Dr. Sima Salahshor is the Founder of ScienceHA, Inc., a scientific advisory and project management firm with focus on life sciences and healthcare related projects and programs. She has worked extensively with early-stage as well as larger corporate companies, and has a background in genetics, diagnostics, commercialization, product evaluation and marketing, and industry partnership development. She has over 20 years experience in oncology and clinical research and has published numerous peer-reviewed articles in the areas of cancer research, biomarker discovery and development and diagnostics.
Dr. Salahshor holds a Bachelor degree in Clinical Chemistry, a Master in Molecular Biology and a PhD in Medical Genetics from Karolinska Institute, Sweden, and is a certified Project Management Professional (PMP) with the Project Management Institute (PMI). Currently, she is an adjunct professor at the University of Toronto, Faculty of Medicine, where she designs and coordinates new courses and teaches graduate level students. During her carrier, she has been active serving on a number of boards of director, advisory committees and mentorship programs.
Industry Expertise (9)
Areas of Expertise (9)
Project Management Institute (PMI): PMP Certification, License #1661589
Karolinska Institute: Ph.D., Medical Genetics
Uppsala University: M.Sc., Molecular Biology
University College of Health Science: B.Sc., Clinical Chemistry
- ScienceHA, Inc.
- Department of Laboratory of Medicine & Pathobiology, Faculty of Medicine, U of T
- The Institute for Management & Innovation, University of Toronto Mississauga, I-CUBE
Sample Talks (5)
Genetics and cancer risk factors
Communication of science to the general public is increasingly recognized as one of the responsibilities of scientists and health care professionals. In this session, principles of genetic inheritance, cancer risk factors, diagnostic and prognostic test methodologies and some of the latest treatment options are reviewed. The goal is to communicate scientific information and developments in the field of cancer genetics to promote better understanding of challenges & opportunities in personalized medicine among both professionals and the general public.
To be or not to be a scientist!
Various career paths available to students in science degree programs are reviewed. We also discuss what skills and qualifications are required to succeed in a graduate or postgraduate program and ultimately thrive as a good scientist. This talk was originally prepared for the "Summer Student Research Program" at the Department of Laboratory of Medicine and Pathobiology, Faculty of Medicine, University of Toronto.
Cell signaling pathways involved in carcinogenesis
Cell signaling pathways in normal and cancer cells will be discussed. We also review recent advancement in cancer treatment, novel drugs and their mechanism of action. This lecture is part of a graduate course that is offered at the University of Toronto, Faculty of Medicine.
Picturing Science: An overview of imaging technologies
In the past decades imaging technologies are increasingly used to model the dynamics and structure of biological systems. Biomedical imaging is now an integral part of biological and medical sciences and is used in both clinical practice and research. In this session some of the latest imaging technologies are reviewed.
Genetic diversity and drug resistance
Why some people respond to a treatment while others don’t? What are the mechanisms of drug resistance? How genetic makeup or dynamic genetic changes in cells contribute to drug resistance? Why a person develops tolerance to a drug? How biomarkers can help predict drug response? These are some of the questions that will be discussed in this session.
- Workshop Leader
Cellular Imaging in Pathobiology (Course ID# LMP1006H)
This course explores the powerful intersection of Physics, Biological science, and Imaging technologies. Some of the lectures will be complemented by laboratory sessions demonstrating these systems. As a result, students will have the opportunity for hands-on experience with state-of-the-art optical, electronic, and digital imaging equipment guided by an experienced staff from the University, hospitals, research facilities, government agencies as well as the industry. This course will focus on the theory, application and implementation of different imaging techniques, and more importantly, on application of biological experimentation relevant to modern biological research or clinical biochemical studies and the common real-life research goal in the industry, hospitals and research laboratories.
Signal Transduction Pathways in Normal and Diseased Tissues (Course ID# LMP1503H)
Signalling Pathways in Cancer: Signal transduction mechanisms will be described and illustrated by defects in specific human disease states.
E-cadherin expression and analysis in pancreas tumors.
Comment on: E-cadherin/catenin complex status in solid pseudopapillary tumor of the pancreas.
Esophageal squamous cell carcinoma is frequently associated with poor prognosis, as a result of high levels of lymph node metastasis. So far, very few genetic abnormalities have been associated with this disease, and its molecular etiology remains largely unknown.
This study is the first demonstration of aberrant nuclear localization of E-cadherin protein in solid pseudopapillary tumors of the pancreas. Whilst the exact mechanism is not know and nuclear E-cadherin is not related to tumor aggression, this staining pattern may be of diagnostic value in concert with beta-catenin staining.
Abrogation of the Wnt-signaling pathway is implicated in the carcinogenesis of several malignancies, especially colorectal cancer where up to 90% of cases are thought to have impaired Wnt signaling. It is less frequently involved in conventional ductal pancreatic adenocarcinoma.
To elucidate the biological dysregulation underlying adenoma formation we examined global gene expression profiles of adenomas and corresponding normal mucosa from an FAP patient. Differential expression of the most significant gene identified in this study was further validated by mRNA in situ hybridization, reverse transcriptase PCR and Northern blotting in different sets of adenomas, tumours and cancer cell lines.
The products of the two mammalian Axin genes (Axin1 and its homologue Axin2) are essential for the degradation of beta catenin, a component of Wnt signalling that is frequently dysregulated in cancer cells.
A 67 year old man with a clinical diagnosis of attenuated familial adenomatous polyposis (AFAP) and a past history of synchronous colon cancers in the transverse colon was also found to have an intraductal papillary mucinous neoplasm (IPMN) of the pancreas.
Mutations and diminished expression of the E-cadherin gene (CDH1) have been identified in a number of epithelial malignancies. Although somatic CDH1 mutations were detected in lobular breast cancer with a frequency ranging from 10-56%, CDH1 alterations in more frequent ductal tumors appear to be rare.
We previously reported that the alpha-1 chain of type 11 collagen (COL11A1), not normally expressed in the colon, was up-regulated in stromal fibroblasts in most sporadic colorectal carcinomas. Patients with germline mutations in the APC gene show, besides colonic polyposis, symptoms of stromal fibroblast involvement, which could be related to COL11A1 expression.
Inactivating mutations have been found in the cell-cell adhesion molecule E-cadherin (CDH1), which acts as a tumor suppressor gene in different kinds of cancers, e.g. primarily diffuse gastric cancer and lobular breast cancer.
Endometrial cancer is the most commonly diagnosed cancer of the female reproductive tract in the United States and other western countries. Although several genes may be altered in these cancers, the molecular events in the development of endometrial carcinoma remain poorly defined.
In order to explore the possible role of E-cadherin in familial cancer, 19 familial breast cancer patients, whose tumours demonstrated loss of heterozygosity (LOH) at the E-cadherin locus, were screened for germline mutations.
Immunohistochemical expression analysis of mismatch repair gene products has been suggested for the prediction of hereditary nonpolyposis colorectal cancer (HNPCC) carrier status in cancer families and the selection of microsatellite instability (MSI)-positive tumors in sporadic colorectal cancer. In this study, we aimed to evaluate hMSH2 and hMLH1 immunohistochemistry in familial and sporadic colorectal cancer.
There is evidence supporting a multistep genetic model for colorectal tumorigenesis. In familial adenomatosis polyposis (FAP), the inherited defect is a mutation in the APC gene. The vast majority of all sporadic colorectal cancers also show mutations in the APC gene, and the tumorigenesis in sporadic colorectal cancer and FAP is assumed to involve the same genes.
Hereditary non-polyposis colorectal cancer (HNPCC) is linked to an inherited defect in the DNA mismatch repair system. DNA from HNPCC tumours shows microsatellite instability (MSI).