Sima Salahshor
Strategic Advisor | Life Sciences & HealthTech Program Management Shiruy, Inc | University of Toronto, Faculty of Medicine
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Biography
Strategic Advisor | Life Sciences & HealthTech Program Management
Dr. Sima Salahshor is an experienced strategist and the Principal at Shiruy, Inc., offering expert strategic program advice and scientific due diligence for the life sciences and healthcare sectors. With a PhD in Medical Genetics from the Karolinska Institute and a PMP certification, she bridges the gap between complex science and commercial implementation.
Dr. Salahshor specializes in leading projects in Oncology, Biomarkers, and Diagnostics, with extensive expertise in Medical Affairs, clinical trials, and the development of medical guidelines and policies. Her portfolio includes advising on HealthTech innovations, such as AI-powered health apps and Medical Devices (SaMD), ensuring their technical feasibility and market readiness.
As a trusted partner for healthcare investment firms and early-to-late-stage pharma, she provides comprehensive product evaluation, marketing strategy, and commercialization roadmaps. Her clinical background is grounded in years of oncology research at renowned institutions such as Princess Margaret Hospital and the Lunenfeld-Tanenbaum Research Institute, where she concentrated on the molecular biology of solid tumors.
Currently an Adjunct Professor at the University of Toronto, Dr. Salahshor also contributes to medical education, mentorship, and patient advocacy, ensuring that health technology and genetic innovations lead to meaningful clinical outcomes.
Industry Expertise
Areas of Expertise
Education
University College of Health Science
B.Sc.
Clinical Chemistry
Uppsala University
M.Sc.
Molecular Biology
Karolinska Institute
Ph.D.
Medical Genetics
Project Management Institute (PMI)
PMP Certification
License #1661589
Affiliations
- University of Toronto, Faculty of Medicine, Department of Laboratory of Medicine and Pathobiology
- Shiruy, Inc
Links
Languages
- Persian
- Swedish
- English
Sample Talks
Bridging the Gap in Cancer Genetics & Personalized Medicine
As personalized medicine evolves, the ability to translate complex genomic data into actionable health insights is critical. I specialize in demystifying the science of cancer genetics for diverse audiences—from healthcare providers and non-profit organizations to the general public. Through strategic sessions and advisory, I break down the complexities of genetic inheritance, diagnostic test methodologies, and next-generation treatment options to foster informed decision-making and improve patient outcomes.
What I Offer to Clients & Partners:
• For Healthcare Providers: Deep-dive reviews into prognostic and diagnostic biomarkers, helping clinical teams stay ahead of the latest oncology treatment paradigms and personalized medicine challenges.
• For Non-Profit Organizations: Expert science communication designed to empower patient communities, translating high-level research into accessible, high-impact advocacy and educational programs.
• For Strategic Clients: Insight into the opportunities and hurdles of personalized medicine, providing the scientific clarity needed for program development and health technology evaluation.
Key Topics Covered:
• Principles of Genetic Inheritance: Understanding familial risk and hereditary cancer syndromes.
• Cancer Risk & Prevention: Science-backed analysis of lifestyle and genetic risk factors.
• Precision Diagnostics: Navigating the landscape of prognostic testing and molecular screening.
• The Future of Oncology: A review of the latest therapeutic developments and health technologies.
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.
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.
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.
Availability
- Keynote
- Moderator
- Panelist
- Workshop Leader
Courses
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.
Cellular Imaging in Pathobiology (Course ID# LMP1100H)
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.
Articles
Frequent accumulation of nuclear E-cadherin and alterations in the Wnt signaling pathway in esophageal squamous cell carcinomas
Modern PathologySima Salahshor, Richard Naidoo, Stefano Serra, Warren Shih, Ming-Sound Tsao, Runjan Chetty & James R Woodgett
2007-12-01
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.
The links between axin and carcinogenesis
Journal of Clinical PathologySima Salahshor and James R Woodgett
2005-03-01
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.
Differential gene expression profile reveals deregulation of pregnancy specific beta1 glycoprotein 9 early during colorectal carcinogenesis
BMC CancerSima Salahshor, Jason Goncalves, Runjan Chetty, Steven Gallinger & James R Woodgett
2005-06-01
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.
Nuclear expression of E-cadherin.
American Journal of Surgical Pathology2008-08-01
Comment on: E-cadherin/catenin complex status in solid pseudopapillary tumor of the pancreas.
E-cadherin in solid pseudopapillary tumors of the pancreas.
Human Pathology2008-09-01
E-cadherin expression and analysis in pancreas tumors.
Nuclear expression of E-cadherin in solid pseudopapillary tumors of the pancreas.
Journal of the Pancreas2007-05-01
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.
Expression of Wnt-signaling pathway proteins in intraductal papillary mucinous neoplasms of the pancreas: a tissue microarray analysis
Human Pathology2005-09-01
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.
Intraductal papillary mucinous neoplasm of the pancreas in a patient with attenuated familial adenomatous polyposis.
Journal of Clinical Pathology2005-01-01
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.
CDH1 mutations are present in both ductal and lobular breast cancer, but promoter allelic variants show no detectable breast cancer risk.
International Journal of Cancer2002-03-01
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.
COL11A1 in FAP polyps and in sporadic colorectal tumors.
BMC Cancer2001-01-01
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.
A germline E-cadherin mutation in a family with gastric and colon cancer.
Journal of Molecular MedicineS. Salahshor H. Hou C. B. Diep A. Loukola H. Zhang T. Liu J. Chen L. Iselius C. Rubio R. A. Lothe L. Aaltonen X.-F. Sun G. Lindmark A. Lindblom
2001-10-01
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.
Screening families with endometrial and colorectal cancers for germline mutations.
Journal of Medical Genetic2001-09-01
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.
Low frequency of E-cadherin alterations in familial breast cancer.
Breast Cancer Research2001-03-01
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.
Microsatellite Instability and hMLH1 and hMSH2 expression analysis in familial and sporadic colorectal cancer.
Lab InvestigationSima Salahshor, Konrad Koelble, Carlos Rubio & Annika Lindblom
2001-04-01
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.
Colorectal cancer with and without microsatellite instability involves different genes.
Genes Chromosomes CancerSima Salahshor, Ulf Kressner, Lars Påhlman, Bengt Glimelius, Gudrun Lindmark, Annika Lindblom
1999-11-01
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.
Microsatellite instability in sporadic colorectal cancer is not an independent prognostic factor.
British Journal of CancerS Salahshor, U Kressner, H Fischer, G Lindmark, B Glimelius, L Påhlman & A Lindblom
1999-09-01
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).
