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Natalie Afonina Shamii Goh

Natalie Afonina Shamii Goh. Where Taxotere comes from…. First used in cancer treatment in 1996 Generic name: Docetaxel In the taxane class of chemotherapy drugs The chemical in Taxotere is a plant-alkaloid that comes from the needles or bark of the European yew tree. How is it administered?.

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Natalie Afonina Shamii Goh

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  1. Natalie Afonina Shamii Goh

  2. Where Taxotere comes from… • First used in cancer treatment in 1996 • Generic name: Docetaxel • In the taxane class of chemotherapy drugs • The chemical in Taxotere is a plant-alkaloid that comes from the needles or bark of the European yew tree.

  3. How is it administered? • Administered intravenously (through IV) in one-hour infusions • No pill form • But a corticosteroid pill is given as pre-medication to reduce complications of fluid retention and allergic reactions • Dosage received is dependent on factors such as height, weight, general health and of course, the type of cancer or condition being treated

  4. How Taxotere Functions-General • It’s a cell-cycle specific drug • This means it attacks the cells during various phases of mitosis. • Taxotere blocks mitosis by inhibiting the assembly of the mitotic spindle between methaphase and anaphase. • Blocks microtubule structures within the cell. • More specifically, it suppresses the dynamic assembly and disassembly of the microtubules. • Reason why taxane also known as an anti-microtubule agent.

  5. How Taxotere Functions-Specifics • Normally, as part of mitotic process, microtubules form a spindle. • A protein called tubulin is required to assemble the microtubules and therefore essential to cell division. • Taxotere binds to the ß-subunit of the tubulin within the microtubules. • Such formation of stable microtubules promotes their polymerization and causes them to form abnormal bundles that do the following: • Resist physiologic disassembly • Accumulate within tumor cells • Inhibit cell division and eventually lead to apoptosis (cell death).

  6. How This Would Cure Cancer • Taxotere binds to the tubulin of fast-growing cells: inhibiting the microtubules so that they can’t form a mitotic spindle. • If the mitotic spindle can’t form, then the cell can’t arrange the chromosomes on the mitotic plate or pull the sister chromatids apart. • Therefore the cell can’t go through with cell division-cancer can’t proliferate.

  7. Works Cited • "Chemotherapy Drugs." ChemoCare. 2005. Clevelend Clinic Foundation. 11 Nov 2008 <http://www.chemocare.com/bio/taxotere.asp>. • "Docetaxel." Wikipedia. 2008. Wikimedia Foundation Incorporation . 11 Nov 2008 <http://en.wikipedia.org/wiki/Docetaxel>. • "Mechanism of Action." Docetaxel . 2008. sanofi-aventic. 11 Nov 2008 <http://www.taxotere.com/oncology/about_Taxotere/mechanism_of_action.aspx>. • Hamilton, Scott. "Taxotere." Chemocare.com. 2005. The Cleveland Clinic Foundation. 11 Nov. 2008 <http://www.chemocare.com/bio/taxotere.asp>. • "Taxotere." Medsafe. 2006. New Zealand Ministry of Health. 11 Nov. 2008      <http://www.medsafe.govt.nz/profs/Datasheet/t/taxotereinf.htm>.

  8. Cutaneous T-Cell Lymphoma&Zolinza By Nick and Amanda http://drugs.healthdiaries.com/spilledpills.jpg http://www.irxmedicine.com/images/products/Zolinza.jpg http://images.rxlist.com/images/rxlist/zolinza1.gif

  9. Cutaneous T-Cell Lymphoma Diagram of the Lymphatic System T-Cell http://integratedsupplements.typepad.com/photos/uncategorized/2008/01/29/tcell.jpg • It is caused by the uncontrolled growth of T-cells (white blood cells) • CTCL mainly affects the skin • It is diagnosed with a biopsy (of the infected organ) • CTCL is a low grade lymphoma • Main forms: Mycosis fungoids and Sézary syndrome • There are many treatments including chemotherapy and phototherapy. • Symptoms include skin lesions that do not heal

  10. Zolinza Basics • Zolinza is also known as Vorinostat or SAHA • It was approved in 2006 • Vorinostat is a Histone deacetylase inhibitor (gene silencer) • It is administered when CTCL persists after other treatments have failed • It is an oral medicine • Zolinza is used to reduce skin lesions or tumors http://www.131.org.cn/article/uploadfile/200709/20070904102241254.gif

  11. More on Histones • Protein complexes to which DNA binds and wraps around • A lot of acetyl groups decreases the ability of histones to bind to the DNA • Leads to chromatin expansion and allows for transcription • A few acetyl groups cause the histones to bind very closely to DNA, which makes it difficult to do transcription http://www.unc.edu/depts/marzluff/histone.jpg

  12. How Vorinostat Works http://www.nature.com/nrd/journal/v1/n4/images/nrd772-f2.jpg • Histone deacetylase removes acetyl groups from the lysine amino acid on histone proteins • Histones bind closer to DNA • Cancers tend to have a lot of HDACs • In vitro, Vorinostat causes accumulation of acetyls on histones, which then induces apoptosis and/or cell cycle arrest

  13. By: Candace Chuck & Dimitri Woods

  14. GLEEVEC!!!!!!

  15. Chronic Myeloid Leukemia or CML • Chronic phase—the earliest stage of CML • Accelerated phase—when CML begins to get worse • Blast phase—the advanced stage of CML

  16. GIST or Intestinal Tumors • Localized  move to different parts (ex. Stomach to the liver) • Kit+ GIST is a rare cancer of the gastrointestinal (GI) tract. Most GISTs develop in the stomach or in the small intestine, and a small percentage develop elsewhere in the GI tract. GIST is difficult to diagnose and to treat because it "hides" in the abdomen, and often does not cause any physical symptoms.

  17. How they are taken…health risks… • Tablet Form (prescribed by doctor) taken daily • occasionally associated with serious side effects, including severe fluid retention in different parts of the body including the lungs and heart, heart failure, low levels of certain blood cells (including children), liver problems, abnormal bleeding, or skin blistering

  18. How IT Works • Ph + CML (Philadelphia Chromosome CML) • It affects cellular replication/reproduction • The Philadelphia Chromosome = fusion of abl (abelson proto-oncogene) with bcr (breakpoint cluster region) = tyrosine kinase • There are several binding sites on tyrosine kinase for ATP • Gleevec works to competitively bind to the active sites of the tyrosine kinase • GIST • It works to turn off the Kit protein • The kit protein is also a mutated protein • Gleevec works in the same way for GIST as it did in PH + CML, but on the Kit protein’s active sites

  19. http://upload.wikimedia.org/wikipedia/en/d/dc/Bleomycin.png BLENOXANE bleomycin sulfate s. (chin + j*lee)

  20. http://www.health.state.mn.us/divs/idepc/dtopics/stds/images/syringe.jpghttp://www.health.state.mn.us/divs/idepc/dtopics/stds/images/syringe.jpg http://kidshealth.org.nz/images/Child%20with%20IV%20drip.gif Bleomycin: an “antineoplastic” (antitumor antibiotic)From bacterium streptomyces verticullusOften used as part of a multiple-drug therapyToo toxic to use as a normal antibiotic Intravenous Intramuscular Rapid absorption, wide distribution in body Subcutaneous (rarely)

  21. types of cancer treated with bleomycin 1. Squamous Cell (a kind of skin cell) Cancer head & neck cervix, penis, & vulva 2. Testicular Cancer 2. Lymphomas http://myhero.com/images/guest/g182185/hero42610/g182185_u47375_LanceArmstrong.jpg http://bbsimg.ngfiles.com/14/14568000/ngbbs4738f8125ddb8.gif http://www.creativepro.com/files/story_images/042204_fg1.jpg

  22. How it works • Inhibition of DNA synthesis • Create free radicals that cause breaks in DNA • Single stranded breaks: only one of the strands in the double helix is affected • Can use other strand to try to correct • Double stranded breaks: both strands are severed • No template for reparation  cell death

  23. Why it works • Overwhelms natural repair systems • Cells stopped at G2 checkpoint  DNA too damage to continue • Also stopped in mitosis

  24. SIDE EFFECTS • Commonly • Fatigue, hair loss, loss of appetite, loss of fertility, vomiting • Not-so-commonly • Drop in bone marrow function • Renal toxicity • Lung inflammation (pneumonitis) – 10% • 1% progress to pulmonary fibrosis  death

  25. Avastin By: Margo and Tim Also Known As Bevacizumab

  26. About Avastin • Cancer types • Metastatic Breast Cancer • Metastatic Colorectal Cancer • Non-Small Cell Lung Cancer • Emphasis on colorectal cancers • Administered • Given through IV infusion • Takes about 90 minutes first time it is given to you • Subsequent times take 30-60 minutes • Given once every two weeks with chemotherapy • Treats metastatic colorectal cancer (MCRC)

  27. What is it? • Drug is actually called bevacizumab • Humanized monoclonal antibody • First available as an angiogenesis inhibitor • Came from a modified mouse antibody • Use • Only approved for metastatic cancers • Cancers which will spread to other parts of body • Controversy over use in treating breast cancer • Only slows tumor growth but does not lengthen patient’s life

  28. How It Works • Anti-angiogenic agent • Angiogenesiss = tumors creating network of blood vessels • Avastin blocks VEGF • Key signal for angiogenesis

  29. By Ellen Zocher Herceptin

  30. Herceptin a.k.a. Trastuzumab http://commons.wikimedia.org/wiki/Image:Herceptin.png http://www.cbc.ca/news/background/cancer/gfx/herceptin_file.jpg  Therapeutic Monoclonal antibody HER2 (Human Epidermal Growth Factor 2) receptor protein

  31. HER2 Normal Cell  Receptor Protein, transmits growth signals

  32. HER2+ cancer cells HER2+ Breast Cancer Cell Produce too many HER2 receptors cells grow/divide more quickly Cancer progresses faster

  33. Herceptin attaches to HER2 cancer cell Immune cells destroy cancerous cell

  34. http://www.herceptin.com/index.jsp

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