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Cancer-MS1
Cancer Pharmacology
| Question | Answer |
|---|---|
| What does thiopurine methyltransferase [TPMT] do? | Metabolize thiopurine drugs. - Because thiopurine drugs are being metabolized you must then give a higher dose. |
| Name 2 thiopurine drugs. | 6-mercaptopurine, azathioprine |
| What is one severe side effect of a high dose of azathioprine? | Severe bone marrow suppression |
| Before treatment with 6-mercaptopurine what do you test? | TPMT [thiopurine methyltransferase] test or enzyme test - If you don't know how quickly the thiopurines are metabolized you might give to much of a dose and kill them. |
| If treating with azanthioprine what would you treat with in addition to increase half life? | Antimetabolites [because TMPT is metabolizing the drug] - You don't want the drug metabolized to quickly because you would need to keep giving more doses. Less metabolized = less times to visit the doctor. :) |
| What are the 3 things you can give a patient that is myelosuppressed [decrease in production of blood cells]? | Erythropoietin [EPO], Granulocyte colony-stimulating factor [G-CSF] and Granulocyte-macrophage colony-stimulating factor[ GM-CSF] |
| What does EPO do? Prevent? | Stimulates production of erythrocytes. Prevents anemia. |
| Where is EPO produced? | 90% kidney, 10% liver |
| How long until see effects of EPO? | 2-6 weeks Remember you the cells have to differentiate and divide. Takes a long time. |
| How is EPO given and what is the half life? | SC [subcutaneous] or IV. 4-13 hr. |
| What are side effects of EPO? | Hypertension, sweating, thrombosis, myocardial infarction, iron deficiency Just think now you have all these RBCs that are gonna clog up the arteries. |
| Which type of cancer do you NOT want to give EPO? | Erythroid-based cancer |
| Which pathway is EPO a ligand for? | JAK/STAT Remember i said "appears to be involved in the immune system". EPO is part of this issue of bone marrow suppression... affecting the immune system |
| What cell normally produces G-CSF [granulocyte-colony stimulating factor? | Immune cells |
| What does G-CSF stimulate? | production of neutrophiles; used in neutropenia |
| What is G-CSF half-life with and without PEGylation? | Without = ~3 hrs, With = 15-80 hrs |
| What are some adverse reactions of G-CSF? | fever and bone pain - think all this production in your bone marrow |
| With what disease should G-CSF not be taken? | leukemia [already has an increase in white blood cells] |
| What normally produces GM-CSF [Granulocyte-macrophage- colony stimulating factor]? | T cells, B cells, mast cells and macrophages |
| What does GM-CSF[Granulocyte-macrophage- colony stimulating factor] stimulate? | production of monocytes [monocytes differentiate into macrophages] and granulocytes |
| What is GM-CSF's [Granulocyte-macrophage- colony stimulating factor] half life? | ~3 hr |
| What are some adverse reactions of GM-CSF [Granulocyte-macrophage- colony stimulating factor]? | fever, rash, bone pain, muscle pain |
| Which drugs are S-Phase specific? | Antimetabolites: thiopurine drugs |
| Which drugs are M-phase specific? | Taxanes, Vinca alkaloids |
| Which drugs are G1-S specific? | Topoisomerase II inhibitors |
| Name 5 cell cycle-nonspecific drugs. | Alkylating agents, Platinum analogs, Anthracyclines, Antitumor antibiotics, Topoisomerase I inhibitors |
| What do alkylating agents do? | Create irreversible changes in DNA [including cross-linking], can also make changes in RNA and protein Just think if you add all these little CH3-CH3 groups they are gonna want to crosslink because they are just floating around. |
| What are side effects of alkylating agents? | mutagenic, teratogenic, carcinogenic. If you change DNA then it is mutagenic [adding alkyls]. Don't give to pregnant women because teratogenic. And generally if you are acquiring mutations [mutagenic] then it will be carcinogenic. So handle with care. |
| Name an alkylating agent. | Cyclophosphamide |
| What is cyclophosphamide used to treat? And what was it originally used for? | Lymphoma, leukemia, prostate, lung, breast and ovarian cancer. Nitrogen mustard or mustard gas |
| Is Cyclophosphamide a non-specific or cell cycle specific drug? Name type. | Non-specific, Alykylating Agent |
| Is Methotrexate a non-specific or cell cycle specific drug? Name type. | Cell Cycle Specific, S-Phase |
| What does Methotrexate do? | Folic acid analog [resembles folic acid], and inhibits dihydrofolate reductase. This retards DNA/RNA synthesis and protein synthesis because lack of Met. - Remember it is an antimetabolite so you need to be taking away something important |
| What is Methotrexate used to treat? | head, neck, breast and lung carcinoma; sarcoma; testicular and bladder tumors |
| What does Dihydrofolate Reductase do? | Reduces dihydrofolic acid [DHF] to tetrahydrofolic acid [THF]. Tetrahydrofolic acid is the active form of folate in humans. |
| What drug creates a folate deficiency? And why is this useful? | Methotrexate [inhibits dihydrofolate reductase]; folate is important in DNA synthesis as well as RNA and protein synthesis |
| Are thiopurines a non-specific or cell cycle specific drug? Name type. | Cell Cycle Specific, S-Phase- antimetabolite. remember all that mumbo jumbo about TPMT and testing for it to see how it is metabolized in the body so you don't kill someone. |
| Name three thiopurines. | 6- Mercaptopurine [6-MP], Azathioprine, 6-Thioguanine [6-TG] |
| Besides as an antimetabolite what are to other uses of thiopurines? | anti-inflammatory and immunosuppressive drugs |
| How do thiopurines work? | block normal purine synthesis. Lead to mutagenesis b/c is thyopurine is incorporated then can have either C or T pair with it |
| Is Fluorouracil [5-FU] a non-specific or cell cycle specific drug? Name type. | Cell Cycle Specific, S-Phase- antimetabolite |
| What is Fluorouracil [5-FU] used to treat? | lung, breast, ovary, prostate, cervix, bladder, head and neck carcinoma; GI adenocarcinoma |
| How does fluorouracil [5FU] work? Give full mechanism. | Block thymidylate synthase -> inhibits pyrimidine synthesis -> inc in dUTP. dUTP incorporated in DNA & usually excised out but a lot so futile -> DNA strand breaks & cell death. Also UTP incorporated in RNA -> inhibits processing to mature RNA |
| What is the vinca alkaloid mechanism? | bind tubulin and prevent mitotic spindle formation [arrest in metaphase] |
| What is vinca alkaloid used to treat? | lymphoma, leukemia, kaposi's sarcoma, breast, cervic, lung, ovary, bladder, testis cancer |
| What type of drug is vinblastine? | Vinca alkaloid |
| What is vinca alkaloid isolated from? | vinca rosea |
| Is Vinblastine a non-specific or cell cycle specific drug? Name type. | Cell Cycle Specific, M-Phase- Vinca Alkaloid |
| Where was Paclitaxel first isolated from? | yew tree bark |
| Where was Taxol first isolated from? | yew tree bark |
| Name two taxoids. | Paclitaxel and Taxol |
| How does Paclitaxel work? | induce polymerization/stabilization of microtubules. Microtubules must be broken down before cells can finish the cell cycle. |
| Which cancers are Taxol used to treat? | Breast and Ovary cancer |
| Is Paclitaxel a non-specific or cell cycle specific drug? Name type. | Cell Cycle Specific, M-Phase [inhibits anaphase] |
| Actinomycin D comes from what bacteria? | streptomyces |
| What is Actinomycin D's mechanism? | intercalates [incorporate] in DNA and inhibits transcription and DNA synthesis. It is a planar molecule so when it intercalates into the DNA it messes up the DNA structure. Just think the bacteria is attacking us... |
| Actinomycin D is used to treat what? | Wilms tumor, Ewing tumor, osteosarcoma, neuroblastoma |
| Is doxorubicin cell cycle specific or non-specific? And what is it's mechanism? And what is another name for it? | Non-specific- anthracycline Intercalates in DNA Adriamycin |
| What is the mechanism for Adriamycin? | intercalates in DNA |
| What is the mechanism for Mitomycin? | After intracellular activation, reacts with DNA and inhibits its synthesis, not as planar as doxorubicin so doesn't intercalate as well but has a nice reactive group that forms adducts [addition of itself] and blocks DNA synthesis |
| What does Mitomycin treat? | carcinoma of head, neck, lung, Gi tract, breast, cervix and bladder |
| What does Bleomycin do? | Chelates metal ions because has lots of sulfyl and nitrogen so very reactive. This produces lots of superoxide and hydroxide free radicals which leads to DNA cleavage, lipid and other peroxidation which eventually will kill the cell |
| What was Camptothecin first isolated from? | Happy Tree |
| What is camptothecin's mechanism? | inhibits topoisomerase I which leads to single strand breaks in DNA, this inhibits replication and transcription |
| Is Camptothecin a non-specific or cell cycle specific drug? Name type. | Non specific because topoisomerase I inhibitor not II. Single-strand breaks only. |
| What are 2 Camptothecin analogues [similar structure and function]? | Topotecan and Irinotecan |
| What was Epipodophyllotoxins first isolated from? | Mayapple plant |
| What is the Epipodophyllotoxin mechanism? | inhibits Topoisomerase II which leads to double-strand breaks in DNA, this causes error in DNA replication and eventually apoptosis |
| What are 2 derivatives [structure came from] of Epipodophyllotoxin? | Etoposide and Teniposide |
| Is Epipodophyllotoxin a non-specific or cell cycle specific drug? Name type. | Cell Cycle Specific, G1-S, TOpoiosomerase II inhibitor |
| What does Cisplatin treat? | Carcinoma of testes, ovary, head, neck, cervix, endometrium; sarcoma, neuroblastoma |
| What is Cisplatin's mechanism? | Causes intra-/interstrand crosslinks in DNA which leads to apoptosis. Think Cysteine causes di-sulfide crosslinks so Cis-platin causes crosslinks also. |
| What drug did Lance Armstrong take to treat his testicular cancer? | Cisplatin |
| What does Arsenic Trioxide treat? | Acute Promyelocytic Leukemia - Think leukocytes are everywhere and arsenic is gonna strait kill ALL of you |
| What is the As2O3 mechanism? | Induces cancer cells to undergo apoptosis |
| Asparaginase + what is used to make it more active? | PEG |
| What is the mechanism of Asparaginase? | Depletes Asparagine levels by converting it to Aspartic Acid and Ammonia. Leukemic cells require high amounts of asparagine because cannot synthesize for themselves. |
| What is Asparaginase used to treat? | Acute Lymphocytic Leukemia |
| What receptor family are sex hormones a part of? | Nuclear Hormone Receptor Family |
| What are Selective Receptor Modulators? | Drugs that do different things in different tissues, ie. Tomoxifin. Antagonist in breast but agonist in cervix and endometrium |
| Name a type of anti-androgen. | Flutamide Think flute is shaped like a penis so Flute-amide treats penis cancer or prostate... :) |
| What does Flutamide treat? | prostate carcinoma |
| What HAVE androgens been used to treat? | metastatic breast cancer [may be bad] |
| What HAVE estrogens been used to treat? | postmenopausal breast cancer and prostate cancer, [but may be bad] |
| Name an anti-estrogen. | Tamoxifen |
| What is tamoxifen used to treat? | postmenopausal breast cancer, metastatic melanoma [controversial] |
| What do aromatase inhibitors do? | prevent the conversion of testosterone to estradiol. - Think aromatics are round and testosterone and estrogen are round so round inhibitors prevent round things. |
| Name an aromatase inhibitor. | Letrozole - "Ohhh tamoxifin isn't working or it's causing cancer!" LET's try LETrozole and LET's inhibit aromatases |
| When is Letrozole used? | Advanced breast cancer, particularly if patient acquires tamoxifen resistance, also may just skip tamoxifen because of its effects on other tissues |
| What kind of drug is Fulvestrant? | Selective estrogen receptor downregulator Some women are full of themselves so lets downregulate that a bit. We'll give them Fulvestrant to downregulate their estrogen so they are full-of-restraint. |
| What does Fulvestrant do? | Leads to destruction of estrogen receptor |
| When is Fulvestrant given? | Given to tamoxifen-resistant patients |
| Retinoic Acid is used to treat what disease? | Acute Promyelocytic Leukemia [APL] |
| What causes Acute Promyelocytic Leukemia? | A balanced translocation between chromosome 15 and 17 which is between PML [promyelocytic leukemia] and RAR [Retinoic Acid Receptor] |
| What is the mechanism for Acute Promyelocytic Leukemia? | PML [promyelocytic leukemia] recruits corepressors instead of coactivators, cells don't differentiate. If you give retinoic acid then it will bind & relieve repression. So able to differentiate. APL- is the build up of these undifferentiated cells |
| What does Tretinoin treat? | APL [Acute Promyelocytic Leukemia], acne vulgaris, keratosis pilaris Think Retinoni treats "Tre" things. Obviously APL, acne, and that third skin thing [skin has keratinocytes so keratosis] |
| What are side effects of Tretinoin? | Sensitivity to sunlight, skin irritation |
| What is the ACID form of Vitamin A? | Tretinoin- all "T" [trans] retinin [retinoic acid] |
| What are tretinoin dosing? | pill, 15 days, every 3 months |
| What does Alitretinoin target? | RAR [retinoic acid receptor] and RXR [retinoid X receptor] - "ALl" RR receptors |
| What does Alitretinoin treat? | AIDS-related Kaposi's sarcoma, severe chronic hand eczema A = Aids and retinoin = skin [eczema] |
| What does Bexarotene target? | RXR [retinoid X receptor] Bex = X so retinoid X |
| What does Bexarotene treat? | cutaneous T cell lymphoma, Off-label: lung cancer, breast cancer, Kaposi's sarcoma Bexarotene = Karotene. karotene is in skin. Skin = cutaneous. Cutaneous T cell Lymphoma. Plus Bextra stuff- lung, breast, Kaposi sarcoma |
| What is Gleevec used to treat? And what is another name for it? | Ph+ Chronic Myeloid Leukemia, Bcr-Abl fusion, Ph+ Acute Lymphocytic Leukemia Imatinib. I'm glee-ful that I met a guy from philly. There are three glee diseases. I'MA in love... |
| What is Imatinib's mechanism? | Tyrosine Kinase Inhibitor for 3 types: Abl, cKit, PDGF Tyrosine Kinases are important for cell proliferation & are often found mutated. I'MA in love with a guy from philly. Not only are there 3 diseases but there are 3 tyrosine kinase inhibitors. |
| Which tyrosine kinase inhibitor is targeted for Gastrointestinal stromal tumors [GIST]? | cKit You "c" there is a "kit" kat in my tumor. |
| What is the most important pathway emanating from the EGF receptor? | RAS, major proto-oncogene |
| EGF is a family of 4 RTKS. What are they? | EGFR, HER2/Neu, EGFR3, EGFR4 |
| Which RTK of the EGF family does not need a ligand for over-expression? | HER2/Neu [30% of breast cancers] |
| Which cancers are HER2/Neu over-expressed in? | breast, ovarian, endometrial and other |
| Which tests are used to test for HER2/Neu? | Fish and Immunohistochemistry |
| What's another name for Trastuzumab? | Herceptin She "Traz" to reason with the "mab" but "her" i mean she s"lipped" "in" the back |
| What is one major symptom of Trastuzumab? | Cardiac dysfunction |
| How is Herceptin given? | IV, every week or every 3 weeks |
| What is the half life of Herceptin? | ~6 days |
| What is the Transtuzumab mechanism? | Humanized monoclonal anti-HER2 antibody |
| What is the Lapatinib mechanism? | Kinase inhibitor for HER2/Neu and EGFR Lapped the effects of other breast cancer treatments. Nib isn't just for neu but also for EGFR. |
| What are symptoms for Lapatinib? | Nausea, vomiting, heartburn, fatigue |
| What is Eriotinib's mechanism? | Kinase Inhibitor |
| What is another name for Eriotinib? | Tarceva |
| What do you use Tarceva to treat? | Non Small Cell Lung Cancer [NSCLC] The tar from the lungs causes cancer |
| What is the life extension benefit for Eriotinib? and what does it treat? | 3 months Non Small Cell Lung Cancer It's ERy how there is so much lung cancer. |
| What are side effects for Tarceva? | rash, diarrhea, fatigue |
| What is the Gefitinib mechanism? | Tyrosine Kinase Inhibitor |
| What is another name for Iressa? | Gefitinib The IRiSes were a GEFT. |
| What do you use Iressa to treat? | NSCLC [Non Small Cell Lung Cancer] I ressa my case. Don't smoke cigarettes. They cause lung cancer. |
| What are some side effects of Gefitinib? | acne, diarrhea, nausea, vomiting |
| What is the mechanism for Cetuximab? | Monoclonal Antibody, prevents EGF binding |
| What is another name for Erbitux? | Cetuximab Notice the tuxes. |
| What do you use Erbitux to treat? | Squamous cell carcinoma and colon cancer. You grow erbs in a garden which might grow like skin in squamous cell carcinoma. What if you ate those "erbs"! Then you would have colon cancer. |
| What do you test for first before treatment with Erbitux? | K-Ras mutations, If you block receptor you block K-RAS pathway but if you already have the mutation in KRAS you don't care because already consitutively active Remember Ras is downstream in a tyrosine kinase pathway. |
| What is Bevacizumab's mechanism? | Vascular endothelial growth factor [VEGF] antibody, angiogenesis inibitor, prevents VEGF from binding to its receptor |
| What is another name for Bevacizumab? | Avastin But avas hun-tin makes my bev izzy mab |
| What is Avastin used to treat? | Metastatic colorectal cancer and non small cell lung cancer [NSCLC]; also off label- macular degeneration instead of Lucentis but comes with more side effects Avastin treats tree from head to butt… hahahaha |
| What is the Sunitinib mechanism? | Inhibitor of VEGFRs, PDGFRs and cKit what's grown in the sun? Peg? no Veg? yes! you got it kit i mean kid. |
| What does Sunitinib treat? | Renal Cell Carcinoma [RCC] and imatinib-resistant GIST After laying in the sun i have to go pee [renal cell carcinoma] and poo [GIST] |
| What is another name for Sunitinib? | Sutent |
| What is the mechanism for Sorafenib? | inhibitor of VEGFR2, VEGFR3, PDGFR, cKit, RAF-1, B-Raf [tyrosine kinase inhibitor and serine threonine inhibitors] SORt of everything- tyrosine kinase inhibs and serine threonine inhibs |
| What does Sorafenib treat? | renal cell carcinoma and unresectable hepatocellular carcinoma. - Sort of the same exceptfin the liver [hepato] |
| What is another name for Sorafenib? | Nexavar SORtA FENIn for the NEX thing |
| What is Vemurafenib's mechanism? | Inhibits V600E B-Raf, but not wild-type B-Raf V and another fenib so serine threonine which means Raf |
| What is Vemurafenib used to treat? | late-stage melanoma Look the vemur i mean lemur got skin cancer!!! |
| What is another name for Vemurafenib? | Zelboraf Zilly boraf that vemur did not! |
| How long is increased life expectancy for Zelboraf? | 6 months, regression 2-18 months |
| What is the mechanism for Bortezomib? | Inhibits active side of 26S proteasome, Bortezomib fits in proteasome and inhibits its activity [prevents proteins that have been ubiquinated from being destroyed] - Bort goes into the port of the proteasome. |
| What is another name for Bortezomib? | Velcade - Velcade makes a blockade in the proteasome. |
| What is Velcade used to treat? | Multiple Myeloma [cancer of plasma cells] Velcade helps the cancer that affects the blockade for the blood. |
| What enzyme adds the methyl group for DNA methylation? | DNA methyl transferase, specifically used for hemimethylated DNA during mitosis |
| What are some of the effects of Hypomethylation of the genome? | Genome instability: chromosome rearrange, activate retrotransposons & growth promoting genes [R-ras] & melanoma antigen (MAGE)] I am hypomethylated about MATCH M-Melanoma antigen, MAGE A-Activate growth genes-R-Ras T-Transpos CH-Chrom rearrange |
| What effects are seen due to hypermethylation of CpG island promoters? | Silencing of tumor suppressors [Rb, BRCA1) If you're hyper and you know it tumor suppress... |
| What does Azacitidine do? | Incorporates into the DNA [looks like cysteine] & directly & irreversibly inhibits DNA methyltransferase, this reactivates tumor suppressor genes. Incorporates into RNA if del hydroxyl group - counteract hypermeth * A to Z you can't hypermethylate me |
| What do you use Azacitidine to treat? | Myelodysplastic syndrome [dysplasia of bone marrow cells] My lod of dys medical stuff is from A to Z. |
| What is another name for Vidaza? | Azacitidine Notice the Z's |
| What does 5-Aza-2'-deoxycytidine do? | similar to 5-Azacytidine but no incorporation into RNA, Incorportates into the DNA [looks like cysteine] and directly and irreversibly inhibits DNA methyltransferase, this reactivates tumor suppressor genes, - A to Z can't hypermethylate me |
| What is another name for Decitabine? | 5-Aza-2'-deoxycytidine Notice "De" and citabine = cytidine |
| What do you treat with Decitabine? | Myelodysplastic syndrome |
| Name 8 histone modifications. | Here Maps Dear Idle Histone- It lived a good life Histone U- ubiquitylation R- ADP Ribosylation M- Methylation A- Acetylation P- Phosphorylation S- Sumoylation D- Deamination I- Proline Isomerization [non-covalent] Histone Lysine- targe |
| What are HDACs and where are they located? | Histone Deacetylases, nucleus, cytoplasm, mitochondria |
| What is Vorinostat/SAHA? | Histone Deacetylase Inhibitor Vor the last time, don't deacetylate my histones. |
| What do you treat with Vorinostat/SAHA? | Cutaneous T-cell lymphoma I need T-cells stat!!! |
| What is another name for Zolinza? | Vorinostat/SAHA Zo you think that dVor is better than stat. |
| What is Romidepsin? | Histone Deacetylase Inhibitor I'm going to rome de whole genome and stop these deacetylations. |
| What is another name for Istodax? | Romidepsin Is dax okay to rome de genome to stop these deacetylations? |
| What do you treat with Istodax? | Cutaneous T-cell lymphoma Is T dax what you use for T-cell lymphoma? |
| What is Romidepsin isolated from? | Chromobacterium violaceum When you rome in chrome sometimes it is violent. |
| What is IL-2 used to treat? | Metastatic renal cell carcinoma and malignant melanoma If you are very Il it is probably metastatic and malignant. From your skin to your pee. |
| What are some side effects of IL-2? | capillary leak |
| What is the IL-2 mechanism? | IL-2 antigen binds to T cell receptor and leads to IL-2 secretion, this leads to activation of monocytes, natural killer cells, T cells |
| What is IFN-a 2a [Interferon] used to treat? | Renal Cell Carcinoma Interferon is interferin with everything even my pee. |
| What do you couple interferon with to extend half life? | Pegylation |
| How is Interferon administered? | Subcutaneous [SC] or Intramuscular [IM] |
| What are some side effects of interferon? | myelosuppression, and flu like symptoms |
| How is interferon induced? | induced by viral infection |
| How is IFN-y induced? | Induced by viral infection |
| What produces IFN-y? | T lymphocytes and NK cells, granulocytes, macrophages |
| How is IFN-y administered? | SC and IV |
| What is IFN-y used to treat? | Renal cell carcinoma Remember it is interferin with your pee. |
| What are some side effects of IFN-y? | Flu like symptoms, GI upset |
| What was Levamisole used to treat and what now used to treat? | colon cancer, melanoma, head and neck cancer. Dewormer for livestock Lemme level with ya. Levamisole is for livestock dewormer. Worms are for the colon. |
| What other use is Levamisole used for? | Cutting cocaine. Here level out that cocaine with some levamisole. |
| What is the mechanism of Levamisole? | Non-specific immunostimulatory properties. Generally enhance immune system. - Think parasites and worms and how when you get rid of them you have in general an enhanced immune response causing Daniel's shit. |
| How can cancer cells escape cytotoxic T lymphocytes? | poor immunogenic self antigens [come from own bodies], poor antigen presenting properties [don't recognize as cell], produce immunosuppressive cytokines, resistant to T cell kill mechanism, resist apoptosis or even induce apoptosis in lymphocytes |
| What is adoptive Immunotherapy? | Remove tumor and stimulate and grow most aggressive interferon producing lymphocytes. Give patient lymphocyte depleting therapy then put new lymphocytes back in. |
| What can adoptive immunotherapy treat? | Metastatic melanoma When you adopt you don't know anything about a kids personality all you see is their skin... goin off appearance. |
| What can they do if you don't have any tumor infiltrating lymphocytes? | can use gene therapy to place T cell receptor into normal cells, then clonaly expand, and inject into patient |
| What can the gene therapy treated T cells treat? | Metastatic melanoma |
| What is a chimeric antigen receptor? | They are engineered receptors that have an arbitrary specificity grafted for monoclonal antibody onto a T cell. These can then be generated for use as adoptive cell therapy. The monoclonal antibody is fused to CD8 or CD28 and then zeta chain. |
| In the case study what disease did the chimeric antigen receptor treat? | chronic lymphocytic leukemia CHronic = CHimeric |
| What is Provenge? | Autologous cellular immunotherapy "cancer vaccine" |
| How does Provenge work? | Isolate patient's leukocytes, especially APCs send to company fuse with prostatic acid phosphatase and GM-CSF then reinfuse into patient |
| What does Provenge treat? | metastatic castration-resistant prostate cancer |
| How much life expectancy can you get from Provenge? | 4 months |
| What are some side effects of Provenge? | fever, fatigue, chills, nausea, joint and headache |
| What is Ipilimumab? | Human monoclonal antibody |
| What does Ipilimumab do? | Blocks CTLA-4 [cytotoxic T lymphocyte-associated antigen 4. This prevents immune system tolerance of cancer cells. I pil not tolerate cancer. |
| What does Ipilimumab treat? | late stage melanoma, clinical trials for prostate and lung cancer |
| What are side effects of Ipilimumab? | potentially fatal immunological adverse effects, GI- diarrhea, stomach pain, constipation, fever |
| What is Denileukin Diftitox? | Immunotoxin "Leuk" = [immune]; "Tox" = [toxin] |
| What is another name for Ontak? | Denileukin Diftitox Have you got "On" "Tak" Difitox? |
| What is the Denileukin Difitox mechanism? | Couple IL-2 with Diphtheria. Brings into cell. IL-2 is cleaved off. Diptheria kills cell. |
| What does Ontak treat? | Cutaneous T cell Lymphoma Tap that, Get on tak T! |
| What is another name for Adcetris? | Brentuximab Vedotin Ad a Tris with Brent to my bucket list. |
| What does Adcetris do? | Antibody conjugated to poison. So antibody binds to cancer cell and is endocytosed with poison. Cleaved. Poison released. Cell dies. |
| What does Adcetris treat? | Refractory Hodgkin's lymphoma and systemic anaplastic large cell lymphoma Ad Hodgy to my bucket list as well as quitting smoking. |
| What is the first successful gene therapy in humans? | SCID-X1 |
| What is SCID-X1? | X-linked IL2RG mutation, encodes common gamma subunit of IL-2, -4, -7, -9, -15, -21 |
| Explain SCID-X1. | IL-2 receptor gamma chain is mutated. Since it affects to many interleukens the immune system is basically dead. Normal treatment is bone marrow transplant but hard to find. |
| What is ONYX-015? | Genetically engineered adenovirus lacking E1B-BBkDa [GENE THERAPY] |
| What is Onyx's mechanism? | The E1B-55kDa gene has been deleted allowing the virus to selectively replicate in and lyse p53-deficient cancer cells |
| What is Onyx used to treat? | Squamous cell carcinoma of the head and neck "On" yo head and neck i'll "nyx" you squamous cell |
| What is the Chinese version of Onyx that is on the market? | Oncorine, used for nasopharyngeal carcinoma Onyx gets an oncor in the nose. |
| What does measles lead to spontaneous regression of? | Leukemias/lymphomas |
| How does Measles kill cancer cells? | kills tumor cells by inducing cell fusions |
| How does measles enter cell? | CD46 receptor, which is frequently overexpressed in tumors. Could use virus to retarget other antibodies like HER2/Neu |
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