Publications

Conferences

Abstract Profiling the classes of the RNA silencing, also known as RNA interference, is an essential mechanism in plants, animals and fungi that functions in gene regulation and defense against foreign nucleic acids. In fungi, RNA silencing has been shown to function primarily in defense against invasive nucleic acids. RNA-silencing- deficient fungi show increased susceptibility to virus infection. Little is known about the classes of RNA editing in virus- derived small RNA which will teach us the nature of self-nonself recognition and ways to modulate RNA modification to control fungal infections.

Abstract ProfilingRNA silencing, also known as RNA interference, is an essential mechanism in plants, animals and fungi that functions in gene regulation and defense against foreign nucleic acids. In fungi, RNA silencing has been shown to function primarily in defense against invasive nucleic acids. RNA-silencing- deficient fungi show increased susceptibility to virus infection. Plant pathogenic fungi also utilize RNA silencing to silence plant host immunity genes through the delivery of fungal small RNAs into plants.

Abstract Background : Gene and mutation discovery in cancers is typically performed by sequencing somatic and germline samples from the same individuals and subtracting germline mutations. However, in biobanked acute myeloid leukaemia (AML) samples, matched germline DNA is frequently unavailable. When germline samples are available, sequencing both germline and somatic samples for each patient significantly increases costs. This study explores whether it is possible to utilise unrelated germline controls to identify ocogenic drivers.

Abstract Mutations of the RAS family of genes are frequent events in AML, occurring in 10% of children and 10-20% of adults. NRASmutations promote proliferation through activation of the Ras/Raf/MEK/ERK signalling pathway. Several MEK inhibitors have shown promising pre-clinical activity in AML, with a number of compounds currently in adult phase I/II clinical trials, including AZD6244, GSK1120212 and AS703026. Given not all patients respond to MEK inhibitor treatment we undertook a comprehensive preclinical evaluation of MEK inhibitors in AML and developed a clinically relevant model of resistance.

Abstract Whole exome sequencing (WES) can detect a high proportion of cancer causing genetic mutations, and therefore has the potential to replace targeted molecular assays and identify additional novel, patient-specific mutations. To test the ability of WES to detect variants of clinical consequence, we compared WES findings to results for FLT3-ITD and NPM1mut obtained by routine pathology testing (high-resolution fragment analysis (HRFA) and Matrix Assisted Laser Desorption/Ionization – Time of Flight Mass Spectrometry (MALDI-TOF) respectively), and to point mutation findings in DNMT3A, IDH1/2, JAK2, KRAS, NRAS and MPL, as determined by Sequenom, across a cohort of 188 AML samples from adults (n = 144) and children (n = 44).

Impact/Awards


Awards


Research Grants

• University of Nebraska-Lincoln travel grants ($1500, FY 2014)

• Center for Excellence in Drought Tolerance Research (CEDTR)-USDA/NIFA (#SA1100029): Identification and characterization of mitogen-activated protein kinases (MAPKs) involved in root nodulation in Glycine max. ($4000, FY 2012/2013).

• MERCK/ AAAS: Anticancer activity of novel ionic triorganotin derivatives against MDA-MB 231 breast cancer cells. ($5000, FY2009).

Awards

• Sigma Xi Masters Research Paper, South Dakota State University, (2012)

• Dean’s List Honoree, University of the District of Columbia, (2006-2009)

• United Nations Mission in Nepal (UNMIN) Scholarship (2002)


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