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Pathologists Medicine, Weill Cornell on the Global Stage Medicine; Pathologist-In-Chief, and Working Groups Vol. 26 • February 2020 PThe NeAwsletteTr of PaHthologyO and LaboLratoryO MedicineG at WeillI CoSrnell MeT dicine grant, which has been funded since 2002 and comprises Contents Research Highlights seven academic research institutions in Boston. He has received several awards and honors, including the Edited by David P. Hajjar, PhD Stowell-Orbison Award from the United States and Canadian 1 Academy of Pathology, the Donald S. Coffey Physician- Research Highlights Scientist Award from the Prostate Cancer Foundation and Welcome to Our New Chair, Massimo Loda, MD Massimo, Loda, MD the Distinguished Mentor Award from Brigham and David D .Thompson Professor Women’s Hospital. Dr. Loda was also elected a member of and Chairman 3 of the Department of the Association of American Physicians in 2015. He serves Pathology and Laboratory on several national advisory boards and NIH study sections Our Renowned Pathologists Medicine, Weill Cornell on the Global Stage Medicine; Pathologist-in-Chief, and working groups. NewYork-Presbyteria n/ Dr. Loda completed his undergraduate studies in 1976 at Weill Cornell Medical Center 4 the University of Witwatersrand in Johannesburg, South Faculty Focus Africa, and received his medical degree in 1980 from the University of Milan. In the mid-1980s, Dr. Loda moved to the 5 Welcome to Our New Chair, United States and completed a residency in anatomic pathology at Harvard Medical School, as well as a fellow - Keynotes Massimo Loda, MD ship in anatomic and molecular pathology at Tufts Medical Dr. Massimo Loda, an inte rnationally renowned molecular Center. Dr. Loda was appointed to Ha rvard Medical School’s 7 pathologist, is our new Chai rman and Pathologist-in-Chief. Dr. faculty in 1992, rising through the ranks to become a Newly Awarded Loda was recruited to Weill Co rnell Medicine and NewYork- Professor of Pathology in 2006. He joined the Dana-Farber Pathology Grants Presbyte rian/Weill Co rnell Medical Center from Dana-Farber Cancer Institute in 1998, where he in 2016 became Chief Cancer Institute in Boston, where he was Chair of the of the Division of Translational and Molecular Oncologic 8 Depa rtment of Oncologic Pathology. Pathology. Congratulations An acclaimed physician-scientist with a focus on urologic Dr. Loda, Professor of Pathology and Laboratory Medicine, Dr. Rhonda K. Yantiss oncology, Dr. Loda uses biochemical and genomic approaches joined Weill Cornell Depa rtment of Pathology and Labora tory to investigate the mechanisms by which prostate cancer Medicine in February 2019. 9 hijacks cell metabolism to allow tumors to flourish. Unlike Residents’ Research Day healthy cells, prostate tumors rely on – and thus create – fat, BIOLOGY OF PROSTATE CANCER According to Massimo Loda, MD or lipids, for energy. Dr. Loda discovered that the molecular 10 pathway responsible for that metabolic activity renders tumor For many years, Dr. Massimo Loda and his research team Welcome New cells vulnerable to targeted treatments, and has identified two have studied the links between the regulation of Resident s/ Fellows such drugs that exploit it with few clinical side effects. Dr. metabolomics and the progression of prostate cancer. Department Leadership Loda has also identified prostate cancer biomarkers that can Today, metabolomics is defined as the quantitative meas - Appointment s/ Promotions predict therapeutic e fficacy. urement of the metabolic response to external stimuli or Dr. Loda is a board-ce rtified pathologist and physician- genetic alterations. It can also detect and quantify low- 11 sci entist with expe rtise in genitourinary cancers, pa rticularly mol ecular weight metabolites produced by living cells. Faculty Publications prostate cancer. He has published more than 360 scholarly The metabolites of living cells are seen as the end prod - in 2019 papers in jou rnals, including Nature and its specialized pub - ucts of the biological hierarchy, starting with activated li cations, Cell, Cancer Cell, New England Jou rnal of Medicine, genes (genome) and extending over the collection of gene Proceedings of the National Academy of Sciences, and Jou rnal transcripts (transcriptome) and proteins (proteome). of Clinical Oncology. Dr. Loda has been consistently funded by Metabolic alterations can occur as a consequence of the National Institutes of Health, the Depa rtment of Defense, genet ic events. Alternatively, metabolic alterations are the American Cancer Society and other organizations. He is pri mary events in cancer but require genetic alterations principal investigator of a National Cancer Institute Specialized in critical pathways for oncogenesis to occur (e.g. isocitrate Program of Research Excellence (SPORE) prostate cancer dehydrogenase mutations). Either way, Professor Loda Research Highlights Figure 1. Prostate cells increased both the synthesis and utilization of fatty acids (FAs) continued from page 1 during cellular transformation and prostate cancer progression. (A) Simplified illustration Exogenous FAs and lipids A LDL of FA synthesis and associated pathways. FATPs CD36 believes that genetic alterations and altered meta - A Glucose LDLR FABP Sources of carbon for de novo FA synthesis bolic pathways go hand in hand in a tumor cell- GLUT derive primarily from glucose and glutamine. Cholesterol In harsh environments, acetate can also be spe cific manner. Thus, simultaneous targeting of Glucose Prostaglandins, used as a carbon source. Once synthesized, Thromboxanes s d i p selected metabolic enzymes and “driving” onco - G6P i L Intracellular (Poly)unsaturated de novo FAs undergo elongation and satura tion Triacylglycerides, x FAs Phosphoglycerides e FAs l p m ELOVL modifications. FAs are also provided by diet genes may be a cancer cell-selective therapeutic G3P Sphingolipids o FADS C Cardiolipids Monounsaturated and they can be uptaken from the circulation approach. FAs Pyruvate through transporters, binding proteins, or SCD Several years ago, he and his colleagues discov - ELOVL passive transport. Diet is the only source of Malonyl-CoA Acetyl-CoA ACC FASN Palmitate essential FAs. Once in the cells, FAs are ered that USP2a binds to and stabilizes fatty acid Oxaloacetate ACLY Citrate Citrate Acetyl-CoA incorporated in more complex structural, Malate ACSS2 TCA Cycle Isocitrate synthase (FASN) by preventing its degradation. This Isocitrate Fumarate Acetylation Acetate storage lipids, and inflammatory mediators α-KG Succinate Mevalonate or (B) oxidized in peroxisomes or mitochon - prompted them to initiate a research program α-KG pathway Succinyl-CoA Internal acetate sources MCT dria to produce energy. GLUT, glucose trans - focused on FASN. Having interests in the etiology Glutamate Acetate porter; LDL, low-density lipoprotein; LDLR, Cholesterol and and pathogenesis of prostate cancer (PCa), his lab - Glutamine Steroid Synthesis low-density lipoprotein receptor; FATPs, oratory investigated the expression of FASN in PCa fatty-acid transport proteins; FABP, fatty- SLC1A5 acid-binding protein; ACLY, ATP citrate lyase; GGlutaminelutamine by immunohistochemistry as well as gene expres - ACC, acetyl-CoA carboxylase; FASN, fatty BB Very long FAs acid synthase; ACSS2, cytoplasmic acetyl- sion profiling demonstrating that FASN is over- Shortened FAs Peroxisome CoA synthetase; SCD, stearoyl-CoA desaturase; ex pressed in aggressive prostate carcinomas. FAs NADH ETC Carnitine Acyl-CoA ELOVL, fatty acid elongase; ␣-KG, ␣-ketog - β-oxidation FADH2 Since it has been reported that FASN expression is Acyl-CoA CPT1 lutarate; G3P, glyceraldehyde-3-phosphate; CPT2 G6P, glucose-6-phosphate; TCA, tricarboxylic highest in androgen-independent bone metastatic ATP Acylcarnitine Acylcarnitine Carnitine acid; MCT, monocarboxylate transporter; disease, they set out to determine whether it con - Carnitine CPT1, carnitine palmitoyltransferase I; CPT2, fers a growth advantage to PCa. Using genetically carnitine palmitoyltransferase II; NADH, engineered human prostate epithelial cells infected reduced nicotinamide adenine dinucleotide; FADH2, reduced flavin adenine dinucleotide; with FASN, they established that FASN can act as a Advanced Online Article. Cite this article as Cold Spring Harb Perspect Med ETC, electron transport chain; ATP, adenosine PCa. Subsequently, Dr. Loda and his colleagues doi: 10.1101/cshperspect.a030569 triphosphate. showed that FASN ge rmline polymorphisms are significantly associated with risk of lethal PCa. G2/M may be therapeutically exploited for hyper - Sci USA 2018. PubMed Significant interactions of BMI with FASN polymor - Hamid AA, Gray KP, Shaw G, MacConaill LE, Evan C, proliferative diseases such as cancer. phisms and FASN tumor expression suggest FASN Bernard B, Loda M, Corcoran NM, Van Allen EM, Professor Loda’s laboratory at Weill Co rnell Medicine Choudhury AD, Sweeney CJ. Compound Genomic as a potential link between obesity and poor PCa Alterations of TP53, PTEN, and RB1 Tumor Suppressors has now been established, and he continues to hit in Localized and Metastatic Prostate Cancer. Eur Urol outcome. Dr. Loda reasons that FASN inhibition major milestones in understanding the pathogenesis 2018. PubMed could reduce PCa-specific mortality, particularly in Wang Z, Cao S, Morris JS, Ahn J, Liu R, Tyekucheva S, of Prostate Cancer. Gao F, Li B, Lu W, Tang X, Wistuba II, Bowden M, Mucci overweight men. Relevant Publications L, Loda M, Parmigiani G, Holmes CC, Wang W. Dr. Loda recently expanded the analysis of metab - Transcriptome Deconvolution of Heterogeneous Tumor Abida W, Cyrta J, Heller
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