C, Isaev K, Johnson TA, Juul M, Kahles A, Kahraman A, Kim Y, Komorowski J, Kumar K, Kumar S, Lee D, Lehmann KV, Li Y, Liu EM, Lochovsky L, Park K, Pich O, Roberts ND, Saksena G, Schumacher SE, Sidiropoulos N, Sieverling L, Sinnott-Armstrong N, Stewart C, Tamborero D, Tubio JMC, Umer HM, Uusküla-Reimand L, Wadelius C, Wadi L, Yao X, Zhang CZ, Zhang J, Haber JE, Hobolth A, Imielinski M, Kellis M, Lawrence MS, von Mering C, Nakagawa H, Raphael BJ, Rubin MA, Sander C, Stein LD, Stuart JM, Tsunoda T, Wheeler DA, Johnson R, Reimand J, Gerstein M, Khurana E, Campbell PJ, López-Bigas N, Weischenfeldt J, Beroukhim R, Martincorena I, Pedersen J, Getz G. Analyses of non-coding somatic drivers in 2,658 cancer whole genomes. Nature 2020, 578: 102-111. PMID: 32025015, PMCID: PMC7054214, DOI: 10.1038/s41586-020-1965-x.Peer-Reviewed Original ResearchConceptsInternational Cancer Genome ConsortiumStructural variantsPoint mutationsDriver discoveryProtein-coding genesNon-coding genesNon-coding regionsPan-cancer analysisDriver point mutationsSomatic driversCancer Genome AtlasRegulatory sequencesCancer genomesUntranslated regionGenome ConsortiumFocal deletionsGenesGenome AtlasGenomeNovel candidatesMutationsRecurrent breakpointsRegion of TP53DiscoveryVariantsSystematic analysis of telomere length and somatic alterations in 31 cancer types
Barthel F, Wei W, Tang M, Martinez-Ledesma E, Hu X, Amin S, Akdemir K, Seth S, Song X, Wang Q, Lichtenberg T, Hu J, Zhang J, Zheng S, Verhaak R. Systematic analysis of telomere length and somatic alterations in 31 cancer types. Nature Genetics 2017, 49: 349-357. PMID: 28135248, PMCID: PMC5571729, DOI: 10.1038/ng.3781.Peer-Reviewed Original ResearchTruncating PREX2 mutations activate its GEF activity and alter gene expression regulation in NRAS-mutant melanoma
Lissanu Deribe Y, Shi Y, Rai K, Nezi L, Amin S, Wu C, Akdemir K, Mahdavi M, Peng Q, Chang Q, Hornigold K, Arold S, Welch H, Garraway L, Chin L. Truncating PREX2 mutations activate its GEF activity and alter gene expression regulation in NRAS-mutant melanoma. Proceedings Of The National Academy Of Sciences Of The United States Of America 2016, 113: e1296-e1305. PMID: 26884185, PMCID: PMC4780599, DOI: 10.1073/pnas.1513801113.Peer-Reviewed Original ResearchConceptsPREX2 mutationsCross-species gene expression analysisGuanine nucleotide exchange factor activityNucleotide exchange factor activityGene expression regulationPI3K/PTEN/Akt pathwayExchange factor activityMelanoma developmentPTEN/AKT pathwayCell cycle regulatorsGene expression analysisExpression regulationGEF activityCytoskeleton organizationCDKN1C geneRegulatory regionsExpression analysisGene expressionCycle regulatorsDNA hypomethylationCell cycleChromosome 11Tumor suppressorBiological pathwaysMechanistic basisThe Cancer Genome Atlas Pan-Cancer analysis project
Chang K, Creighton C, Davis C, Donehower L, Drummond J, Wheeler D, Ally A, Balasundaram M, Birol I, Butterfield Y, Chu A, Chuah E, Chun H, Dhalla N, Guin R, Hirst M, Hirst C, Holt R, Jones S, Lee D, Li H, Marra M, Mayo M, Moore R, Mungall A, Robertson A, Schein J, Sipahimalani P, Tam A, Thiessen N, Varhol R, Beroukhim R, Bhatt A, Brooks A, Cherniack A, Freeman S, Gabriel S, Helman E, Jung J, Meyerson M, Ojesina A, Pedamallu C, Saksena G, Schumacher S, Tabak B, Zack T, Lander E, Bristow C, Hadjipanayis A, Haseley P, Kucherlapati R, Lee S, Lee E, Luquette L, Mahadeshwar H, Pantazi A, Parfenov M, Park P, Protopopov A, Ren X, Santoso N, Seidman J, Seth S, Song X, Tang J, Xi R, Xu A, Yang L, Zeng D, Auman J, Balu S, Buda E, Fan C, Hoadley K, Jones C, Meng S, Mieczkowski P, Parker J, Perou C, Roach J, Shi Y, Silva G, Tan D, Veluvolu U, Waring S, Wilkerson M, Wu J, Zhao W, Bodenheimer T, Hayes D, Hoyle A, Jeffreys S, Mose L, Simons J, Soloway M, Baylin S, Berman B, Bootwalla M, Danilova L, Herman J, Hinoue T, Laird P, Rhie S, Shen H, Triche T, Weisenberger D, Carter S, Cibulskis K, Chin L, Zhang J, Getz G, Sougnez C, Wang M, Saksena G, Carter S, Cibulskis K, Chin L, Zhang J, Getz G, Dinh H, Doddapaneni H, Gibbs R, Gunaratne P, Han Y, Kalra D, Kovar C, Lewis L, Morgan M, Morton D, Muzny D, Reid J, Xi L, Cho J, DiCara D, Frazer S, Gehlenborg N, Heiman D, Kim J, Lawrence M, Lin P, Liu Y, Noble M, Stojanov P, Voet D, Zhang H, Zou L, Stewart C, Bernard B, Bressler R, Eakin A, Iype L, Knijnenburg T, Kramer R, Kreisberg R, Leinonen K, Lin J, Liu Y, Miller M, Reynolds S, Rovira H, Shmulevich I, Thorsson V, Yang D, Zhang W, Amin S, Wu C, Wu C, Akbani R, Aldape K, Baggerly K, Broom B, Casasent T, Cleland J, Creighton C, Dodda D, Edgerton M, Han L, Herbrich S, Ju Z, Kim H, Lerner S, Li J, Liang H, Liu W, Lorenzi P, Lu Y, Melott J, Mills G, Nguyen L, Su X, Verhaak R, Wang W, Weinstein J, Wong A, Yang Y, Yao J, Yao R, Yoshihara K, Yuan Y, Yung A, Zhang N, Zheng S, Ryan M, Kane D, Aksoy B, Ciriello G, Dresdner G, Gao J, Gross B, Jacobsen A, Kahles A, Ladanyi M, Lee W, Lehmann K, Miller M, Ramirez R, Rätsch G, Reva B, Sander C, Schultz N, Senbabaoglu Y, Shen R, Sinha R, Sumer S, Sun Y, Taylor B, Weinhold N, Fei S, Spellman P, Benz C, Carlin D, Cline M, Craft B, Ellrott K, Goldman M, Haussler D, Ma S, Ng S, Paull E, Radenbaugh A, Salama S, Sokolov A, Stuart J, Swatloski T, Uzunangelov V, Waltman P, Yau C, Zhu J, Hamilton S, Getz G, Sougnez C, Abbott S, Abbott R, Dees N, Delehaunty K, Ding L, Dooling D, Eldred J, Fronick C, Fulton R, Fulton L, Kalicki-Veizer J, Kanchi K, Kandoth C, Koboldt D, Larson D, Ley T, Lin L, Lu C, Magrini V, Mardis E, McLellan M, McMichael J, Miller C, O'Laughlin M, Pohl C, Schmidt H, Smith S, Walker J, Wallis J, Wendl M, Wilson R, Wylie T, Zhang Q, Burton R, Jensen M, Kahn A, Pihl T, Pot D, Wan Y, Levine D, Black A, Bowen J, Frick J, Gastier-Foster J, Harper H, Helsel C, Leraas K, Lichtenberg T, McAllister C, Ramirez N, Sharpe S, Wise L, Zmuda E, Chanock S, Davidsen T, Demchok J, Eley G, Felau I, Ozenberger B, Sheth M, Sofia H, Staudt L, Tarnuzzer R, Wang Z, Yang L, Zhang J, Omberg L, Margolin A, Raphael B, Vandin F, Wu H, Leiserson M, Benz S, Vaske C, Noushmehr H, Knijnenburg T, Wolf D, Veer L, Collisson E, Anastassiou D, Yang T, Lopez-Bigas N, Gonzalez-Perez A, Tamborero D, Xia Z, Li W, Cho D, Przytycka T, Hamilton M, McGuire S, Nelander S, Johansson P, Jörnsten R, Kling T, Sanchez J. The Cancer Genome Atlas Pan-Cancer analysis project. Nature Genetics 2013, 45: 1113-1120. PMID: 24071849, PMCID: PMC3919969, DOI: 10.1038/ng.2764.Peer-Reviewed Original ResearchIntegrating Gene and Mir Expression Profiles and Regulatory Network Structures to Define Aberrent Feed Forward Loops with Functional and Clinical Implications in Myeloma.
Fulciniti M, Li Y, Wang X, Samur M, Yan Z, Amin S, Li C, Anderson K, Munshi N. Integrating Gene and Mir Expression Profiles and Regulatory Network Structures to Define Aberrent Feed Forward Loops with Functional and Clinical Implications in Myeloma. Blood 2012, 120: 2386. DOI: 10.1182/blood.v120.21.2386.2386.Peer-Reviewed Original ResearchFeed-forward loopRegulatory network structureGene/sGene expressionExpression profilesMiR expression profilesGene expression profile analysisNormal plasma cellsLarge regulatory networkExpression profile analysisOncogenic effectsExpression profile dataMaster TFsNegative feedback regulationRegulatory networksOncogenomic analysisDifferential genesRegulatory loopMolecular impactHeterogeneous genetic backgroundMiRNA expressionFeedback regulationMiR profilesGenetic backgroundMalignant phenotypeGene expression profile alone is inadequate in predicting complete response in multiple myeloma
Amin S, Yip W, Minvielle S, Broyl A, Li Y, Hanlon B, Swanson D, Shah P, Moreau P, van der Holt B, van Duin M, Magrangeas F, Pieter Sonneveld P, Anderson K, Li C, Avet-Loiseau H, Munshi N. Gene expression profile alone is inadequate in predicting complete response in multiple myeloma. Leukemia 2014, 28: 2229-2234. PMID: 24732597, PMCID: PMC4198516, DOI: 10.1038/leu.2014.140.Peer-Reviewed Original Research
2022
Glioma progression is shaped by genetic evolution and microenvironment interactions
Varn F, Johnson K, Martinek J, Huse J, Nasrallah M, Wesseling P, Cooper L, Malta T, Wade T, Sabedot T, Brat D, Gould P, Wöehrer A, Aldape K, Ismail A, Sivajothi S, Barthel F, Kim H, Kocakavuk E, Ahmed N, White K, Datta I, Moon H, Pollock S, Goldfarb C, Lee G, Garofano L, Anderson K, Nehar-Belaid D, Barnholtz-Sloan J, Bakas S, Byrne A, D’Angelo F, Gan H, Khasraw M, Migliozzi S, Ormond D, Paek S, Van Meir E, Walenkamp A, Watts C, Weiss T, Weller M, Palucka K, Stead L, Poisson L, Noushmehr H, Iavarone A, Verhaak R, Consortium T, Varn F, Johnson K, Martinek J, Huse J, Nasrallah M, Wesseling P, Cooper L, Malta T, Wade T, Sabedot T, Brat D, Gould P, Wöehrer A, Aldape K, Ismail A, Sivajothi S, Barthel F, Kim H, Kocakavuk E, Ahmed N, White K, Datta I, Moon H, Pollock S, Goldfarb C, Lee G, Garofano L, Anderson K, Nehar-Belaid D, Barnholtz-Sloan J, Bakas S, Byrne A, D’Angelo F, Gan H, Khasraw M, Migliozzi S, Ormond D, Paek S, Van Meir E, Walenkamp A, Watts C, Weiss T, Weller M, Alfaro K, Amin S, Ashley D, Bock C, Brodbelt A, Bulsara K, Castro A, Connelly J, Costello J, de Groot J, Finocchiaro G, French P, Golebiewska A, Hau A, Hong C, Horbinski C, Kannan K, Kouwenhoven M, Lasorella A, LaViolette P, Ligon K, Lowman A, Mehta S, Miletic H, Molinaro A, Ng H, Niclou S, Niers J, Phillips J, Rabadan R, Rao G, Reifenberger G, Sanai N, Short S, Smitt P, Sloan A, Smits M, Snyder J, Suzuki H, Tabatabai G, Tanner G, Tomaszewski W, Wells M, Westerman B, Wheeler H, Xie J, Yung W, Zadeh G, Zhao J, Palucka K, Stead L, Poisson L, Noushmehr H, Iavarone A, Verhaak R. Glioma progression is shaped by genetic evolution and microenvironment interactions. Cell 2022, 185: 2184-2199.e16. PMID: 35649412, PMCID: PMC9189056, DOI: 10.1016/j.cell.2022.04.038.Peer-Reviewed Original ResearchConceptsSpecific ligand-receptor interactionsMicroenvironment interactionsDNA sequencing dataGlioma progressionLigand-receptor interactionsNeoplastic cellsSignaling programsCell statesSequencing dataGenetic evolutionGenetic changesIDH wild-type tumorsIsocitrate dehydrogenaseMesenchymal transitionSomatic alterationsDistinct mannerActive tumor growthIDH-mutant gliomasPotential targetTherapy resistanceAdult patientsDisease progressionPossible roleCellsTumor growthLive-Cell Imaging Shows Uneven Segregation of Extrachromosomal DNA Elements and Transcriptionally Active Extrachromosomal DNA Hubs in Cancer
Yi E, Gujar A, Guthrie M, Kim H, Zhao D, Johnson K, Amin S, Costa M, Yu Q, Das S, Jillette N, Clow P, Cheng A, Verhaak R. Live-Cell Imaging Shows Uneven Segregation of Extrachromosomal DNA Elements and Transcriptionally Active Extrachromosomal DNA Hubs in Cancer. Cancer Discovery 2022, 12: 468-483. PMID: 34819316, PMCID: PMC8831456, DOI: 10.1158/2159-8290.cd-21-1376.Peer-Reviewed Original ResearchConceptsExtrachromosomal DNA elementsDNA elementsUneven segregationRNA polymerase IILive-cell imagingPolymerase IIOffspring cellsGene transcriptionCell line modelsEcDNAsRandom segregationGenetic materialLiving cellsCopy numberLive cellsIndividual cellsTumor evolutionMitosisInheritance patternBreakpoint sequencesIssue featureTranscriptionFluorescent markersPatient tissuesCells
2021
Reprogramming of bivalent chromatin states in NRAS mutant melanoma suggests PRC2 inhibition as a therapeutic strategy
Terranova C, Tang M, Maitituoheti M, Raman A, Ghosh A, Schulz J, Amin S, Orouji E, Tomczak K, Sarkar S, Oba J, Creasy C, Wu C, Khan S, Lazcano R, Wani K, Singh A, Barrodia P, Zhao D, Chen K, Haydu L, Wang W, Lazar A, Woodman S, Bernatchez C, Rai K. Reprogramming of bivalent chromatin states in NRAS mutant melanoma suggests PRC2 inhibition as a therapeutic strategy. Cell Reports 2021, 36: 109410. PMID: 34289358, PMCID: PMC8369408, DOI: 10.1016/j.celrep.2021.109410.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell Line, TumorCell ProliferationChromatinEnhancer of Zeste Homolog 2 ProteinFemaleGTP PhosphohydrolasesHistonesHumansMelanocytesMelanomaMembrane ProteinsMesodermMice, NudeMitogen-Activated Protein Kinase KinasesMutationNeoplasm MetastasisPolycomb Repressive Complex 2Transcription, GeneticTumor BurdenConceptsHistone H3 lysine 27 trimethylationH3 lysine 27 trimethylationBivalent chromatin stateCell identity genesLysine 27 trimethylationKey epigenetic alterationsNRAS mutantsMaster transcription factorBivalent domainsChromatin statePRC2 inhibitionEpigenetic elementsTranscription factorsEpigenetic alterationsGenetic driversMesenchymal phenotypeNRAS-mutant melanomaState profilingTherapeutic vulnerabilitiesInvasive capacityPharmacological inhibitionMutantsTherapeutic strategiesMelanoma samplesMutant melanoma patients