BIO 501 The Biology of Cancer

BIO 501 The Biology of Cancer
Introduction to 501 Folder Title: Intro501 Online: Intro501(NoTP) Updated: January 10, 2015

NewsWeek Oct. 26, 2009

Phenomenology of Cancer: What are the features that cancers present in human populations?
Extent and Clinical Patterns of Cancers Epidemiology of Cancers Classification and Nomenclature What do these features tell us about the basic biology of cancer? What do these features tell us about Diagnosis, Management (therapy), and Prevention of Cancers? Folder title: Intro501: The first part of this course defines the cancer problem is terms of its epidemiology and public health impact. It then classifies the 200 or more clinical human cancers, and relates these to the underlying biology of cancer.

What Models of Cancers Do We Actually Use in Cancer Biology and Cancer Medicine?
Neoplastic and Normal Cell Lines in Culture Transformed Normal Cells Freshly-derived Cancer Cells Genetically Engineered Cells Engineered Tissues (3-Dimensional Cell Cultures) Animal Models in Cancer Research and Cancer Medicine (“Pre-Clinical Trials”) Inbred Animal Models Veterinary Animals Animal-Human Engineered Hybrid Models Clinical Cancer in Patients Clinical Trials (Phase I, Phase II, and Phase III)

What are Cancer Cells Like? How do Cancer Cells “Talk” to each other?
As Isolated Cells? In Tumor-bearing Animals? In Patients? Characteristics of Cancer Cells in Culture How does a Cancer Cell “Talk” to Itself and Its Neoplastic Neighbors? Why are cancer cells in cell culture Immortal? Tumor Cell Populations and Tumor Tissues in vivo How do Cancer Cells “Talk” to each other? How do Cancer Cells “Talk” to normal cells? What do cancer cells “hear” from the host? Why don’t cancer cells know how old they are and when to die? Growth Patterns of Experimental and Clinical Cancers How Do Cancer Cells Change and Progress in Malignant Potential? What are the Patterns of Invasion & Spread to Distant Sites? Folder title: Intro501: The course then proceeds to discuss the natural history of cancers and relates these features to the underlying basic biology.

What are Cancers like in Patients? What do clinicians see?
What are they dealing with? The Story of Kuyler Van Nocker and Neuroblastoma (See Slide 49 for Video Link) William Bunn: Boy Police-Officer and Neuroblastoma (See Slide 24 for Video Link) Kelley Mitchell and Ewing’s Sarcoma (See Slide 50) Taylor Black and Neuroblastoma See UntreedReads.com Daydreams and Diaries By Tim Black (Taylor Black’s Father)

What Features are Seen in Cancer Genetics?
What does modern genomics tell us about cancer biology, origins of cancer, cancer diagnosis and treatment? What are the crucial features of cancer cell genomes? What are the hereditary patterns in tumor-bearing hosts? What are the clonal origins of cancers? What do Proteomics (the spectrum of expressed proteins) and Epigenetics* tell us about Cancer origins and progression? *(modification of genes and gene-products) Folder title: Intro501: The phenomenology and natural history of cancer are intimately related to the genetics of cancer cells and of the cancer-bearing host.

Differentiation and Cancer: Cancer as an expression of abberrant differentiation
How are genes expressed and controlled in cancer? Can the malignant state be reversed to normal? Why are oncofetal genes often re-expressed in cancers? Folder title: Intro501: Gene expression is also crucial in the appearance and subsequent natural history of cancers.

Biological Mechanisms Underlying Cancer Phenomenology
Cell Cycle, Proliferation, Signalling, and Immunogenicity Cellular Senescence, Immortalization, and Cancer Cell Death (Genetically-programmed cell death; Apoptosis) Telomeres and Cell Ageing Autophagy (Inter-cellular “cannibalism”) and Cancer Intra-cellular signaling Growth Factors and Receptors Inter-cellular Communication Cell Movement Gene Expression and Differentiation Control Normal Immune Responses and Immune Escape Protein Structure, Function, and Modification Onco-fetal gene products Folder title: Intro501: A major element of this course is the relating of the natural history of cancers to their underlying biological and biochemical mechanisms.

Basic Biology in the Diagnosis and Therapy of Cancers
Modalities in Cancer Management Host Response Modifiers Genetics and Cancer Management Immunotherapy & Immunodiagnosis of Cancers Cancer Chemotherapy New Approaches to Cancer Management Specific Targeted Therapy (See Slides 42, Molecular Signaling in Cancer & Slide 43, The RAS Pathway for an examples of a cell signaling pathways in cancer. “Phenotherapy” of Cancer? Folder title: Intro501: A major element of this course is the relating of the natural history of cancers to their underlying biological and biochemical mechanisms.

To Enter your name on your NXT Transmitter (Revised January 10, 2015)
For NXT Transmitter (Off-white) Press grey button with white oval in the middle Get screen with a wrench on it Press upper right button (square with two bubbles) “Find Channel” (Channel 41) Press Right Arrow 4 times to get to “Your ID” Grey Button (Left arrow under abc will clear characters) Enter your name (first five letters OK) using the letters shown on each key. If you want a “c”, hit the abc key three times in quick succession. When your name is entered hit the grey button. You will get a smiley face. _______________________________________________________________ To Send in a “Response to Leader” Question at any time during class: Use Cntrl F8. (Your ID but not your name will show) Type in your message. I will get an icon on my screen to see what was asked. 447Intro: 447Grad1 Please read carefully the details concerning BIO 447 that are presented in the various BIO 447 Setup links in the first group of boxes on the course Home Page. Note especially that I do not give (or grade) exams for students who never come to class. If you prefer not to go to course presentations and discussions, BIO 447 is not for you.

To Respond to Turning Point Questions in Class:
Using the NXT Transmitter (Revised January 10, 2015 Put your last name onto your transmitter under “Your ID” for NXT If you borrow a transmitter from us, fill out an index card, take instruction form, leave the device ID unchanged on the borrowed transmitter. We will know who y ou are form the index card that you filled out on the date when you borrowed our transmitter. Do not change the “BIO” designation. We are using Channel 41 in this room. NXT should find Channel 41 when you hit “Find Channel”. You get a smiley face. Respond to the question as directed on the question itself. With NXT you have to hit the square response button in the upper left below the screen in order to get to the blank screen that is presentation mode. Screen will show whether your response has been received. Your device will also show a check when your name has been received. If you have problem with your NXT transmitter we can provide a paper back-up form if absolutely unavoidable. However, you must hand in the back-up form with your response at the same time that the question is being responded to by the rest of the class. You must identify yourself with your SUID photo card when you hand in a back-up form so we know that the form has been filled out by the person who hands it in. We count persons in class and match that number with the TP responses + Backup Forms. If the numbers don’t agree, we hand out paper forms one-at-a-time. The person or persons who have someone else respond for them will be dismissed from the class

The Next Two Slides are Turning Point Quiz Question Slides
You may not use any notes or electronic devices other than your NXT transmitter. No computers. No phones. No talking or consulting. Make sure that your desk is clear. These are graded quizzes that make up 40% of the overall course grade. They are designed for both you and me to determine whether you are paying attention and following what is going on. You can send a “Response to Leader” while a TP Slide is open. Give it a try. You can communicate with me.

With your name entered under Device ID: To get a blank screen that accepts your response: repeatedly push the black square button in the upper left of the NXT device. When you get the blank screen, respond to the question: I am here! Yes No Response Counter

This is a fill-in-the-blank question: Fetal Genes that are re-expressed in cancerous adult tissues are called _ _ _ _ -fetal genes Rank Responses 1 2 3 4 5 6

Course Evaluation, Grading, and Maintenance of Standards
Three In-Class Exams, 100 Pts Each Tuesday February 17th, After Classes 1 to 10 Tuesday, March 31st, After Classes 11 to 19 Tuesday April 28th, after Classes 20 to 27 (Last Day of Class) Class Participation Components at Every Class: Based on Responses Using Turning Point NXT-Transmitters 200 Points Maximum Possible (40% of Course Grade)

To Send in a “Response to Leader” Question at any time during class:
Course Web-Site Integrated Web-site at is a crucial element of this course. See Class Schedule and Graphics On Course Main Web-Page To Send in a “Response to Leader” Question at any time during class: Use Cntrl F8. (Your ID but not your name will show) Type in your message. I will get an icon on my screen to see what was asked.

Textbook: Biology of Cancer Robert A. Weinberg Garland Science, 2014
Second Edition CD with Movies, Mini-lectures, Pathways in Cancer Poster, Powerpoint and JPEG Versions of Textbook Graphics 501Text

Scope of Disciplines in Basic Sciences Involved in Biology of Cancer
Cell Biology Genetics Molecular Biology Biochemistry Immunology Microbiology/Virology Developmental Biology Physiology Environmental Biology Histology Pathobiology Pharmacology Epidemiology Neurobiology Organic Chemistry Physics Statistics Computer Information Sciences

Some Conceptual Goals in Biology of Cancer Course
Overview of Cancer Biology: What Does One Study? How Do Cancer Biologists Think? How Are Questioned Formulated? How are Experiments and Trials Designed? What (Who) Do Cancer Biologists Work On? What are the Real Questions and the Limitations? What are the Currently Best Prospects for: Improved Understanding of the Biology of Cancer? Improved Diagnosis, Management, and Cures? What Do Terms in Oncology Mean? What is Cancer Like: As a Biological Manifestation? As a Clinical Problem? As a Problem for People?

Why Study the Biology of Cancer?
Cancer Incidence, Morbidity, and Mortality 1,638,910 New Cases US; 1,660,290 (2013); 1,665,540 (2014) ~12,000,000 New Cases per Year - World-Wide 580,350 Deaths US ; 585,720 (2014) 1,590 Deaths per Day – 2013 U.S. ; 1,605 (2014) ~6,000,000 Deaths per Year - World-Wide 1 in 200 out of 310 Million (US) will present with Cancer in 2014 Lifetime Risk of presenting with Cancer ~ 40% (assuming 80-year lifespan and no change in incidence 1 in 600 will die of Cancer in 2014 (0.18% of US Population) Lifetime Risk of Death ~13% Protracted, Degenerative, Dehumanizing Diseases 1.8% of Cancer Deaths are Children ages 1 to 14 (10,800 deaths per year)

Cancer in Children William Bunn: 8-Year-old Police Officer July, 2010
Filename: BoyPoliceman11July10.doc Video 1 - 2 minutes and 32 seconds Video 2 1 1/2 minutes - actual funeral Refers to Stem Cell Transplants and Chemotherapy for Neuroblastoma in final 5 seconds of clip Video 3: Kuyler Van Nocker and Neuroblastoma (Slide 49)

Cancer and Other Causes of Death in Children
Number of Children 0 to 5 Years Old: Million 6 to 11 Years Old Million 12 to 17 Yrs Old Million Cancer Deaths in Children 140 per million children/year 75 Million Children = 10,500 Cancer Deaths per Year 1.8 % of total Cancer Deaths per Year Gun Deaths in Children Ages 0 to 14 per Year: 3,400 Gun Deaths per Year (Accidental and Deliberate Homicide) School Shootings per Year Tripled since 1995 Sharpton News; January 16, 2013 116,000 Guns Deaths in Children since 1979

How This Course in Cancer Biology is Set Up
Part 1: What is Cancer like as a collection of diseases? (Topics: Intro501; Clinical Patterns, Epidemiology, Classifications, Model Systems) Part 2: How do Cancers get that way? (Topics: Cancer Cell Properties, Cancer Cell Interactions, Progression, Growth, Invasion and Metastasis, Cancer Genetics, Cancer Virology) Part 3: What can we do about it? (Topics: War on cancer , Cancer Therapy, Cancer Immunology, Immunotherapy of Cancer; Clinical Management

Why Study the Biology of Cancer? Biology as the Basis For:
Improved Diagnosis Improved Management Increased Survival Time Long-Term Cures Prevention Chance for cure or extended survival depends strongly on where patient goes for diagnosis and where patient is treated! (See Newsweek, Oct. 26, 2009) “What You Don’t Know Might Kill You,

Why Biology of Cancer Now? The Knowledge Base
Advances in Molecular Genetics Genomics and Proteonomics Cellular and Humoral Immunity Inter-cellular Communication and Regulation Cytokines, Growth Factors, Receptors Membrane Structure and Function Membrane Adhesion Receptors and Ligands Membrane Transport Intra-cellular Pathways and Regulatory Cascades Cell Cycle Control Regulation of Nuclear Gene Expression Normal and Aberrant Differentiation Pathways to Cell Death or to Cellular Immortalization BioKnow

Biotechnology & the Cancer Problem the Technological Tools Now Available
Genetics, Cell, and Molecular Biology Gene Identification, Isolation, Cloning, & Sequencing Structure, Relationships, & Functions of Gene Products Directed Protein Synthesis, Site-Directed Mutagensis Cell Separation and Cell Culture In Situ Cell Labelling and Dynamic Functions Cellular and Humoral Immunity Monoclonal Antibodies Radio-immunoassays In Situ Labelling and Diagnosis Biophysical Tools Magnetic Resonance, CAT Scan, X-Ray Radio-isotope Labelling Electron Microscopy Live Animal Models and Tumor Model Systems Inbred Animals Genetically Engineered Animals BioTools

Molecular and Cellular Anomalies in Cancer
Abberant Genes and Gene Expression

Banding pattern of normal metaphase human chromosomes
Figure 1.11a The Biology of Cancer (© Garland Science 2007)

using chromosome specific DNA probes with different fluorescent dyes
Fluorescent in situ hybridization (FISH) of normal metaphase human chromosomes using chromosome specific DNA probes with different fluorescent dyes Figure 1.11b The Biology of Cancer (© Garland Science 2007)

Aneuploidy in Human Hepatocellular Carcinoma Cell Line
Chromosome number, structure of individual defined numbered chromosomes, and fine structure as shown by banding patterns are grossly abnormal in advanced cancers. (Compare to the previous slide of normal chromosomal structures.). Hsr = homogeneously staining region due to endoreduplication of chromosomal segments resulting in gene amplification

Aneuploid karyotype of human breast cancer cell.
Note “scrambling” of colors demonstrating chromosomal reciprocal translocations Note intermixing of chromosomal components between and among chromosomes. What are the chances that this cell will express normal behavior if it is viable? Figure 1.11c The Biology of Cancer (© Garland Science 2007)

Intra-chromosonal inversion by M-band fluorescent in situ hybridization(mFISH)
Figure 1.11d The Biology of Cancer (© Garland Science 2007)

Gene Expression DNA Array Analysis
mRNA’s From 142 different human tumors Red = elevated expression 1800 HumanGenes Green = diminished expression Figure The Biology of Cancer (© Garland Science 2007)

Molecular and Cellular Anomalies in Cancer
Aberrant Cell Structures and Cell Behavior Role of the Cytoskeleton In Cell Adhesion, Cell Division, Cell Migration

Intermediate filaments
Cytoskeleton: Actin microfilaments Microtubules Intermediate filaments Figure 1.14a The Biology of Cancer (© Garland Science 2007)

Intermediate Filaments of epithelial cell (keratin) in green
Plasma membrane in blue Figure 1.14b The Biology of Cancer (© Garland Science 2007)

3T3 Mouse Fibroblast attached to fibronectin extra-cellular matrix by integrin receptors
Figure 1.14d The Biology of Cancer (© Garland Science 2007)

Motility of a Fish Keratocyte
Actin microfilament leading edge Figure 1.15c The Biology of Cancer (© Garland Science 2007)

The Complexity of Signaling Factors, Receptors, and Pathways
Why is Cancer This Way? What can we do about it? The Complexity of Signaling Factors, Receptors, and Pathways

Increased T Cell Adhesion
Growth Factors and Receptors: Signal Transduction Across Membranes Ras Pathway Increased T Cell Adhesion R T K Growth Factors R T K Antigen PMA Integrins GAP T C R SHC GRB2 GTP CD-GEGII β1 Ras β1 β1 SOS Ras P β2 β2 GEF P P GDP Lck PLC-ε PI3K p120- GAP RalGDS P Raf Rac Rap1A p190-B Ral GTP P MEKs PAKs PLD RalBP1 Rho PLD Pathway Review: Ras is a membrane-associated guanine nucleotide-binding protein that is normally activated in response to the binding of extracellular signals, such as growth factors, RTKs (Receptor Tyrosine Kinases), TCR (T-Cell Receptors) and PMA (Phorbol-12 Myristate-13 Acetate). Ras signaling affects many cellular functions, which includes cell proliferation, apoptosis, migration, fate specification, and differentiation. Ras acts as a binary signal switch cycling between ON and OFF states, which are characterized in terms of a small molecule, a guanine nucleotide, bound to the protein. In the resting cell, Ras is tightly bound to GDP (Guanosine Diphosphate), which is exchanged for GTP (Guanosine Triphosphate) upon binding of extracellular stimuli to cell membrane receptors. In the GTP-bound form, Ras interacts specifically with so-called effector proteins, thereby initiating cascades of protein-protein interactions that may finally lead to cell proliferation. To return to the inactive OFF state, Ras cleaves off the terminal phosphate moiety, the Gamma-Phosphate, of GTP in an enzymatic process, the intrinsic GTPase reaction. The remaining GDP-bound Ras is no longer able to interact with effectors, it is switched OFF. Ras is thought to activate a number of signaling pathways, including the Raf/MEK/ERK (Extracellular Signal-Regulated Kinases) pathway, the MEKK/SEK/JNK (Jun N-terminal Kinases) pathway, a PI3K (Phosphatidylinositol 3-Kinase)/Akt/NF-KappaB (Nuclear Factor-Kappa B) pathway, a p120-GAP/p190-B/Rac/NF-KappaB pathway, and a Raf/MEKK1/IKK (I-KappaB Kinase)/I-KappaB/NF-KappaB pathway. Most growth factors that signal through RTKs or heterotrimeric GPCR (G-Protein Coupled Receptors) stimulate Ras by recruiting the GEF (Guanine-Nucleotide Exchange Factor) SOS (Son of Sevenless) to the membrane. SOS exists in a complex with the adapter protein GRB2 (Growth Factor Receptor-Bound Protein-2). Upon receptor activation, the GRB2/SOS complex is translocated to the membrane by binding of GRB2 to tyrosyl-phosphorylated residues in RTKs or additional adapter proteins. GTP-bound Ras recruits and activates Raf. Raf initiates a cascade of protein phosphorylation by first phosphorylating MEKs. Phosphorylated MEK in turn phosphorylates ERKs. Phosphorylated ERK moves from the cytoplasm into the nucleus where it subsequently phosphorylates a number of transcription factors, including the specific transcription factor called Elk1. Phosphorylated transcription factors turn on transcription (gene expression) of specific sets of target genes. The activity of Ras is limited by the hydrolysis of GTP back to GDP by GAP (GTPase Activating Proteins) (Ref.1). A second effector is PI3K, which synthesizes several lipid second messengers that activate small G proteins such as Rac and CDC42 (Cell Division Cycle-42). Rac also has multiple effectors, one of which is the serine threonine kinase PAKs (p21 Activated Kinases). The PI3K-mediated survival signal is also triggered by the activation of Akt/PKB (Protein Kinase-B). The third and most recently established effector is the Ral guanine nucleotide exchange factor, RalGDS (Ral-Guanine Nucleotide Dissociation Stimulator). RalGDS is a GEF (Guanine Nucleotide Exchange Factor) for the small GTPase Ral. Currently, five Ral GEFs have been identified; RalGDS, Rgl, Rlf, Rgr and RalGEF2 that are direct targets for Ras (Ref.2). They provide a mechanism for Ral activation by extracellular signals via a variety of receptors, including GPCR and RTKs. Reactive free radicals and cellular redox stress have been proposed to directly activate Ras. NO (Nitric Oxide) promotes the direct post translational modification of Ras by single S-nitrosylation at Cys118. These results in stimulation of guanine nucleotide exchange, possibly by destabilization associates with other effectors, leading to transduction of Ras mediated signals through multiple pathways. In addition to Raf, PI3K and RalGDS other Ras effectors have been proposed, including p120GAP, PKC-zeta, Rin1, AF6, and NF1 GAP (Ref.3). TCR engagement also leads to the activation of Ras via a signaling pathway involving the activation of p56 (Lck) and PKC (Protein Kinase-C). Biochemical and genetic studies have now confirmed the functional relevance of Ras effectors. The Raf protein kinase family controls the activation of the MAPK (Mitogen-Activated Protein Kinases) pathway and plays a major role in controlling proliferation and differentiation. The PI3K mediates some of the Ras-dependent actin cytoskeleton remodeling and protection against apoptosis. The third bonafide Ras effector is RalGDS, regulates multiple processes including receptor endocytosis, cytoskeletal changes, and DNA synthesis. The Ras-Raf-MEK-ERK pathway features several oncogenes and is deregulated in approximately 30% of all human cancers. It has also emerged as a prime target for antitumor therapy (Ref.4). References: 1. Gay B, Suarez S, Caravatti G, Furet P, Meyer T, Schoepfer J. Selective GRB2 SH2 inhibitors as anti-Ras therapy. Int. J. Cancer Oct 8;83(2): PubMed ID: 2. Emel Okan et al. The small-GTPase RelA activates transcription of the urokinase plasminogen activator receptor (uPAR) gene via an AP1-dependent mechanism. ONCOGENE 5 April 2001, Volume 20, Number 15, Pages PubMed ID: 3. Diaz-Meco MT, Lozano J, Municio MM, Berra E, Frutos S, Sanz L, Moscat J. Evidence for the in vitro and in vivo interaction of Ras with protein kinase C zeta. J. Biol. Chem Dec 16;269(50): PubMed ID: 4. Kolch W. Ras/Raf signalling and emerging pharmacotherapeutic targets. Expert Opin. Pharmacother Jun;3(6): PubMed ID: MEKK1 CDC42 P Cytoskeleton Actin ERKs Stress Fibers and Focal Adhesions JNKK ERKs JNK JNK c-Jun Elk1 ATF2 Gene Expression c-Fos 2009 ProteinLounge.com C

Molecular Signaling in Cancer (From Quigen.com)

Thoughts on Conversations in a Crowded Room

The Next Two Slides are Turning Point Quiz Question Slides
You may not use any notes or electronic devices other than your NXT transmitter. No computers. No phones. No talking or consulting. Make sure that your desk is clear. These are graded quizzes that make up 40% of the overall course grade. They are designed for both you and me to determine whether you are paying attention and following what is going on. You can send a “Response to Leader” while a TP Slide is open. Give it a try. You can communicate with me.

This slide is showing the karyotype of a human breast cancer cell
This slide is showing the karyotype of a human breast cancer cell. What is this slide illustrating about cancer genetics? (you can abbreviate as long as I can figure out what you are trying to say.

Mouse mammary cancer cell lines established in 1903 are still viable and still in use. This illustrates a key property of cancer cells that is unique to cancer cells and that contributes in a major way to their pathogenicity. One answer is all that is needed. These cell lines illustrate that cancer cells are ___ ___ ___ ___ ___ ___ ___ ___ or That these cancer cells have been ___ ___ ___ ___ ___ ___ ___ ___ ___ ___ ___ ____

Cancer Biology and Clinical Treatment
The Impact of the Health-care System About Kuyler Van Nocker and Neuroblastoma

Week Two: The Story of Kelley Mitchell and Ewings Sarcoma
Cancer Treatment | PBS NewsHour | Jan. 1, 2001 | PBS Jan 1, ELIZABETH BRACKETT: Last year, Kelley Mitchell lost her battle against cancer. But before the 16-year-old died, she agreed to try a highly ... Last Presentation: The Story of Taylor Black and Neuroblastoma (“Daydreams and Diaries” - UntreedReads.com OnLine Story of Taylor Black by Tim Black)

Intro501 Stops Here for 2014 Go to: Cancer2013_ACS.pptx
American Cancer Society Facts and Figures for 2014

On a scale of 1 to 5 rate: #1 = -2 = I’m pretty much lost, Please slow down and repeat. #2 = -1 = I’m struggling. I follow some of it, but I’m having hard time. #3 = 0 = I’m OK. I understand most of it. I’ll figure the rest out later. #4 =+1 = I doing OK. No Problem. #5 = +2 = This is no sweat. Please get moving before I get totally bored.

Yifan Gong and Twinkle Chowdhury will present the Graduate Research seminar on Tuesday, January 14 at 3:30 in 106 Life Sciences Complex. Yifan's Title: COX-2 in brain: Regulation of COX-2 and its role as a neuromodulator in seizure generation Yifan's Advisor: Dr. Jim Hewett Twinkle's title: Glutamate-mediated neuronal cell death pathways Twinkle's Advisor: Dr. Sandra Hewett

Regulation of Gene Expression by Transcription Factors:
General and Specialized Transcription Factors Figure The Biology of Cancer (© Garland Science 2007)

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