Learning from Cancer to Advance Drug Development for Neurodegeneration
Posted September 03, 2015
Age-related diseases frequently occur together and are often considered manifestations of aging. However, there is evidence of an inverse relationship between cancer and neurodegenerative disease. Cancer patients have a lower risk of Parkinson's, Alzheimer's, and other neurodegenerative diseases, and the reverse is also true. Many cancer drug targets overlap with targets for neurodegeneration; thus research on cancer biology may advance therapeutic development for neurodegenerative disorders.
On June 11, 2015, researchers in cancer and neuroscience convened at the New York Academy of Sciences for the symposium Learning from Cancer to Advance Neurodegeneration Drug Discovery and Development. The talks focused on research related to both fields, highlighting insights about cell biology and function that can be gleaned from these seemingly disparate diseases. The plenary address introduced epidemiological and biological evidence for the connections between cancer and neurodegenerative disorders. Speakers described common molecular mechanisms as well as clinical possibilities for repurposing cancer therapies for Alzheimer's and related dementias. The symposium was presented by the Alzheimer's Drug Discovery Foundation and the Academy's Brain Dysfunction Discussion Group.
Use the tabs above to find a meeting report and multimedia from this event.
Presentations available from:
Kurt R. Brunden, PhD (University of Pennsylvania)
Stuart K. Calderwood, PhD (Harvard Medical School)
Jane A. Driver, MD, MPH (Brigham and Women's Hospital)
Gary Landreth, PhD (Case Western Reserve University)
Tamara Maes, PhD (Oryzon Genomics)
David M. Roy, PhD (Memorial Sloan-Kettering Cancer Center)
Stephen M. Strittmatter, MD, PhD (Yale University School of Medicine)
Li-Huei Tsai, PhD (Massachusetts Institute of Technology)
R. Scott Turner, MD, PhD (Georgetown University)
Hui Zheng, PhD (Baylor College of Medicine)
The Brain Dysfunction Discussion Group is proudly supported by
How to cite this eBriefing
The New York Academy of Sciences. Learning from Cancer to Advance Drug Development for Neurodegeneration. Academy eBriefings. 2015. Available at: www.nyas.org/BDDGCancer-eB
Epidemiological and biological evidence
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Catala-Lopez F, Tabares-Seisdedos R. Alzheimer's disease and cancer: the need of putting research into context with previous published systematic reviews. J Cancer Res Clin Oncol. 2015;141:569-70.
Driver JA. Inverse association between cancer and neurodegenerative disease: review of the epidemiologic and biological evidence. Biogerontology. 2014;15:547-57.
Driver JA, Beiser A, Au R, et al. Inverse association between cancer and Alzheimer's disease: results from the Framingham Heart Study. BMJ. 2012;344:e1442.
Ganguli M. Cancer and dementia: It's complicated. Alzheimer Dis Assoc Disord. 2015;29:177-82.
Ibanez K, Boullosa C, Tabares-Seisdedos R, et al. Molecular evidence for the inverse comorbidity between central nervous system disorders and cancers detected by transcriptomic meta-analyses. PLoS Genet. 2014;10:e1004173.
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Tabares-Seisdedos R, Rubenstein JL. Inverse cancer comorbidity: a serendipitous opportunity to gain insight into CNS disorders. Nat Rev Neurosci. 2013;14:293-304.
Genomic instability and DNA repair in neurological diseases
Dobbin MM, Madabhushi R, Pan L, et al. SIRT1 collaborates with ATM and HDAC1 to maintain genomic stability in neurons. Nat Neurosci. 2013;16:1008-15.
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Madabhushi R, Gao F, Pfenning AR, et al. Activity-induced DNA breaks govern the expression of neuronal early-response genes. Cell. 2015;161:1592-1605.
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Wang WY, Pan L, Su SC, et al. Interaction of FUS and HDAC1 regulates DNA damage response and repair in neurons. Nat Neurosci. 2013;16:1383-91.
LSD1 inhibitors in cancer and neurodegenerative diseases
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Harris WJ, Huang X, Lynch JT, et al. The histone demethylase KDM1A sustains the oncogenic potential of MLL-AF9 leukemia stem cells. Cancer Cell. 2012;21:473-87.
Maes T, Carceller E, Salas J, et al. Advances in the development of histone lysine demethylase inhibitors. Curr Opin Pharmacol. 2015;23:52-60.
Bromodomain inhibitors in glioblastoma and neurodegenerative diseases
Belkina AC, Blanton WP, Nikolajczyk BS, Denis GV. The double bromodomain protein Brd2 promotes B cell expansion and mitogenesis. J Leukoc Biol. 2014;95:451-60.
Belkina AC, Nikolajczyk BS, Denis GV. BET protein function is required for inflammation: Brd2 genetic disruption and BET inhibitor JQ1 impair mouse macrophage inflammatory responses. J Immunol. 2013;190:3670-8.
Johnstone S, Johhnsone A, Penas C, et al. Development of highly potent, selective bet bromodomain inhibitors that are CNS penetrant and effective in rodent models of brain cancer. Neuro Oncol. 2014;16(suppl 5):v75.
Pastori C, Daniel M, Penas C, et al. BET bromodomain proteins are required for glioblastoma cell proliferation. Epigenetics. 2014;9:611-20.
Rademakers R. C9orf72 repeat expansions in patients with ALS and FTD. Lancet Neurol. 2012;11:297-8.
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Bexarotene in Alzheimer's disease
Cramer PE, Cirrito JR, Wesson DW, et al. ApoE-directed therapeutics rapidly clear β-amyloid and reverse deficits in AD mouse models. Science. 2012;335:1503-6.
Madrekar-Colucci S, Karlo JC, Landreth GE. Mechanisms underlying the rapid peroxisome proliferator-activated receptor-γ-mediated amyloid clearance and reversal of cognitive deficits in a murine model of Alzheimer's disease. J Neurosci. 2012;32:10117-28.
Mandrekar-Colucci S, Landreth GE. Nuclear receptors as therapeutic targets for Alzheimer's disease. Expert Opin Ther Targets. 2011;15:1085-97.
O'Hare E, Jeggo R, Kim EM, et al. Lack of support for bexarotene as a treatment for Alzheimer's disease. Neuropharmacology. 2015. [Epub ahead of print.]
Tousi B. The emerging role of bexarotene in the treatment of Alzheimer's disease: current evidence. Neuropsychiatr Dis Treat. 2015;11:311-5.
Protein chaperones in cancer and neurodegeneration
Calderwood SK, Stevenson MA, Murshid A. Heat shock proteins, autoimmunity, and cancer treatment. Autoimmune Dis. 2012;2012:486069.
Chen Y, Wang B, Liu D, et al. Hsp90 chaperone inhibitor 17-AAG attenuates Aβ-induced synaptic toxicity and memory impairment. J Neurosci. 2014;34:2464-70.
Gong J, Weng D, Eguchi T, et al. Targeting the hsp70 gene delays mammary tumor initiation and inhibits tumor cell metastasis. Oncogene. 2015. [Epub ahead of print.]
Kamal A, Boehm MF, Burrows FJ. Therapeutic and diagnostic implications of Hsp90 activation. Trends Mol Med. 2004;19:283-90.
Watanabe S, Ageta-Ishihara N, Nagatsu S, et al. SIRT1 overexpression ameliorates a mouse model of SOD1-linked amyotrophic lateral sclerosis via HSF1/HSP70i chaperone system. Mol Brain. 2014;7:62.
Zhang Y, Murshid A, Prince T, Calderwood SK. Protein kinase A regulates molecular chaperone transcription and protein aggregation. PLoS One. 2011;6:e28950.
PARK2 in Parkinson's disease and cancer
Gong Y, Zack TI, Morris LG, et al. Pan-cancer genetic analysis identifies PARK2 as a master regulator of G1/S cyclins. Nat Genet. 2014;46:588-94.
Morris LG, Veeriah S, Chan TA. Genetic determinants at the interface of cancer and neurodegenerative disease. Oncogene. 2010;29:3453-64.
Veeriah S, Taylor BS, Meng S, et al. Somatic mutations of the Parkinson's disease-associated gene PARK2 in glioblastoma and other human malignancies. Nat Genet. 2010;42:77-82.
Nilotinib in Alzheimer's and Parkinson's diseases
Lonskaya I, Hebron ML, Desforges NM, et al. Nilotinib-induced autophagic changes increase endogenous parkin level and ubiquitination, leading to amyloid clearance. J Mol Med (Berl). 2014;92:373-86.
Lonskaya I, Hebron ML, Desforges, NM, et al. Tyrosine kinase inhibition increases functional parkin-Beclin-1 interaction and enhances amyloid clearance and cognitive performance. EMBO Mol Med. 2013;5:1247-62.
TFEB and PTEN clearance of neurofibrillary tangles
Brunden KR, Trojanowski JQ, Lee VM. Advances in tau-focused drug discovery for Alzheimer's disease and related tauopathies. Nat Rev Drug Discov. 2009;8:783-93.
Choi AM, Ryter SW, Levine B. Autophagy in human health and disease. N Engl J Med. 2013;368:1845-6.
Polito VA, Li H, Martini-Stoica H, et al. Selective clearance of aberrant tau proteins and rescue of neurotoxicity by transcription factor EB. EMBO Mol Med. 2014;6:1142-60.
Microtubule-stabilizing drugs for tauopathies
Brunden KR, Yao Y, Potuzak JS, et al. The characterization of microtubule-stabilizing drugs as possible therapeutic agents for Alzheimer's disease and related tauopathies. Pharmacol Res. 2011;63:341-51.
Brunden KR, Zhang B, Carroll J, et al. Epothilone D improves microtubule density, axonal integrity, and cognition in a transgenic mouse model of tauopathy. J Neurosci. 2010;30:13861-6.
Irwin DJ, Cohen TJ, Grossman M, et al. Acetylated tau, a novel pathological signature in Alzheimer's disease and other tauopathies. Brain. 2012;135(Pt 3):807-18.
Lou K, Yao Y, Hoye AT, et al. Brain-penetrant, orally bioavailable microtubule-stabilizing small molecules are potential candidate therapeutics for Alzheimer's disease and related tauopathies. J Med Chem. 2014;57:6116-27.
Mukhtar E, Adhami VM, Mukhtar H. Targeting microtubules by natural agents for cancer therapy. Mol Cancer Ther. 2014;13:275-84.
Zhang B, Carroll J, Trojanowski JQ, et al. The microtubule-stabilizing agent, epothilone D, reduces axonal dysfunction, neurotoxicity, cognitive deficits, and Alzheimer-like pathology in an interventional study with aged tau transgenic mice. J Neurosci. 2012;32:3601-11.
Fyn inhibition for Alzheimer's disease
Gimbel DA, Nygaard HB, Coffey EE, et al. Memory impairment in transgenic Alzheimer mice requires cellular prion protein. J Neurosci. 2010;30:6367-74.
Kaufman AC, Salazar SV, Haas LT, et al. Fyn inhibition rescues established memory and synapse loss in Alzheimer mice. Ann Neurol. 2015;77:953-71.
Kostylev MA, Kaufman AC, Nygaard HB, et al. Prion-protein-interacting amyloid-β oligomers of high molecular weight are tightly correlated with memory impairment in multiple Alzheimer mouse models. J Biol Chem. 2015. [Epub ahead of print.]
Um JW, Kaufman AC, Kostylev M, et al. Metabotropic glutamate receptor 5 is a coreceptor for Alzheimer aβ oligomer bound to cellular prion protein. Neuron. 2013;79:887-902.
Um JW, Nygaard HB, Heiss JK, et al. Alzheimer amyloid-β oligomer bound to postsynaptic prion protein activates Fyn to impair neurons. Nat Neurosci. 2012;15:1227-35.
Institutes and Industry
Alzheimer's Drug Discovery Foundation
Foundations providing seed funding to accelerate Alzheimer's disease drug candidates through the pipeline.
Alzheimer's Disease Cooperative Study
U.S. Government initiative for Alzheimer's disease clinical trials.
Belfer Neurodegeneration Consortium
Multi-institutional initiative that focuses on alternative hypotheses for neuroprotection in Alzheimer's disease.
Diagnostic and therapeutic discovery company that conducted clinical trials of bexarotene in Alzheimer's disease.
Drug discovery company cofounded by Claes Wahlestedt that focuses on epigenetics. Drugs in development include EP11313.
Drug discovery company focused on cancer and neurodegenerative diseases. Drugs in development include ORY-1001 for acute leukemia and ORY-2001 for Alzheimer's disease.
Drug discovery company cofounded by Gary Landreth that focuses on using retinoid X receptor agonists, such as bexarotene, in Alzheimer's disease.
Clinical trials of oncology drugs or targets for neurodegenerative diseases
Completed phase II trial of Bexarotene in Alzheimer's disease.
Phase IIa trial of AZD0530 in mild Alzheimer's disease.
Completed phase I trial of Epothilone D in Alzheimer's disease.
Phase I trial of AZD0530 in Alzheimer's disease.
Phase I trial of TPI-287 in a primary four-repeat tauopathy, progressive supranuclear palsy, or corticobasal degeneration.
Howard Fillit, MD
Howard Fillit, a geriatrician, neuroscientist, and expert in Alzheimer's disease, is the founding executive director of the Alzheimer's Drug Discovery Foundation (ADDF). The foundation's mission is to accelerate the discovery and development of drugs to prevent, treat, and cure AD, related dementias, and cognitive aging. Fillit has had a distinguished academic medicine career at The Rockefeller University and Mount Sinai School of Medicine, where he is a clinical professor of geriatrics and medicine and a professor of neurobiology. He is the senior editor of the Textbook of Geriatric Medicine and Gerontology. Fillit was previously the corporate medical director for Medicare at New York Life, responsible for over 125 000 Medicare managed-care members in five regional markets. He has received several awards and honors, including the Rita Hayworth Award for Lifetime Achievement. He also serves as a consultant to pharmaceutical and biotechnology companies, health care organizations, and philanthropies.
Diana Shineman, PhD
Diana Shineman is the director for scientific affairs at the Alzheimer's Drug Discovery Foundation, where she develops and manages drug discovery and development grant programs and strategic initiatives. Shineman led an interdisciplinary effort to standardize animal model study design to improve research efficiency and translatability. She earned her PhD in cell and molecular biology in 2008 from the University of Pennsylvania, where she worked in the Center for Neurodegenerative Disease Research led by Drs. Virginia Lee and John Trojanowski. She also worked as an editorial intern for the Journal of Clinical Investigation and was an active member of the Penn Biotechnology Group. Shineman was a Howard Hughes Undergraduate Research Scholar.
Sonya Dougal, PhD
The New York Academy of Sciences
Sonya Dougal is the director of Life Sciences Discussion Groups at the New York Academy of Sciences. She develops an annual portfolio of scientific symposia on life sciences and biomedical research. Dougal has over 14 years of experience in scientific research and program management in academia, industry, and nonprofits. She holds a PhD in cognitive psychology from the University of Pittsburgh. She was the recipient of a Ruth L. Kirschstein National Research Service Award from the National Institutes of Health for her postdoctoral training as a cognitive neuroscientist in the laboratory of Elizabeth Phelps at New York University.
Jane A. Driver, MD, MPH
Jane A. Driver is a member of the Geriatrics Research Education and Clinical Center (GRECC) at VA Boston Healthcare System Division of Aging at Brigham and Women's Hospital and of the Division of Medical Oncology at Dana-Farber Cancer Institute. She is also an assistant professor at Harvard Medical School. Trained as both a geriatrician and an oncologist, her research focuses on the epidemiology, prediction, and prevention of cancer and neurodegenerative disease. She is investigating the link between cancer and Alzheimer's disease, as well as new methods of early diagnosis of Alzheimer's disease. She has received research grants from the Department of Veterans Affairs, the Hartford Foundation, the Parkinson's Disease Foundation, and Harvard Medical School. Driver works with vulnerable elderly veterans with memory disorders and teaches in geriatrics and oncology. She is codirector of the Older Adult Hematologic Malignancy Program at the Dana-Farber Cancer Institute.
Kurt R. Brunden, PhD
Kurt R. Brunden is director of drug discovery and a research professor in the Center for Neurodegenerative Disease Research (CNDR) at the University of Pennsylvania, where he oversees drug discovery programs in the areas of Alzheimer's disease, frontotemporal lobar degeneration, and Parkinson's disease. Before joining CNDR Brunden was an executive in the biotechnology sector, managing drug discovery programs in AD, cognitive enhancement, schizophrenia, inflammation, metabolic disease, and cancer. Before working in industry, Brunden was an NIH-funded faculty member in the Biochemistry Department at the University of Mississippi Medical Center, with a research focus on the regulation of myelination. He obtained his PhD in biochemistry from Purdue University and completed a postdoctoral fellowship at the Mayo Clinic.
Stuart K. Calderwood, PhD
Stuart K. Calderwood obtained his PhD from Newcastle University, UK, and carried out postdoctoral fellowships studying the mammalian stress response at Newcastle University and Stanford University. He joined the Dana-Farber Cancer Institute at Harvard Medical School, where he and studied the transcription of molecular chaperone genes. He later became director of the Molecular Stress Response Center and a professor of medicine at Boston University and then director of Molecular and Cellular Biology and a professor of radiation oncology at Beth Israel Deaconess Medical Center and Harvard Medical School. Calderwood studies the regulation of molecular chaperone gene expression in cancer and aging as well as the immune properties of heat shock proteins. His research has been continuously funded through the National Cancer Institute since 1986 and he has been a member of multiple National Institutes of Health study sections.
Gary Landreth, PhD
Gary Landreth completed his PhD in neuroscience at the University of Michigan, with a year of study at the National Institute of Medical Research in London, UK. He did postdoctoral work in the Department of Neurobiology at Stanford University. Landreth was appointed to the faculty of the Medical University of South Carolina, where he worked for 9 years, and moved to Case Western Reserve University and the Alzheimer Research Laboratory in 1989. He is currently a professor in the Department of Neurosciences, focusing on the investigation of Alzheimer's disease and the development of new drugs for its treatment.
Tamara Maes, PhD
Tamara Maes received her PhD in biotechnology from the University of Ghent, Belgium, where she worked on developmental genetics. She was a European Union postdoctoral fellow at the Council for Scientific Research (CSIC) in Barcelona, Spain, and founded Oryzon in 2000, becoming its chief scientific officer. The company identified biomarkers for minimally invasive detection of endometrial cancer in postmenopausal women, developing its first marketed product, GynEC-Dx, in the diagnostics area. The company also identified early human biomarkers in several neurodegenerative disorders, and in 2008 proposed to start a drug discovery program for LSD1. This program split into two branches, with molecules optimized for CNS uses and oncological indications. The oncology drug, ORY-1001, received orphan drug status from the European Medicine Agency and is currently in clinical phase I/IIA trials for acute leukemia. It has recently been licensed to Roche. The CNS drug, ORY-2001, is a dual LSD1-MAOB inhibitor expected to enter the clinic for the treatment of Alzheimer's disease by the end of 2015.
David M. Roy, PhD
David Roy is in his final year at the Weill Cornell/Rockefeller/Sloan-Kettering Tri-Institutional MD-PhD Program in New York. While in medical school, he completed a two-year Howard Hughes Medical Institute research fellowship, studying the role of PTPRD in cancer. He received his PhD from Weill Cornell Medical College in 2015 under the supervision of Dr. Timothy Chan at Memorial Sloan-Kettering Cancer Center. His graduate work focused on studying genomic alterations in glioma and developing computational strategies to identify driver genes involved in malignant transformation and metastasis. He is currently exploring the role of arm-level copy number alterations in cancer progression.
Stephen M. Strittmatter, MD, PhD
Stephen M. Strittmatter completed MD and PhD training at Johns Hopkins University, studying with Dr. Solomon H. Snyder. He moved to Massachusetts General Hospital for a medical internship and an adult neurology residency. While there he worked as a research fellow with Dr. Mark Fishman, exploring the molecular basis of axonal guidance. He joined the faculty of Yale University in 1993, where he currently holds the Vincent Coates Professorship of Neurology and is a founding director of the Yale Cellular Neuroscience, Neurodegeneration and Repair Interdepartmental Program. He is also director of the Yale Memory Disorders Clinic. His work has contributed to defining a molecular basis for axonal guidance during development and neural repair after adult injury. More recently, his laboratory has also explored ligand-receptor interactions in degenerative dementias. Work on amyloid-β oligomer toxicity has defined a pathway from PrPC to mGluR5 to Fyn.
Li-Huei Tsai, PhD
Li-Huei Tsai is the director of the Picower Institute for Learning and Memory and the Picower Professor of Neuroscience at the Massachusetts Institute of Technology. She is interested in the mechanisms of neurological disorders accompanied by learning and memory impairments—both neurodegenerative disorders such as Alzheimer's disease and neurodevelopmental disorders. She has studied neuronal development and function in the developing and adult brain, as well as how neuronal function and circuitry may be dysregulated in disorders of cognitive impairment. Her lab identified histone deacetylase 2 (HDAC2) as a key negative regulator of genes implicated in activity regulation, synaptogenesis, and synaptic plasticity. She received her PhD from the University of Texas Southwestern Medical Center and completed postdoctoral training at Cold Spring Harbor Laboratory and Massachusetts General Hospital. Tsai joined the faculty at Harvard Medical School and was named an investigator of Howard Hughes Medical Institute before joining the Picower Institute.
R. Scott Turner, MD, PhD
R. Scott Turner is a professor of neurology and the director of the Memory Disorders Program at Georgetown University Medical Center. He was previously chief of the Neurology Service at the Veterans Affairs Ann Arbor Healthcare System and an associate professor and associate chair in the Department of Neurology at the University of Michigan, Ann Arbor. He holds MD and PhD degrees from Emory University and completed internship, residency, and fellowship training at the University of Pennsylvania. He is board certified in psychiatry and neurology. Turner lectures widely and serves as a reviewer for granting agencies and biomedical journals. He directs clinical studies sponsored by industry and the National Institutes of Health. Most recently, he was the principal investigator of a multicenter, randomized, double-blind, placebo-controlled phase II trial of resveratrol for mild–moderate Alzheimer's disease, in collaboration with the National Institute on Aging–funded Alzheimer's Disease Cooperative Study (ADCS).
Claes Wahlestedt, MD, PhD
Claes Wahlestedt is the Leonard M. Miller Professor and associate dean and center director for therapeutic innovation at the University of Miami Miller School of Medicine. His research focuses on epigenetics, mammalian transcriptomics, noncoding RNAs, cancer, neuroscience, and drug discovery in several therapeutic areas. Wahlestedt obtained his MD and PhD degrees from Lund University, Sweden, and has worked in academia and in the pharmaceutical industry. Before joining the University of Miami, he was a professor and director of neuroscience at the Florida campus of the Scripps Research Institute, and previously an endowed professor of pharmacogenomics and chair of the Department for Genomics and Bioinformatics at the Karolinska Institute, Sweden. He has directed large drug discovery and biotechnology teams in the pharmaceutical industry for Astra-Zeneca, Pharmacia & Upjohn, and Pharmacia Corporation. His most recent biotechnology start-ups are CURNA Inc. (focusing on noncoding RNAs; acquired by OPKO Health in 2011) and Epigenetix Inc. (focusing on chromatin regulators).
Hui Zheng, PhD
Hui Zheng holds a PhD from Baylor College of Medicine. She studies the biological and pathophysiological functions of the amyloid precursor protein (APP) and presenilins. Her work revealed APP as a synaptic adhesion protein and identified an intriguing role of presenilins in skin tumorigenesis. Recently, Zheng expanded her focus to investigate the neuron-glia signaling pathways and intracellular clearance mechanisms in neuronal health and Alzheimer's disease. Zheng holds the Huffington Foundation Endowed Chair and directs the Huffington Center on Aging at Baylor College of Medicine. She has also researched Alzheimer's disease at Merck Research Laboratories. She serves on the Cellular & Molecular Biology of Neurodegeneration (CMND) Study Section and is a member of the BrightFocus Foundation Scientific Advisory Committee and the Alzheimer's Association Medical & Scientific Advisory Council.
Jennifer Cable lives in New York City, where she experiments with different outlets to communicate science. She enjoys bringing science to scientists and nonscientists alike. She writes for Nature Structural and Molecular Biology, Bitesize Bio, Under the Microscope, and the Nature New York blog. She received a PhD from the University of North Carolina at Chapel Hill for her research in investigating the structure/function relationship of proteins.