Mr. Jamie Magrill, BSc - The Hebrew University of Jerusalem - Graduate Research Assistant

Mr. Jamie Magrill

BSc

The Hebrew University of Jerusalem

Graduate Research Assistant

Jerusalem | Israel

Main Specialties: Biology

ORCID logohttps://orcid.org/0000-0003-0124-7323


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Mr. Jamie Magrill, BSc - The Hebrew University of Jerusalem - Graduate Research Assistant

Mr. Jamie Magrill

BSc

Introduction

Bilingual Bachelor of Science, Honours in Biology with Distinction, graduated from the University of British Columbia with a focus on Cancer, Pathology and Diabetes research. Experience working in highly focused research environments including at the UBC Life Sciences Institute investigating the relationship between pancreatic cancer and diabetes via precursor lesion formation in mouse models with differing endogenous insulin levels, and at IMRIC investigating epigenetic transmission of diabetes and the metabolic syndrome. Previous experience at the Vancouver Prostate Center working on Notch signalling pathways in bladder cancer, and at the BC Cancer Agency with the BC Ovarian Cancer Research Team, investigating and validating clinically applicable molecular-based classification systems for endometrial and ovarian carcinoma subtypes. Enthusiastic and experienced researcher with a desire to pursue a degree in medicine, while seeking new opportunities and challenges in the fields of Biomedical and Cancer Research. Extensive experience with aquatic emergencies, rapid-response first aid in fast-paced, team-based environments. Enthusiastic volunteer, involved with special needs children swim programs, handicapped and special needs adults through adaptive swim programs, knowledgeable in teaching strategies and human kinetics in aquatic environments. Passionate about STEM Outreach and Education, working with Let's Talk Science UBC, Genome BC, the Vancouver Public Library and other STEM non-profits to bring science to the general public. Constantly striving to improve and exceed expectations.

Primary Affiliation: The Hebrew University of Jerusalem - Jerusalem , Israel

Specialties:

Research Interests:


View Mr. Jamie Magrill’s Resume / CV

Education

May 2018
University of British Columbia
Hon BSc

Experience

Aug 2018
Israel Student Research Scholarship
Research Assistant
$2000 CAD
May 2018
NSERC Undergraduate Student Research Award (USRA)
Research Assistant
$4500 CAD
May 2016
UBC Faculty of Medicine Summer Student Research Program Award (SSRP)
Co-op Student
$2800 CAD

Publications

7Publications

139Reads

10Profile Views

Endogenous Hyperinsulinemia Contributes to Pancreatic Cancer Development.

Cell Metab 2019 Sep 1;30(3):403-404. Epub 2019 Aug 1.

Department of Cellular and Physiological Sciences, Life Sciences Institute, University of British Columbia, Vancouver, BC, Canada. Electronic address:

The incidence of cancers, including pancreatic ductal adenocarcinoma (PDAC), continues to rise alongside the global obesity and diabetes epidemics. This rise suggests that factors modulated by environment or lifestyle play a key role, but the mechanisms by which obesity and type 2 diabetes promote cancer remain unclear. Obesity and type 2 diabetes are associated with elevations in circulating insulin and glucose, as well as systemic low grade inflammation, which have been proposed to contribute to cancer initiation or progression. Primary hyperinsulinemia, defined as circulating insulin in excess of what is required for glucose homeostasis and independent of insulin resistance, can be found in 30% of obese adults (Trico et al., 2018). Hyperinsulinemia is associated with PDAC, independent of BMI (Tsujimoto et al., 2017). Nevertheless, the cause and effect relationship between hyperinsulinemia and cancer remains to be determined directly.

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http://dx.doi.org/10.1016/j.cmet.2019.07.003DOI Listing
September 2019
55 Reads
20.565 Impact Factor

Expression of L1 retrotransposon open reading frame protein 1 (L1ORF1p) in gynecologic cancers.

Hum Pathol 2019 Jun 17. Epub 2019 Jun 17.

Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, BC, Canada; Department of Molecular Oncology, BC Cancer Agency, Vancouver, BC, Canada. Electronic address:

LINE-1 (L1) retrotransposons are mobile genetic elements capable of "copy-and-pasting" their own sequences into random genomic loci and one of the proteins it uses to achieve mobility is LINE-1 open reading frame 1 protein (L1ORF1p). L1ORF1p expression is found across many epithelial cancers, including small cohorts of ovarian and endometrial cancers, and is highly expressed in cancers with mutant p53 expressions. Here we aimed to gain insights into L1ORF1p expression levels within specific histotypes of ovarian cancers: high grade serous (n=585), low grade serous (n=26), clear cell (n=132), endometrioid (n=148), and mucinous (n=32) ovarian cancers, as well as endometrial cancers (n=607) using tissue microarray (TMA's). We demonstrated that L1ORF1p expression is associated with advanced stage and serous histotype in gynecological cancers. Like previous studies, we found a higher proportion of L1ORF1p expression in cases with aberrant p53 expression. We evaluated the expression of L1ORF1p in serous tubal intraepithelial carcinomas (STICs) (n=6) and p53 signature lesions (n=2) in fallopian tubes. Three STIC cases displayed aberrant p53 overexpression with corresponding L1ORF1p expression in the same tissues, but such correlation was not seen in the two p53 signature lesions, suggesting that L1 protein may be expressed after dysplastic transformation. The remaining three STIC cases have TP53 nonsense mutations with absent p53 expression but a strong and clear L1ORF1p expression within the STIC lesions. While L1ORF1p may not be prognostic in gynecological cancers, it may be useful clinically as a diagnostic IHC marker for p53 null STIC lesions and this warrants further investigation.

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http://dx.doi.org/10.1016/j.humpath.2019.06.001DOI Listing
June 2019
13 Reads
3.014 Impact Factor

DICER1 hot-spot mutations in ovarian gynandroblastoma.

Histopathology 2018 Aug 5;73(2):306-313. Epub 2018 Jun 5.

Institute of Pathology, Medizin Campus Bodensee, Friedrichshafen, Germany.

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http://dx.doi.org/10.1111/his.13630DOI Listing
August 2018
12 Reads
3.453 Impact Factor

Tubo-Ovarian Transitional Cell Carcinoma and High-grade Serous Carcinoma Show Subtly Different Immunohistochemistry Profiles.

Int J Gynecol Pathol 2018 Jul 27. Epub 2018 Jul 27.

British Columbia Cancer Agency (J.M., A.N.K., A.T., D.C., D.G.H.) Department of Pathology, University of British Columbia (A.N.K., B.T.-C., C.C., A.C., C.B.G., D.G.H.), Vancouver, British Columbia, Canada Memorial Sloan Kettering Cancer Center, New York, New York (R.S.) Department of Pathology, Maastricht University Medical Center, Maastricht, The Netherlands (S.H.) Department of Women's Health, Tübingen University Hospital, Tübingen (S.K.) Department of Gynecologic Oncology, Kliniken Essen Mitte, Essen (A.D.B.) Gynecologic Oncology Center, Kiel (J.P.) Institute of Pathology, Friedrichshafen (F.K.), Germany.

Tubo-ovarian transitional cell carcinoma (TCC) is grouped with high-grade serous carcinoma (HGSC) in the current World Health Organization classification. TCC is associated with BRCA mutations and a better prognosis compared with HGSC. Previous papers examining the immunohistochemical features of TCC have studied limited numbers of samples. No marker reflecting the biological difference between TCC and HGSC is known. We collected a large cohort of TCC to determine whether TCC and HGSC could be distinguished by immunohistochemistry. A tissue microarray was built from 89 TCC and a control cohort of 232 conventional HGSC. Immunohistochemistry was performed, scored, and statistically analyzed for routine markers of HGSC and urothelial tumors: PAX8, WT1, p53, p16, ER, p63, and GATA3. Using scoring cutoffs commonly employed in clinical practice, the immunohistochemical profile of TCC was indistinguishable from HGSC for all markers. However, more detailed scoring criteria revealed statistically significant differences between the 2 groups of tumors with respect to ER, PAX8, and WT1. HGSC showed more diffuse and intense staining for PAX8 (P=0.004 and 0.001, respectively) and WT1 (P=0.002 and 0.002, respectively); conversely, TCC showed more intense staining for ER (P=0.007). TCC and HGSC therefore show subtle differences in their immunohistochemical profiles which might reflect underlying (epi)genetic differences. Further studies using proteomic analysis will focus on the identification of differentially expressed proteins that might serve as markers of TCC-like differentiation, which could help explain biologic differences between TCC and HGSC and might identify other cases of HGSC with a better prognosis.

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http://dx.doi.org/10.1097/PGP.0000000000000538DOI Listing
July 2018
28 Reads
2.006 Impact Factor

Final validation of the ProMisE molecular classifier for endometrial carcinoma in a large population-based case series.

Ann Oncol 2018 05;29(5):1180-1188

Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, Canada.

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http://dx.doi.org/10.1093/annonc/mdy058DOI Listing
May 2018
3 Reads
7.040 Impact Factor

Evaluation of endometrial carcinoma prognostic immunohistochemistry markers in the context of molecular classification.

J Pathol Clin Res 2017 Oct 14;3(4):279-293. Epub 2017 Oct 14.

BC Cancer AgencyVancouverBCCanada.

Molecular subclassification of endometrial carcinoma (EC) with Proactive Molecular Risk Classifier for Endometrial Cancer (ProMisE) identifies four subtypes [DNA polymerase epsilon () mutant, mismatch repair-deficient, p53 wild-type (wt), and p53 abnormal]. The aim of this study was to evaluate additional EC biomarkers in the context of these subtypes. Tissue microarrays encompassing 460 previously characterized ECs were assessed for L1-cell adhesion molecule (L1CAM), progesterone receptor (PR), estrogen receptor (ER) alpha, stathmin, and phosphatase and tensin homolog (PTEN), by immunohistochemistry (IHC). Associations with clinicopathological parameters, molecular subtype, and outcomes were determined. About 413 ECs (75% endometrioid, >15% serous) had complete data. L1CAM overexpression was found in 16%, associated with older age, lower body mass index (BMI), advanced stage, grade 3 (97%), non-endometrioid histology (84%), deep myometrial invasion, lymphovascular space invasion (LVSI), and ER-negative, PR-negative status. Tumours overexpressing L1CAM were associated with poor outcomes {hazard ratio (HR) [95% confidence interval (CI)] 3.35 [2.10-5.23] for disease-specific survival [DSS], ?

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http://dx.doi.org/10.1002/cjp2.82DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5653931PMC
October 2017
19 Reads
6.253 Impact Factor

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University of British Columbia

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