Regarding techniques of proteomics, there is:
|
|
- Neil Sims
- 5 years ago
- Views:
Transcription
1 Molecular الحلقة biology 14 واألخيرة To put you back in the context; the discussion was about Trancriptomics (the study of transcription). The following topic will be PROTEOMICS, which is the study of proteins, analysis of large sets of proteins. An important property of the field is the high throughput, which means that we're dealing with tens, hundreds, maybe thousands of specimens and genes Genomics Vs. Proteomics: Genomics are constant relatively: same genome for an individual along life (minor changes). Proteomics are dynamic: changes happen in min's, hours along the day (sleep/wake, eat/starve ). Regarding techniques of proteomics, there is: Slide#75 Mass spectrometry: An old method which went back in use, it measures mass/charge ratio. Consists of: -Ion source: Ionization of the specimen. -Mass analyzer: separation of ions based on size. -Detector: to detect if there is an ion or not, and where is it detected. Now every peptide has a distinct profile, that might not be enough so we need another go (in the first time we detect general properties of protein, maybe the protein family, so we need to specify this more).. Another ion source and mass analyzer are used, one of the proteins of the first go will be fragmented and separated in the analyzer, detected finally on the detector, and now we know which exact protein is this. An advantage of this method is that we can analyze a large number of proteins within one experiment AFTER being processed in liquid chromatography (this separates them based on size, polarity ). e.g. A blood sample is a complex sample that contains many proteins, we can identify all proteins by the aforementioned method. Extra note : in the figure, HPLC: highperformance liquid chromatography. CID: chemically induced dynamic sth Slide#77: (مصفوفة= array Protein microarray: (recall that Expression array Forwardphase Backwardphase Protein microarray Interaction array Functional array
2 -In forward phase, different probes (Antibodies usually) are on the array, distributed as spots. When the protein sample is administered on the array the antibodies will bind to their compatible proteins. So the goal of this (forwardphase) is to detect if the PROTEINS are present. Hundreds of proteins can be detected in the trial, each for its Ab. -In backward-phase, the goal is to find ONE or two proteins only, using one or two Ab and many specimens (hundreds). Forward One specimen Many probes Many proteins to detect(protein profile will result) Forward Vs. Backward: Backward Many specimens One or two probes One or two proteins to detect Slide#78: Interaction array: Human and fly have high gene homology, so where did human complexity come from? Not only expression! Modification, phosphorylation, glycosylation.. give role (protein-protein interactions). And this method is to detect these interactions. -The array contains known molecule ligands, let's say it contains proteins Now when the specimen protein is added it bind and interacts with protein 2, 50 for say now I know that my protein reacts with 2 and 50. Slide#79: Functional array(aka enzymatic microarray): The goal is to know which substrate is for that specific enzyme, so the array contains enzymes, then the substrate is added, for example it reacted and gave products by enzyme #10 Enzyme #10 is the catalyst for this reaction. Expression Vs. Interaction Vs. Functional Expression Interaction Functional Does protein Does protein Does substrate exist? interact? react? Slide#80: Protein-Protein interaction: When studying a specific mutation (defective protein), we want to know what are the relationships and effects on other proteins in the cell. e.g. in the cell cylce (right figure), there are proteins A,B,C each one can regulate a point in the cycle, and can interact with other proteins. On the left figure (taken for multiple sclerosis disease) you can see the connections that make a network of interactions. So the purpose of studying protein-protein interaction is to predict the possibility of developing a disease if a gene was mutated. e.g. gene 1 can strongly affect genes 11,12,13 if mutated, while 13 can weakly affect 4,5,6.. just a network. Slide#81: The future of biomedicine is PERSONAL MEDICINE! :Giving the most suitable treatment depending on the expression profile of genes. Slide#83 The figure shows cancer steps, simple; tumor is at first a benign mass of cells that can be removed UNCONTROLLED
3 proliferation Accumulation of mutations one cell will become aggressive Proliferation cancer invasion and metastasis. Slide#84 Clonal= come from one cell origin. -Not all cells in tumor are homogenous, clusters of different clones can be found due to different mutations. Slide#85 -Hereditary 10% (Colon, eye, breast..) -As for estrogen, women with increased TIME or AMOUNT of estrogen have higher breast cancer susceptibility. Exogenously administered estrogen may help women at menopause and decrease osteoporosis, but must be given carefully. -Smoking is carcinogen -H. Pylori causes cancer by changing the environment of the stomach. -Liver cancer is #2 in Egypt! Due to high HCV infections. -#1 is Bilharsza, causing bladder cancer. Slide#86 & 87: Normal body cells have homeostasis, a balance between growth and death, #dying cells= #proliferating. If # proliferating cells or #dying cells tumors cancers. So on the balance; Oncogenes genes that increase cell proliferation. Tumor supressor genes increase genes that cell death and supress proliferation. Slide#89: Oncogene, when it is normal it is called proto-oncogene; normally it: Proliferation DIFFERENTIATION (because it leads to cell death faster) Cell survival BUT when mutated, the oncogene gives UNCONTROLLED: Proliferation DIFFERENTIATION Cell survival Slide#89 Extremely important (compare to tumor suppressor gene mutations in the next page) Oncogene mutations are DOMAINANT; one allele mutation is enough to cause cancer. The mechanism is GAIN of function; "Gain of function mutations change the gene product such that it gains a new and abnormal function. - Wikipedia" In the next 3 slides, examples of the 3 functions of oncogenes; cell proliferation, differentiation, and survival. Slide#90 Proliferation; The Ras gene: -Mutated in 95% of pancreatic cancers. -20% of other cancers. -Mechanism: Ras protein is activated by a receptor (e.g. epithelial growth factor receptor-egfr(erbb), or HER2) it attaches to the membrane from the inside (a key step) activation of a kinase (Raf) activation of another kinase (MEK)
4 activation of another kinase (ERK) ERK will do its job inside the nucleus; activating transcription factors, causing transcription of some genes, e.g. cyclind1 induce cell proliferation by inducing the cell cycle from G1 to S phase. CyclinD1 also phosphorylate Rb gene (retinoblastoma), inactivating it, allowing cell proliferation. Note: breast cancer can develop via Ras mutation activation of HER2 receptor gene amplification "A selective increase in the number of copies of a gene coding for a specific protein without a proportional increase in other genes.- Wikipedia". The chromosome may look thicker in some bands. Suggested therapy: inhibition of the enzyme that helps Ras protein binding the membrane (blocking the key step aforementioned). It worked perfectly in labs on mice, but failed on clinical trials. Slide#91: Differentiation; Promylocyte(PML)/RARα gene. This gene when mutated blocks differentiation on a certain cell of the lineage which is the Promyelocyte thus leading to overproliferation of it Promyelocytic leukemia. Suggested therapy: drug to induce cell differentiation rather than proliferation. Slide#92: Survival(prevention of cell death); Akt: Akt is activated by a kinase (PIP3- Phosphatidyl inositol triphosphate) which is activated by a receptor (e.g. receptor A7) Akt activates Bcl-2 blocks mitochondrial induced apoptosis no apoptosis accumulation of mutations Cancer. Slide#93: Tumor suppressor genes inhibit proliferation and induce cell death. Type of mutation is RECESSIVE (Both alleles must be mutated). Loss of function mutation "are the result of gene product having less or no function.-wikipedia". -In children born with 1 Rb allele deleted, if the other is mutated this will cause loss of function eye cancer. Slide#94: How RB works? (see figure) - Sequestration binding of E2F (elongation factor 2) inhibiting G1 to S progression in the cell cycle. If Rb was phosphorylated inhibited cant bind E2F G1 to S will progress normal. (Recall that Rb gets phosporylated by cyclingd1 which expression is increased by the Ras pathway) Slide#95: P53 is a tumor suppressor gene, activated by DNA damage. -If the damage can be repaired cell cycle will be arrested repair will take place cell will return to its cycle. -If the damage was huge Appoptosis. -How P53 works? -It induces p21 (a protein) expression
5 p21 will inhibit 1)Cdk's (cyclin dependant kinase) inhibiting cell cycle. 2)PCNA (Proliferating cell nuclear antigen) inhibiting DNA replication. Slide#96: Genetic model of colorectal cancer: ordered sequential mutations resulting in metastatic cancer. Discovered by Bert Vogelstein, the model didn't work on all types of cancer. -One mutation isn t enough to make the cell cancerous, mutations must be accumulated. -Normal cell APC mutation dysplastic cell Ras mutation intermediate adenoma another mutation late adenoma another carcinoma another metastatic cancer. -Some companies are developing kits to decide if a certain case of colorectal cancer has a Ras mutation or not, providing treatment upon result (personalized medicine). Slide#97: In traditional treatment of cancer, many cases will not completely be cured, some cancerous cells might survive because they have different mutation cancer may reappear. 2)HER2 amplification give HERCEPTIN (a drug). i.e. give the drug for the specific mutation according to patient profile. The slide shows molecular diagnosis of cancer. Not all were explained. (Brca1 results in DNA damage). Slide#98: A patient may complain of a metastasis without knowing where is the primary cancer, this microarray classifies types of cancers looking at expression profile so we can tell which is the primary tumor. Slide#99: Triple-negative breast cancer, i.e: 1) ER -ve (estrogen receptor) 2)PR -ve (progesterone receptor) 3)HER2 -ve This type of cancer is too aggressive chemotherapy. A new trend of understanding the triple ve breast cancer to give better treatment, by analyzing expression profile found out that there are 6 different classes of it based on distinct gene set expression! e.g. metabolism, androgen receptor, stem cell genes related triple negative breast cancer. Solution: give 2 or 3 types of cancer therapy. e.g. of personalized medicine: a lady with breast cancer. Suspect: 1) Estrogen receptor mutation, overexpression, amplification, hyperactivity give ER (estrogen receptor) inhibitor.
6 Slide#100: Hallmark of cancers: Only the bold line points were explained with example of each. Notes: Cancer cells are recognized and killed by the immune system (because they carry different protein and mutations). Some cells can avoid immune destruction by suppression and reduction of immune system, e.g. fake proteins that can inactivate immune cells. العلم نور وتشريف لصاحبه فاطلب هديت فنون العلم واألدبا العلمكنز وذخر ال فناء له نعم القرين إذا ما صاحب صحبا
CELL CYCLE REGULATION AND CANCER. Cellular Reproduction II
CELL CYCLE REGULATION AND CANCER Cellular Reproduction II THE CELL CYCLE Interphase G1- gap phase 1- cell grows and develops S- DNA synthesis phase- cell replicates each chromosome G2- gap phase 2- cell
More informationMolecular biology :- Cancer genetics lecture 11
Molecular biology :- Cancer genetics lecture 11 -We have talked about 2 group of genes that is involved in cellular transformation : proto-oncogenes and tumour suppressor genes, and it isn t enough to
More informationIntroduction. Cancer Biology. Tumor-suppressor genes. Proto-oncogenes. DNA stability genes. Mechanisms of carcinogenesis.
Cancer Biology Chapter 18 Eric J. Hall., Amato Giaccia, Radiobiology for the Radiologist Introduction Tissue homeostasis depends on the regulated cell division and self-elimination (programmed cell death)
More informationMultistep nature of cancer development. Cancer genes
Multistep nature of cancer development Phenotypic progression loss of control over cell growth/death (neoplasm) invasiveness (carcinoma) distal spread (metastatic tumor) Genetic progression multiple genetic
More informationKaryotype analysis reveals transloction of chromosome 22 to 9 in CML chronic myelogenous leukemia has fusion protein Bcr-Abl
Chapt. 18 Cancer Molecular Biology of Cancer Student Learning Outcomes: Describe cancer diseases in which cells no longer respond Describe how cancers come from genomic mutations (inherited or somatic)
More informationDetermination Differentiation. determinated precursor specialized cell
Biology of Cancer -Developmental Biology: Determination and Differentiation -Cell Cycle Regulation -Tumor genes: Proto-Oncogenes, Tumor supressor genes -Tumor-Progression -Example for Tumor-Progression:
More informationChapt 15: Molecular Genetics of Cell Cycle and Cancer
Chapt 15: Molecular Genetics of Cell Cycle and Cancer Student Learning Outcomes: Describe the cell cycle: steps taken by a cell to duplicate itself = cell division; Interphase (G1, S and G2), Mitosis.
More informationCELL BIOLOGY - CLUTCH CH CANCER.
!! www.clutchprep.com CONCEPT: OVERVIEW OF CANCER Cancer is a disease which is primarily caused from misregulated cell division, which form There are two types of tumors - Benign tumors remain confined
More informationCancer genetics
Cancer genetics General information about tumorogenesis. Cancer induced by viruses. The role of somatic mutations in cancer production. Oncogenes and Tumor Suppressor Genes (TSG). Hereditary cancer. 1
More informationCancer and Gene Alterations - 1
Cancer and Gene Alterations - 1 Cancer and Gene Alteration As we know, cancer is a disease of unregulated cell growth. Although we looked at some of the features of cancer when we discussed mitosis checkpoints,
More informationoncogenes-and- tumour-suppressor-genes)
Special topics in tumor biochemistry oncogenes-and- tumour-suppressor-genes) Speaker: Prof. Jiunn-Jye Chuu E-Mail: jjchuu@mail.stust.edu.tw Genetic Basis of Cancer Cancer-causing mutations Disease of aging
More informationA class of genes that normally suppress cell proliferation. p53 and Rb..ect. suppressor gene products can release cells. hyperproliferation.
Tumor Suppressor Genes A class of genes that normally suppress cell proliferation. p53 and Rb..ect Mutations that inactivate the tumor suppressor gene products can release cells from growth suppression
More informationEarly Embryonic Development
Early Embryonic Development Maternal effect gene products set the stage by controlling the expression of the first embryonic genes. 1. Transcription factors 2. Receptors 3. Regulatory proteins Maternal
More informationSection D: The Molecular Biology of Cancer
CHAPTER 19 THE ORGANIZATION AND CONTROL OF EUKARYOTIC GENOMES Section D: The Molecular Biology of Cancer 1. Cancer results from genetic changes that affect the cell cycle 2. Oncogene proteins and faulty
More informationDeregulation of signal transduction and cell cycle in Cancer
Deregulation of signal transduction and cell cycle in Cancer Tuangporn Suthiphongchai, Ph.D. Department of Biochemistry Faculty of Science, Mahidol University Email: tuangporn.sut@mahidol.ac.th Room Pr324
More informationNeoplasia 18 lecture 6. Dr Heyam Awad MD, FRCPath
Neoplasia 18 lecture 6 Dr Heyam Awad MD, FRCPath ILOS 1. understand the role of TGF beta, contact inhibition and APC in tumorigenesis. 2. implement the above knowledge in understanding histopathology reports.
More informationCancer Genetics. What is Cancer? Cancer Classification. Medical Genetics. Uncontrolled growth of cells. Not all tumors are cancerous
Session8 Medical Genetics Cancer Genetics J avad Jamshidi F a s a U n i v e r s i t y o f M e d i c a l S c i e n c e s, N o v e m b e r 2 0 1 7 What is Cancer? Uncontrolled growth of cells Not all tumors
More informationIntroduction to Cancer Biology
Introduction to Cancer Biology Robin Hesketh Multiple choice questions (choose the one correct answer from the five choices) Which ONE of the following is a tumour suppressor? a. AKT b. APC c. BCL2 d.
More informationCancer and Oncogenes Bioscience in the 21 st Century. Linda Lowe-Krentz
Cancer and Oncogenes Bioscience in the 21 st Century Linda Lowe-Krentz December 1, 2010 Just a Few Numbers Becoming Cancer Genetic Defects Drugs Our friends and family 25 More mutations as 20 you get older
More informationChapter 12. Regulation of Cell Division. AP Biology
Chapter 12. Regulation of Cell Division Coordination of cell division! Multicellular organism " need to coordinate across different parts of organism! timing of cell division! rates of cell division "
More informationCancer Biology How a cell responds to DNA Damage
1 Cancer Biology How a cell responds to DNA Damage Jann Sarkaria Department of Oncology Mayo Clinic 2 EDUCATIONAL GOALS How proteins can transmit signals to each other. The definition of a tumor suppressor
More informationRegulation of Cell Division. AP Biology
Regulation of Cell Division 2006-2007 Coordination of cell division A multicellular organism needs to coordinate cell division across different tissues & organs critical for normal growth, development
More informationProf. R. V. Skibbens
Prof. R. V. Skibbens December 2, 2011 BIOS 10: BioScience in the 21 st Century Cell Cycle, Cell Division and Cancer (Part 2) Directionality The Cell Cycle clock goes in only one direction S-phase cells
More informationCancer. The fundamental defect is. unregulated cell division. Properties of Cancerous Cells. Causes of Cancer. Altered growth and proliferation
Cancer The fundamental defect is unregulated cell division. Properties of Cancerous Cells Altered growth and proliferation Loss of growth factor dependence Loss of contact inhibition Immortalization Alterated
More informationRegulation of Cell Division (Ch. 12)
Regulation of Cell Division (Ch. 12) Coordination of cell division A multicellular organism needs to coordinate cell division across different tissues & organs critical for normal growth, development &
More informationDevelopment of Carcinoma Pathways
The Construction of Genetic Pathway to Colorectal Cancer Moriah Wright, MD Clinical Fellow in Colorectal Surgery Creighton University School of Medicine Management of Colon and Diseases February 23, 2019
More informationComputer Science, Biology, and Biomedical Informatics (CoSBBI) Outline. Molecular Biology of Cancer AND. Goals/Expectations. David Boone 7/1/2015
Goals/Expectations Computer Science, Biology, and Biomedical (CoSBBI) We want to excite you about the world of computer science, biology, and biomedical informatics. Experience what it is like to be a
More informationRegulation of Cell Division
Regulation of Cell Division Two HeLa cancer cells are just completing cytokinesis. Explain how the cell division of cancer cells like these is misregulated. Identify genetic and other changes that might
More informationFunctional Limitations
Regulation of the Cell Cycle Chapter 12 Pg. 228 245 Functional Limitations Various factors determine whether and when a cell divides. Two functional limitations for cell size limit growth or influence
More information609G: Concepts of Cancer Genetics and Treatments (3 credits)
Master of Chemical and Life Sciences Program College of Computer, Mathematical, and Natural Sciences 609G: Concepts of Cancer Genetics and Treatments (3 credits) Text books: Principles of Cancer Genetics,
More informationCancer and Oncogenes Bioscience in the 21 st Century. Linda Lowe-Krentz October 11, 2013
Cancer and Oncogenes Bioscience in the 21 st Century Linda Lowe-Krentz October 11, 2013 Just a Few Numbers Becoming Cancer Genetic Defects Drugs Our friends and family 200 180 160 140 120 100 80 60 40
More informationSection D. Genes whose Mutation can lead to Initiation
This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike License. Your use of this material constitutes acceptance of that license and the conditions of use of materials on this
More informationIntroduction to Genetics
Introduction to Genetics Table of contents Chromosome DNA Protein synthesis Mutation Genetic disorder Relationship between genes and cancer Genetic testing Technical concern 2 All living organisms consist
More informationCancer. The fundamental defect is. unregulated cell division. Properties of Cancerous Cells. Causes of Cancer. Altered growth and proliferation
Cancer The fundamental defect is unregulated cell division. Properties of Cancerous Cells Altered growth and proliferation Loss of growth factor dependence Loss of contact inhibition Immortalization Alterated
More informationChapter 18- Oncogenes, tumor suppressors & Cancer
Chapter 18- Oncogenes, tumor suppressors & Cancer - Previously we have talked about cancer which is an uncontrolled cell proliferation and we have discussed about the definition of benign, malignant, metastasis
More informationnumber Done by Corrected by Doctor Maha Shomaf
number 19 Done by Waseem Abo-Obeida Corrected by Abdullah Zreiqat Doctor Maha Shomaf Carcinogenesis: the molecular basis of cancer. Non-lethal genetic damage lies at the heart of carcinogenesis and leads
More informationTUMOR-SUPPRESSOR GENES. Molecular Oncology Michael Lea
TUMOR-SUPPRESSOR GENES Molecular Oncology 2011 Michael Lea TUMOR-SUPPRESSOR GENES - Lecture Outline 1. Summary of tumor suppressor genes 2. P53 3. Rb 4. BRCA1 and 2 5. APC and DCC 6. PTEN and PPA2 7. LKB1
More informationRAS Genes. The ras superfamily of genes encodes small GTP binding proteins that are responsible for the regulation of many cellular processes.
۱ RAS Genes The ras superfamily of genes encodes small GTP binding proteins that are responsible for the regulation of many cellular processes. Oncogenic ras genes in human cells include H ras, N ras,
More informationp53 and Apoptosis: Master Guardian and Executioner Part 2
p53 and Apoptosis: Master Guardian and Executioner Part 2 p14arf in human cells is a antagonist of Mdm2. The expression of ARF causes a rapid increase in p53 levels, so what would you suggest?.. The enemy
More informationDivision Ave. High School AP Biology
Regulation of Cell Division 2008-2009 Coordination of cell division A multicellular organism needs to coordinate cell division across different tissues & organs u critical for normal growth, development
More informationMitosis and the Cell Cycle
Mitosis and the Cell Cycle Chapter 12 The Cell Cycle: Cell Growth & Cell Division Where it all began You started as a cell smaller than a period at the end of a sentence Getting from there to here Cell
More information- A cancer is an uncontrolled, independent proliferation of robust, healthy cells.
1 Cancer A. What is it? - A cancer is an uncontrolled, independent proliferation of robust, healthy cells. * In some the rate is fast; in others, slow; but in all cancers the cells never stop dividing.
More informationBCHM3972 Human Molecular Cell Biology (Advanced) 2013 Course University of Sydney
BCHM3972 Human Molecular Cell Biology (Advanced) 2013 Course University of Sydney Page 2: Immune Mechanisms & Molecular Biology of Host Defence (Prof Campbell) Page 45: Infection and Implications for Cell
More informationMohammed El-Khateeb. Tumor Genetics. MGL-12 May 13 th Chapter 22 slide 1 台大農藝系遺傳學
Mohammed El-Khateeb Tumor Genetics MGL-12 May 13 th 2014 台大農藝系遺傳學 601 20000 Chapter 22 slide 1 Cancer Genetics Types of Genetic Alterations in Cancer Evidence that Mutations Cause Cancer Multistage Model
More informationCancer Cells. It would take another 20 years and a revolution in the techniques of biological research to answer these questions.
Cancer Cells Cancer, then, is a disease in which a single normal body cell undergoes a genetic transformation into a cancer cell. This cell and its descendants, proliferating across many years, produce
More informationBIO360 Fall 2013 Quiz 1
BIO360 Fall 2013 Quiz 1 1. Examine the diagram below. There are two homologous copies of chromosome one and the allele of YFG carried on the light gray chromosome has undergone a loss-of-function mutation.
More informationTHE EUKARYOTIC CELL CYCLE AND CANCER
THE EUKARYOTIC CELL CYCLE AND CANCER ABOUT THIS WORKSHEET This worksheet complements the Click and Learn The Eukaryotic Cell Cycle and Cancer developed in conjunction with the 2013 Holiday Lectures on
More informationChapter 9. Cells Grow and Reproduce
Chapter 9 Cells Grow and Reproduce DNA Replication DNA polymerase Addition of a nucleotide to the 3 end of a growing strand Use dntps as substrate Release of pyrophosphate Initiation of Replication Replication
More informationBiochemistry of Carcinogenesis. Lecture # 35 Alexander N. Koval
Biochemistry of Carcinogenesis Lecture # 35 Alexander N. Koval What is Cancer? The term "cancer" refers to a group of diseases in which cells grow and spread unrestrained throughout the body. It is difficult
More informationCancer. Questions about cancer. What is cancer? What causes unregulated cell growth? What regulates cell growth? What causes DNA damage?
Questions about cancer What is cancer? Cancer Gil McVean, Department of Statistics, Oxford What causes unregulated cell growth? What regulates cell growth? What causes DNA damage? What are the steps in
More informationLecture 8 Neoplasia II. Dr. Nabila Hamdi MD, PhD
Lecture 8 Neoplasia II Dr. Nabila Hamdi MD, PhD ILOs Understand the definition of neoplasia. List the classification of neoplasia. Describe the general characters of benign tumors. Understand the nomenclature
More information34 Cancer. Lecture Outline, 11/30/05. Cancer is caused by mutant genes. Changes in growth properties of cancer cells
34 Cancer Lecture Outline, 11/30/05 Review the Cell cycle Cancer is a genetic disease Oncogenes and roto-oncogenes Normally romote cell growth. Become oncogenic after oint mutations, dulications, deletion
More informationProblem Set 8 Key 1 of 8
7.06 2003 Problem Set 8 Key 1 of 8 7.06 2003 Problem Set 8 Key 1. As a bright MD/PhD, you are interested in questions about the control of cell number in the body. Recently, you've seen three patients
More informationBiochemistry of Cancer and Tumor Markers
Biochemistry of Cancer and Tumor Markers The term cancer applies to a group of diseases in which cells grow abnormally and form a malignant tumor. It is a long term multistage genetic process. The first
More informationProf. R. V. Skibbens. Cell Cycle, Cell Division and Cancer (Part 2)
Prof. R. V. Skibbens November 22, 2010 BIOS 10: BioScience in the 21 st Century Cell Cycle, Cell Division and Cancer (Part 2) Directionality - clocks go in only one direction G1 doesn t have replication-inducing
More informationApoptosis Oncogenes. Srbová Martina
Apoptosis Oncogenes Srbová Martina Cell Cycle Control point Cyclin B Cdk1 Cyclin D Cdk4 Cdk6 Cyclin A Cdk2 Cyclin E Cdk2 Cyclin-dependent kinase (Cdk) have to bind a cyclin to become active Regulation
More informationHST.161 Molecular Biology and Genetics in Modern Medicine Fall 2007
MIT OpenCourseWare http://ocw.mit.edu HST.161 Molecular Biology and Genetics in Modern Medicine Fall 2007 For information about citing these materials or our Terms of Use, visit: http://ocw.mit.edu/terms.
More informationLecture 10. G1/S Regulation and Cell Cycle Checkpoints. G1/S regulation and growth control G2 repair checkpoint Spindle assembly or mitotic checkpoint
Lecture 10 G1/S Regulation and Cell Cycle Checkpoints Outline: G1/S regulation and growth control G2 repair checkpoint Spindle assembly or mitotic checkpoint Paper: The roles of Fzy/Cdc20 and Fzr/Cdh1
More informationc) Macrophages and B cells present antigens to helper T_-cells. (Fill in blanks.) 2 points
Question 1 You are an immunologist who wants to make the big bucks. You decide to leave the world of science and get a job as a script-consultant on a new medical drama (ER-like) show. You test the writers
More information2015 AP Biology Unit #4 Quiz 1 Cell Communication, Cancer and The Cell Cycle Week of November
Name: Class: Date: 2015 AP Biology Unit #4 Quiz 1 Cell Communication, Cancer and The Cell Cycle Week of 16-20 November Multiple Choice Identify the choice that best completes the statement or answers the
More informationOverview of the core ideas in cancer research
Overview of the core ideas in cancer research Paul Edwards Cancer Research UK Cambridge Institute and Department of Pathology, University of Cambridge This lecture Overview of the ideas that provide the
More informationLecture 1: Carcinogenesis
Lecture 1: Carcinogenesis Anti-cancer (oncology agents): These are perhaps the most dangerous of drugs, other than the narcotic analgesics. This is due to their toxicities. Killing or inhibiting cancer
More informationThe Biology and Genetics of Cells and Organisms The Biology of Cancer
The Biology and Genetics of Cells and Organisms The Biology of Cancer Mendel and Genetics How many distinct genes are present in the genomes of mammals? - 21,000 for human. - Genetic information is carried
More informationSrc-INACTIVE / Src-INACTIVE
Biology 169 -- Exam 1 February 2003 Answer each question, noting carefully the instructions for each. Repeat- Read the instructions for each question before answering!!! Be as specific as possible in each
More informationCANCER. Inherited Cancer Syndromes. Affects 25% of US population. Kills 19% of US population (2nd largest killer after heart disease)
CANCER Affects 25% of US population Kills 19% of US population (2nd largest killer after heart disease) NOT one disease but 200-300 different defects Etiologic Factors In Cancer: Relative contributions
More informationGenetics and Cancer Ch 20
Genetics and Cancer Ch 20 Cancer is genetic Hereditary cancers Predisposition genes Ex. some forms of colon cancer Sporadic cancers ~90% of cancers Descendants of cancerous cells all cancerous (clonal)
More informationCell Death and Cancer. SNC 2D Ms. Papaiconomou
Cell Death and Cancer SNC 2D Ms. Papaiconomou How do cells die? Necrosis Death due to unexpected and accidental cell damage. This is an unregulated cell death. Causes: toxins, radiation, trauma, lack of
More informationDiagnostic test Suggested website label Description Hospitals available
Diagnostic test Suggested website label Description Hospitals available Abbott Molecular Inc, PATHVYSION HER-2 DNA Probe Kit (FISH) PathVysion kit A diagnostic tool used to determine whether a particular
More informationCancer. October is National Breast Cancer Awareness Month
Cancer October is National Breast Cancer Awareness Month Objectives 1: Gene regulation Explain how cells in all the different parts of your body develop such different characteristics and functions. Contrast
More informationA Genetic Program for Embryonic Development
Concept 18.4: A program of differential gene expression leads to the different cell types in a multicellular organism During embryonic development, a fertilized egg gives rise to many different cell types
More informationBiology is the only subject in which multiplication is the same thing as division
The Cell Cycle Biology is the only subject in which multiplication is the same thing as division Why do cells divide? For reproduction asexual reproduction For growth one-celled organisms from fertilized
More informationRegulation of cell cycle. Dr. SARRAY Sameh, Ph.D
Regulation of cell cycle Dr. SARRAY Sameh, Ph.D Control of cell cycle: Checkpoints Are the cell cycle controls mechanisms in eukaryotic cells. These checkpoints verify whether the processes at each phase
More information1. Basic principles 2. 6 hallmark features 3. Abnormal cell proliferation: mechanisms 4. Carcinogens: examples. Major Principles:
Carcinogenesis 1. Basic principles 2. 6 hallmark features 3. Abnormal cell proliferation: mechanisms 4. Carcinogens: examples Carcinogenesis Major Principles: 1. Nonlethal genetic damage is central to
More informationDr Rodney Itaki Lecturer Anatomical Pathology Discipline. University of Papua New Guinea School of Medicine & Health Sciences Division of Pathology
Neoplasia Dr Rodney Itaki Lecturer Anatomical Pathology Discipline University of Papua New Guinea School of Medicine & Health Sciences Division of Pathology General Considerations Overview: Neoplasia uncontrolled,
More informationLESSON 3.2 WORKBOOK. How do normal cells become cancer cells? Workbook Lesson 3.2
For a complete list of defined terms, see the Glossary. Transformation the process by which a cell acquires characteristics of a tumor cell. LESSON 3.2 WORKBOOK How do normal cells become cancer cells?
More informationTumor suppressor genes D R. S H O S S E I N I - A S L
Tumor suppressor genes 1 D R. S H O S S E I N I - A S L What is a Tumor Suppressor Gene? 2 A tumor suppressor gene is a type of cancer gene that is created by loss-of function mutations. In contrast to
More information2015 AP Biology Unit #4 Test Cell Communication, Cancer, Heredity and The Cell Cycle Week of 30 November
Class: Date: 2015 AP Biology Unit #4 Test Cell Communication, Cancer, Heredity and The Cell Cycle Week of 30 November Multiple Choice 1 point each Identify the choice that best completes the statement
More informationCancer arises from the mutation of a normal gene. A factor which brings about a mutation is called a mutagen.
Cancer Single cells divide by mitosis to form many cells. This cells undergo physical and chemical changes in order to perform specific functions. (we say the cells have Differentiated) in this way we
More informationOncogenes and Tumor Suppressors MCB 5068 November 12, 2013 Jason Weber
Oncogenes and Tumor Suppressors MCB 5068 November 12, 2013 Jason Weber jweber@dom.wustl.edu Oncogenes & Cancer DNA Tumor Viruses Simian Virus 40 p300 prb p53 Large T Antigen Human Adenovirus p300 E1A
More informationAmerican Society of Cytopathology Core Curriculum in Molecular Biology
American Society of Cytopathology Core Curriculum in Molecular Biology American Society of Cytopathology Core Curriculum in Molecular Biology Chapter 1 Molecular Basis of Cancer Molecular Oncology Keisha
More informationmirna Dr. S Hosseini-Asl
mirna Dr. S Hosseini-Asl 1 2 MicroRNAs (mirnas) are small noncoding RNAs which enhance the cleavage or translational repression of specific mrna with recognition site(s) in the 3 - untranslated region
More informationGenetics of Cancer Lecture 32 Cancer II. Prof. Bevin Engelward, MIT Biological Engineering Department
Genetics of Cancer Lecture 32 Cancer II rof. Bevin Engelward, MIT Biological Engineering Department Why Cancer Matters New Cancer Cases in 1997 Cancer Deaths in 1997 Genetics of Cancer: Today: What types
More information7.012 Problem Set 6 Solutions
Name Section 7.012 Problem Set 6 Solutions Question 1 The viral family Orthomyxoviridae contains the influenza A, B and C viruses. These viruses have a (-)ss RNA genome surrounded by a capsid composed
More informationDisorders of Cell Growth & Neoplasia. Lecture 4 Molecular basis of cancer
General Pathology VPM 152 Disorders of Cell Growth & Neoplasia Lecture 4 Molecular basis of cancer Enrique Aburto Apr 2010 Skin tumor in a 10-year-old Rottweiler. Considering the external appearance and
More informationYour World: Fighting Cancer with Biotechnology
Cancer Education Project Your World: Fighting Cancer with Biotechnology Overview: This series of 6 activities is designed to accompany Your World: Fighting Cancer with Biotechnology magazine available
More informationMohammed El-Khateeb. Tumor Genetics. MGL-12 July 21 st 2013 台大農藝系遺傳學 Chapter 22 slide 1
Mohammed El-Khateeb Tumor Genetics MGL-12 July 21 st 2013 台大農藝系遺傳學 601 20000 Chapter 22 slide 1 Cellular Basis of Cancer Cancer is a collection of diseases characterized by abnormal and uncontrolled growth
More informationOncology 101. Cancer Basics
Oncology 101 Cancer Basics What Will You Learn? What is Cancer and How Does It Develop? Cancer Diagnosis and Staging Cancer Treatment What is Cancer? Cancer is a group of more than 100 different diseases
More informationTest Bank for Robbins and Cotran Pathologic Basis of Disease 9th Edition by Kumar
Link full download:https://getbooksolutions.com/download/test-bank-for-robbinsand-cotran-pathologic-basis-of-disease-9th-edition-by-kumar Test Bank for Robbins and Cotran Pathologic Basis of Disease 9th
More informationOncogenes and Tumor. supressors
Oncogenes and Tumor supressors From history to therapeutics Serge ROCHE Neoplastic transformation TUMOR SURESSOR ONCOGENE ONCOGENES History 1911 1960 1980 2001 Transforming retrovirus RSV v-src is an oncogene
More informationEnzyme-coupled Receptors. Cell-surface receptors 1. Ion-channel-coupled receptors 2. G-protein-coupled receptors 3. Enzyme-coupled receptors
Enzyme-coupled Receptors Cell-surface receptors 1. Ion-channel-coupled receptors 2. G-protein-coupled receptors 3. Enzyme-coupled receptors Cell-surface receptors allow a flow of ions across the plasma
More informationSSN SBPM Workshop Exam One. Short Answer Questions & Answers
SSN SBPM Workshop Exam One Short Answer Questions & Answers 1. Describe the effects of DNA damage on the cell cycle. ANS : DNA damage causes cell cycle arrest at a G2 checkpoint. This arrest allows time
More informationGeneral Biology 1004 Chapter 11 Lecture Handout, Summer 2005 Dr. Frisby
Slide 1 CHAPTER 11 Gene Regulation PowerPoint Lecture Slides for Essential Biology, Second Edition & Essential Biology with Physiology Presentation prepared by Chris C. Romero Neil Campbell, Jane Reece,
More informationRegulation of the Cell Cycle
Regulation of the Cell Cycle 21 I. OVERVIEW Quiescent differentiated cell / can be induced to re-enter the active cell cycle. urvival Cell division Apoptosis 1 Daughter cells Apoptic cell enescent cell
More informationNegative Regulation of c-myc Oncogenic Activity Through the Tumor Suppressor PP2A-B56α
Negative Regulation of c-myc Oncogenic Activity Through the Tumor Suppressor PP2A-B56α Mahnaz Janghorban, PhD Dr. Rosalie Sears lab 2/8/2015 Zanjan University Content 1. Background (keywords: c-myc, PP2A,
More informationMolecular Cell Biology. Prof. D. Karunagaran. Department of Biotechnology. Indian Institute of Technology Madras
Molecular Cell Biology Prof. D. Karunagaran Department of Biotechnology Indian Institute of Technology Madras Module 9 Molecular Basis of Cancer, Oncogenes and Tumor Suppressor Genes Lecture 2 Genes Associated
More informationCell Division. non-mitotic cell. Dividing (mitotic) cell. (This movie has been sped up.) These chromosomes have been marked with RED fluorescence.
Cell Division These chromosomes have been marked with RED fluorescence. DNA is found in the cell nucleus Dividing (mitotic) cell non-mitotic cell (This movie has been sped up.) Cell Division and Cancer
More informationTest Bank for Robbins and Cotran Pathologic Basis of Disease 9th Edition by Kumar
Link full download: http://testbankair.com/download/test-bank-for-robbins-cotran-pathologic-basis-of-disease-9th-edition-bykumar-abbas-and-aster Test Bank for Robbins and Cotran Pathologic Basis of Disease
More informationPart II The Cell Cell Division, Chapter 2 Outline of class notes
Part II The Cell Cell Division, Chapter 2 Outline of class notes 1 Cellular Division Overview Types of Cell Division Chromosomal Number The Cell Cycle Mitoses Cancer Cells In Vitro Fertilization Infertility
More informationVIII Curso Internacional del PIRRECV. Some molecular mechanisms of cancer
VIII Curso Internacional del PIRRECV Some molecular mechanisms of cancer Laboratorio de Comunicaciones Celulares, Centro FONDAP Estudios Moleculares de la Celula (CEMC), ICBM, Facultad de Medicina, Universidad
More informationChapter 4 Cellular Oncogenes ~ 4.6 -
Chapter 4 Cellular Oncogenes - 4.2 ~ 4.6 - Many retroviruses carrying oncogenes have been found in chickens and mice However, attempts undertaken during the 1970s to isolate viruses from most types of
More information