Professor Michael Lisanti

Chair in Translational Medicine

  • Cockcroft 201d
  • T: +44 (0)161 295 0240
  • E: m.p.lisanti@salford.ac.uk

Office Times

Please e-mail for an appointment

Biography

I have been an active research scientist for over 30 years.

I began my education at New York University, graduating Magna Cum Laude in Chemistry. I obtained my MD-PhD degrees at Cornell University Medical College in Cell Biology and Genetics. From 1992-96, I was a Fellow at the Whitehead Institute at MIT. After several distinguished appointments at the Albert Einstein College of Medicine and the Kimmel Centre, I joined the Breakthrough Breast Cancer Research Unit in 2012 as Professor of Cancer Biology, at The University of Manchester, in the United Kingdom (UK).

Following my appointment to the Kimmel Cancer Centre in 2006, I was selected for the leadership of the Program in Molecular Biology and Genetics of Cancer. In 2009, I became the Chair of the Department of Stem Cell Biology and Regenerative Medicine at Thomas Jefferson University. I also served as the former Editor-in-Chief of the American Journal of Pathology. In Manchester, I previously held the Muriel Edith Rickman Chair of Breast Oncology.

Teaching

Previously, I have lectured in various MD and PhD level graduate courses in Biochemistry, Cell Biology, Pharmacology, Pathology and Clinical Medicine, among others. 

Research Interests

Research Achievements:

1. Compartmentalisation of Signal Transduction: The “Caveolae Signalling Hypothesis”. In 1993-94, my laboratory was among the first to propose that signal transduction takes place in an organized fashion, within lipid rafts and caveolae, which are specialized domains at the cell surface. This mechanism includes G-proteins, Src-like kinases, NOS, and the Ras-MAP kinase signalling, as well as many other pathways. This signalling model was heretical in the early 1990s, and is now well accepted today.

2. Compartmentalisation of Tumour Metabolism. In 2009, my laboratory was the first to propose the “Reverse Warburg Effect”. This new model for cancer metabolism will facilitate the development of novel diagnostics and therapeutics, driving personalised cancer therapy.

3. Stromal Cav-1 as a Biomarker. In 2009, my laboratory discovered a new prognostic biomarker, which has now been validated in >10 different countries word-wide for breast cancer. Its prognostic value has also been extended to DCIS lesions (early breast cancers), prostate cancers, and metastatic melanoma, and it may well represent a universal or widely-applicable cancer biomarker for stratified medicine.

More specifically, my laboratory has shown that a loss of stromal Cav-1 predicts early tumour recurrence, metastasis, drug-resistance, and overall poor survival in breast cancer patients, at diagnosis, before poor clinical outcome has occurred.

Research Interests:

1. Anti-Cancer Therapies. My current research programme is focused on epithelial-stromal interactions and metabolic-symbiosis in cancer. The concept that tumor-host interactions are crucial in tumor progression is now well-accepted. In fact, the English Surgeon Stephen Paget first proposed the “seed and soil” hypothesis in 1889, which states that cancer cells (“the seeds”) metastasize systemically and grow best in the most tumor-promoting host organs or the most “fertile soil.”

In this context, tumor cells corrupt or transform their microenvironment in order to generate new blood vessels to support their oxygen requirements. Closely linked to this idea, we and others have begun to view cancer as a “parasitic disease” that “steals” energy-rich metabolites from the host microenvironment.

The tumor stroma, which is composed of fibroblasts, adipocytes, endothelial cells and macrophages, lies in extremely close proximity to cancer cells, and can directly promote tumor growth. Recent studies indicated that the tumor microenvironment can help determine clinical outcome in human cancer patients and may also confer drug-resistance and treatment failure, leading to tumor recurrence and metastasis.

My research laboratory at the University of Salford will also focus on the repurposing of existing FDA-approved drugs as new cancer therapies and on new drug discovery targeting cancer metabolism.

2. Anti-Ageing Therapies.  Another critical goal of my laboratory is to broadly apply our drug discovery skills to a variety of ageing-associated human diseases (cancer, heart disease, diabetes and dementia). In this context, we will target various aging-associated biological processes, such as mitochondrial dysfunction, inflammation, and senescence, which we believe are the root cause of ageing. 

We will also explore the inter-relationship of these factors with accumulated damage that occurs during the ageing process, and the retention of insoluble debris, such as beta-amyloid and lipofuscin.  We believe that these types of experimental approaches will ultimately increase “health-span”, the healthy years of life. In this regard, it is important to note that advanced chronological age is the single most significant risk factor for the development of most cancer types.

Qualifications and Memberships

Fellow, Royal Society for the encouragement of Arts, Manufactures and Commerce (RSA)

American Society for Investigative Pathology (ASIP)

American Association for Cancer Research (AACR)

1981-85: BA in Chemistry, Magna Cum Laude, New York University, New York, USA

1985-92: MD-PhD, Cornell University Tri-Institutional MD-PhD Program (Cornell University, together with Rockefeller University and Memorial Sloan-Kettering), New York, USA

1992-97: Whitehead Institute Fellow, Affiliated with Dr. Harvey Lodish's Laboratory, Whitehead Institute, Massachusetts Institute of Technology (MIT)

Publications

Martinez-Outschoorn UE, Peiris-Pagés M, Pestell RG, Sotgia F, Lisanti MP. Cancer metabolism: a therapeutic perspective. Nat Rev Clin Oncol. 2017 Jan; 14(1):11-31.

Ozsvari B, Fiorillo M, Bonuccelli G, Cappello AR, Frattaruolo L, Sotgia F, Trowbridge R, Foster R, Lisanti MP. Mitoriboscins: Mitochondrial-based therapeutics targeting cancer stem cells (CSCs), bacteria and pathogenic yeast. Oncotarget. 2017 Jul 7. doi: 10.18632/oncotarget.19084. [Epub ahead of print]

Martinez-Outschoorn UE, Sotgia F, Lisanti MP. Caveolae and signalling in cancer. Nat Rev Cancer. 2015 Apr;15(4):225-37.

Peiris-Pagès M, Martinez-Outschoorn UE, Pestell RG, Sotgia F, Lisanti MP. Cancer stem cell metabolism. Breast Cancer Res. 2016 May 24; 18(1):55.

Fiorillo M, Lamb R, Tanowitz HB, Cappello AR, Martinez-Outschoorn UE, Sotgia F, Lisanti MP. Bedaquiline, an FDA-approved antibiotic, inhibits mitochondrial function and potently blocks the proliferative expansion of stem-like cancer cells (CSCs). Aging (Albany NY). 2016 Aug; 8(8): 1593-607.

Farnie G, Sotgia F, Lisanti MP. High mitochondrial mass identifies a sub-population of stem-like cancer cells that are chemo-resistant. Oncotarget. 2015 Oct 13;6(31):30472-86.