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Lectures 5 and 6

by: Nathaniel Bautz

Lectures 5 and 6 MICROBIO 160

Nathaniel Bautz
GPA 2.9
MICROBIO 160 - Biology of Cancer and AIDS
Mitchell Walkowicz

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Here are the notes for lectures 5 and 6
MICROBIO 160 - Biology of Cancer and AIDS
Mitchell Walkowicz
Class Notes
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This 4 page Class Notes was uploaded by Nathaniel Bautz on Friday February 13, 2015. The Class Notes belongs to MICROBIO 160 at University of Massachusetts taught by Mitchell Walkowicz in Spring2015. Since its upload, it has received 102 views. For similar materials see MICROBIO 160 - Biology of Cancer and AIDS in Biology at University of Massachusetts.

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Date Created: 02/13/15
LECTURE 5 Pro le of a Cancer Cell Characteristics of a Normal cell 0 90 VVVVV Reproduce themselves exactly Stop reproducing at the right time Stick together in the right place Selfdestruct if they are damaged Become specialized or mature The Cell Cycle and Checkpoints gt gt gt G1 checkpoint Metaphase checkpoint G2 checkpoint Cancer Begins with DNA Damage gt DNA damage or mutation as a result of I Exposure to radiation I Exposure to toxins I Hormonal abnormalities I Inherited abnormalities I Nutrition and died I Tobacco use I Viral infection How Cancer Cells Develop gt Cancer mutations are progressive and happens in multiple steps Hallmarks of Cancer Cells VVVVVVV Cancer cells exhibit a decreased dependence on external growth factors Exhibit decreased density dependent growth inhibition Cancer cell proliferation is anchorage independent Cancer cells have limitless replicative potential Stimulates sustained angiogenesis Cancer cells are able to evade apoptosis Cancer cells are involved in tissue invasion and metastasis How Growth Factors Work gt gt gt gt Growth factors Receptor Signaling molecules Transcription factors Telomeres DNA Unlaced gt gt gt Telomeres seal off the ends of chromosomes which contains the cell s genetic information As cells replicate telomeres can fray allowing chromosomes to become damaged This becomes increasingly common with age Scientists discovered a protein called telomerase which maintains the telomeres keeping chromosomes intact longer Telomeres Aging and Progeria gt gt gt gt VVVVVV Telomerase enzyme Normally expressed in an early embryo Miss expression accounts for cancer cell Immortality 0 Profile of a Cancer Cell Summary Selfsufficiency in growth signals Evading apoptosis Insensitivity to anti growth signals Sustained angiogenesis Tissue invasion and metastasis Limitless replication potential LECTURE 6 How Cancer Shrew 393 Typical Cancer Progression VVVVV Normal Hyperplasia Mild dysplasia Carcinoma in situ Cancer 393 Primary and Secondary Cancer gt gt gt gt The main reason cancer can be difficult to cure is that it can spread to another part of the body from where it started The cancer that is growing where it started in the body is called the 39primary cancer39 The place a cancer spreads to and starts growing are called the 39secondary cancer39 or 39metastasis39 In order to spread some cells from the primary cancer must break away travel to another part of the body and start growing there 393 Cancer Spread and Mortality gt gt gt gt 90 of Cancer Deaths Occur Because of Where Cancer Ends Up Not Where It Begins Research shows that most metastatic cancers induce premetastatic niches or landing pads allowing cancerous cells to colonize a secondary organ When cancer cells travel to a vital organ they often overwhelm the cells and cause it to shut down By the time a tumor is found cancer cells may have been present for some years but the immune system has controlled their proliferation 393 How Hematologic Cancers Cause Death gt gt gt gt gt Nonsolid tumors Hematologic blood cancers kill because the components of the blood are no longer fulfilling their duties The immune system is no longer working effectively The platelet count drops causing hemorrhage Red cells are significantly reduced causing reduced oxygen and the patient has a heart attack gt Increased white blood cells lead to really viscous blood effectively clogging the arteries How Solid Tumors Cause Death gt Solid tumors kill in very mechanical ways gt Ovarian cancer kills you by obstructing your bowel as does colon cancer and most other cancers of the GI tract Lung cancers usually kill by eroding into an artery or obstructing the airway gt Breast cancers typically kill by metastases in the brain causing increased intracranial pressure gt More than 40 percent of cancer patients die from malnutrition not the cancer itself gt Tumors induce a hyper metabolic state and secrete a substance called cachectin TNF x that results in weakness and weight loss Cancer metastasis and their symptoms gt Brain I Headaches I Seizures I Vertigo gt Lymph nodes I Lymphadenopathy gt Respiratory I Cough I Hemoptysis I Dyspnea gt Liver I Hepatomegaly I J aundice gt Skeletal I Pain I Fractures Vasculogensis and Angiogenesis gt Vasculogenesis is the term used for the formation of new blood vessels when there are no preexisting ones gt The term angiogenesis denotes the formation of new blood vessels from preexisting ones Dr Judah Folkman Pioneer in Tumor Angiogenesis gt While working for the Navy in 1960 s on blood substitutes he began experimenting with tumors and found that all grew to the same size and stopped gt Hypothesized that the tumors could not grow beyond a certain size without a blood supply and that tumors must have some mechanism to induce the formation of blood vessels Tumor Angiogenesis gt When they number only 100300 the cancer cells have created new fullyfunctioning blood vessels Avastin Inhibits Angiogenesis gt Lucentis and Avastin have been called miracle drugs because they are the first treatments that can actually reverse some vision loss from advanced macular degeneration There are three main ways a cancer spreads gt Local spread gt Through the blood circulation gt Through the lymphatic system Steps Involved in the Metastatic Process gt The ability to invade differs among cancer cells and tumors gt Blood ow patterns often dictate where cancers will spread to gt Relatively few cancer cells survive the voyage through the blood stream gt Cancer cells are able to invade because I Decreased adhesiveness I Activated motility I Protease production odern Medicine Modem Problems BiomedicineImmunologics avastinbevacizumab mab monoclonal antibody 5 billion USDyr world wide Chemo 250K Chemo plus avastin 500K Difference in time without progression months PersonalizedGenome based Medicine Biomarker gene mutation shown to be associated with good response to a given treatment Good 5 months without increase in tumor size Avastin was once used to treat breast cancer Colon and lung cancer biomarkers are still being evaluated ore Money Medicine Macular degeneration Lucentis is a purified form of avastin 2000dose VS 20 dose Offlabel use Infections with Avastin due to sloppy procedure M gt gt gt gt gt gt V vvvvvzvvv


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