Lesson 1: Foundations to Set the Stage<\/p>\n\n\n\n
Focusing on Cellular Structure and Function<\/p>\n\n\n\n
The Normal Cell Cycle
-The cell cycle refers to the ordered seres of processes of DNA replication and mitosis, or cell division<\/p>\n\n\n\n
-Cell nucleus regulates these processes by gathering and processing complexes molecular information<\/p>\n\n\n\n
Interphase and Mitotic Phase
Cell division produces two identical cells through these two major phases<\/p>\n\n\n\n
During interphase:
Cell grows and DNA is replicated through the following three steps:<\/p>\n\n\n\n
1: First growth phase (G1 or first gap)<\/p>\n\n\n\n
2: Synthesis phase (S phase)<\/p>\n\n\n\n
3:Mitotic Phse (M phase)<\/p>\n\n\n\n
First Growth Phase (G1 or first gap)
-cells increase in size<\/p>\n\n\n\n
-reproduce RNA<\/p>\n\n\n\n
-“quality assurance” test that the cell will be ready to synthesis DNA<\/p>\n\n\n\n
-Length of time is variable, can be from hours to days<\/p>\n\n\n\n
Synthesis Phase (S phase)
-DNA replicates<\/p>\n\n\n\n
-Results in the formation of identical pairs of DNA (chromatids)<\/p>\n\n\n\n
-which are attached a t the centromere<\/p>\n\n\n\n
-lasts 2-10 hours<\/p>\n\n\n\n
Mitotic Phase (M phase)
-Replicated chromosomes are aligned, separated, and move into 2 new, identical daughter cells<\/p>\n\n\n\n
-takes about 30-60 minutes<\/p>\n\n\n\n
Major points of cell regulation are entry and exit from
-G1 checkpoint<\/p>\n\n\n\n
-S Phase<\/p>\n\n\n\n
-G2 checkpoint<\/p>\n\n\n\n
-M phase<\/p>\n\n\n\n
Restriction Point
-The transition from the resting phase into an actively dividing phase (G0-G1) is a point where cellular transformation can occur<\/p>\n\n\n\n
-During this time, cells pass through a transition phase known as a restriction point<\/p>\n\n\n\n
-Extracellular growth factors trigger reentry into G1, and GF are required to send the cells past the restriction point, or the point of no return<\/p>\n\n\n\n
G0 Phase (resting phase)
-After mitosis, cells may enter back into the G1 phase or go into a resting phase, known as G0<\/p>\n\n\n\n
-Most cells in the human body reside in G0<\/p>\n\n\n\n
-Exceptions to this are those that are (Resting in G0 phase)
-Exceptions to this are those that are metabollically active, such as<\/p>\n\n\n\n
-granulocytes<\/p>\n\n\n\n
-and the epithelium of the GI tract<\/p>\n\n\n\n
Cell Cycling Time
Amount of time from mitosis to mitosis<\/p>\n\n\n\n
Cell cycle video and image
http:\/\/highered.mheducation.com\/sites\/0072495855\/student_view0\/chapter2\/animation__how_the_cell_cycle_works.html<\/p>\n\n\n\n
Check points in the Cell Cycle: Keeping it All Under Control
-The cell cycle is carefully controlled through a series of checkpoints<\/p>\n\n\n\n
-Variation in duplication or distribution of chromosomes during cell division can alter the genetic information passed on to daughter cells, leading to cellular dysfunction and disease, such as cancer<\/p>\n\n\n\n
-These checkpoints monitor for DNA integrity and control progression through mitosis<\/p>\n\n\n\n
Progression through the cell cycle is controlled through two proteins:<\/p>\n\n\n\n
-Cyclin-CDK complex allows the cell to progress through each phase of the cell cycle<\/p>\n\n\n\n
Locations of proteins Cyclins (D, E, A, B) and CDKs
-(G0-G1) : Cyclin D and CDK 4\/6<\/p>\n\n\n\n
-Early S: Cyclin E and CDK 1\/2<\/p>\n\n\n\n
-Late S: Cyclin A and CDK 1\/2<\/p>\n\n\n\n
-G2: CDK 1\/2 and cyclin A<\/p>\n\n\n\n
-Before M: CDK 1 and Cyclin B<\/p>\n\n\n\n
Inhibitory proteins
-prevent progression of the cycle when DNA damage is detected<\/p>\n\n\n\n
-An example of an inhibitory protein is p53 (AKA TP53)<\/p>\n\n\n\n
DNA Damage Checkpoints
-If DNA damage is present, cells are programmed to stop dividing or undergo apoptosis (programmed cell death)<\/p>\n\n\n\n
-The retinoblastoma protein (Rb), p53, and p21 are some of the most well-understood inhibitory proteins (IP)<\/p>\n\n\n\n
Inhibitory proteins p53
-Levels of this IP regulate several important target genes<\/p>\n\n\n\n
-Will increase when DNA damage is present<\/p>\n\n\n\n
-Protects against inappropriate signal proliferation<\/p>\n\n\n\n
-sometimes called the “suicide gene”<\/p>\n\n\n\n
M Phase Checkpoints
When the cells prepare to divide, the chromosomes line up in the mitotic spindle.<\/p>\n\n\n\n
If the chromosomes are not properly aligned, division is not allowed to continue<\/p>\n\n\n\n
Immunity<\/p>\n\n\n\n
Cells of the Immune System<\/p>\n\n\n\n
Pluripotent Stem Cell -A stem cell that can differentiate into any cell type except for extraembryotic tissue, does not yet have a function<\/p>\n\n\n\n Myeolid Precursor Cells Lymphoid Precursor Cells Lines of Defense: The Immune System’s Response to Attack 1: Innate Innate Immunity -Does not retain memory of the entity<\/p>\n\n\n\n -Involves the following: Adaptive Immunity -leads to immune system memory<\/p>\n\n\n\n -Humoral immunity<\/p>\n\n\n\n -Cell-mediated immunity<\/p>\n\n\n\n -Regulatory T-cells<\/p>\n\n\n\n Humoral Immunity B-Cell -Can recognize antigens whether they are freely circulating in the blood or attached to surface of a microbe<\/p>\n\n\n\n -When dividing, can become plasma cells which will then begin secreting antibodies that are unique to that antigen<\/p>\n\n\n\n Plasma Cells -Some will go to the BM where they will continue to secrete antibodies sometimes for years<\/p>\n\n\n\n Cell-Mediated Immunity -more effective against antigens within cells<\/p>\n\n\n\n Regulatory T-cells AKA suppressor T-Cells T-Cell -Recognize phagocytized fragments of an antigen that are put on the surface of antigen-presenting cells<\/p>\n\n\n\n Helper T-Cells (CD4+) -Help B Cells to respond<\/p>\n\n\n\n -rapidly divide, in an effort to stay ahead of the antigen dividsion<\/p>\n\n\n\n -some will turn into effector cells, which secrete different kinds of cytokines<\/p>\n\n\n\n -respond similarly to B-Cells<\/p>\n\n\n\n Cytotoxic T-Cells (CD8+) -rapidly divide, become mature cells, and start killing antigens<\/p>\n\n\n\n Cytokines -Tasked with eliminating the antigen<\/p>\n\n\n\n -Multifunctional subsances having proinflammatory, anti-inflammatory, and regulatory functions in the immune system<\/p>\n\n\n\n Cytokines Include.. -Tumor necrosis factors<\/p>\n\n\n\n -Transforming GFs<\/p>\n\n\n\n -Interleukins (IL -1, -2, -3, -4, -6, -8, -10, and -15)<\/p>\n\n\n\n -These cytokines regulate antibody production and the functions of B and T cells as well as interact with antigen-presenting cells and NKCs<\/p>\n\n\n\n Benign Tumors -Do not invade neighboring tissue<\/p>\n\n\n\n -DO not metastasize to distant sites<\/p>\n\n\n\n -the cells well differentiated in that they look like the parent cell<\/p>\n\n\n\n Characteristics of Cancer Cells -Cell structure is different from parent tissue (no as well differentiated)<\/p>\n\n\n\n -Cell division is uncontrolled<\/p>\n\n\n\n -Cells are loosely adherent without contact inhibition<\/p>\n\n\n\n -Cells are able to invade neighboring tissue<\/p>\n\n\n\n -Cells can migrate and metastasize to distant sites<\/p>\n\n\n\n -Can stimulate the development of new blood vessels to supply the tumor (angiogenesis)<\/p>\n\n\n\n Proto-oncogene -large family of genes that code for proteins and enzymes that turn on the cell cyle<\/p>\n\n\n\n Oncogene Examples of oncogoenes<\/p>\n\n\n\n -EGFR inhibitor therapies are known to cause cutaneous reactions<\/p>\n\n\n\n Tumor suppressor genes -in the presence of malignancies, they bind to DNA with intention of repairing or activating apoptosis<\/p>\n\n\n\n -for it to be turned on it must be expressed or “opened” in the DNA helix so that it can be transcribed or copied<\/p>\n\n\n\n p53 -activates apoptosis when the cell is damaged beyond repair or too old to function<\/p>\n\n\n\n -more than 50% of solid tumors, the gene is mutated and unable to perform its normal function<\/p>\n\n\n\n Growth Signals Signal transduction Signal transduction steps<\/p>\n\n\n\n Dimerization<\/p>\n\n\n\n Protein tyrosine kinases phosphorylates -the message is now send via a “bucket bridage”, or passing the message from one molecule to other signaling molecules until the message gets first into the cell nucleus<\/p>\n\n\n\n -where it is transcribed<\/p>\n\n\n\n Pathways mitogen-activating protein kinase (Raf-1\/MAPK) pathway -decrease disease-free survival time in some pts<\/p>\n\n\n\n mammalian target of rapamycin (mTOR) survival pathway -role in angiogenesis<\/p>\n\n\n\n phosphoinositide 3-kinases (PI3K) Neoadjuvant Treatment -examples: chemo, radiation therapy, hormone therapy<\/p>\n\n\n\n Adjuvant therapy -Examples: chemo, radiation therapy, hormone therapy, targeted therapy, or biologic therapy<\/p>\n\n\n\n Dose density -reduction of time between treatments to achieve higher concentration than in a standard treatment plan<\/p>\n\n\n\n Dose intensity -smaller doses of chemotherapy given more frequently<\/p>\n\n\n\n Relative dose intensity (RDI) Oral Chemotherapy Nonadherence Overadherence Factor affecting adherence Lesson 2: Alkylating Agents<\/p>\n\n\n\n Alkylating Agents Alkylating Agent Subgroups -Platinum-based (cisplatin{Planitol}, carboplatin{Paraplatin}): do not possess an alkyl group<\/p>\n\n\n\n -nitrosoureas<\/p>\n\n\n\n Nitrosoureas -able to cross the blood-brain barrier (effective in treating some brain tumors, melanomas, lymphomas)<\/p>\n\n\n\n -Carmustine (BiCNU) -pulmonary monitoring recommended<\/p>\n\n\n\n Carboplatin (Paraplatin) -possibility for a hypersensitivity reaction which is rash, urticaria, erythema, pruritis, rarely bronchospasm and hypotensision<\/p>\n\n\n\n -notify RN if itching, scratchy throat, difficulty breathing, rash<\/p>\n\n\n\n -Blood count, particularly platelets, monitored because thrombocytopenia is a dose-limiting toxicity<\/p>\n\n\n\n -Oral dosage: 1-5mg\/kg\/day<\/p>\n\n\n\n Cisplatin (Planitol) -nephrotoxic (IV hydration 2-3 L per day) -ovarian and testicular<\/p>\n\n\n\n Cyclophosphamide (Cytoxin) -hemorrhagic cystitis (dysuria, hematuria, hemorrhage)<\/p>\n\n\n\n -DC treatment if hemorrhagic cystitis<\/p>\n\n\n\n -adequate hydration<\/p>\n\n\n\n Oxaliplatin -irritant and vesicant, extra caution with the IV site<\/p>\n\n\n\n -peripheral neuropathy is a dose-limiting side effect (exacerbated by cold temperatures)<\/p>\n\n\n\n -avoid cold drinks and foods, wearing gloves and warm shoes<\/p>\n\n\n\n -avoid breathing cold air<\/p>\n\n\n\n Intrathecal Chemotherapy -Often used to treat leukemia and lymphoma that has spread to the CNS since most IV chemo does not cross the blood-brain barrier<\/p>\n\n\n\n -only MTX and cytarabine via this route<\/p>\n\n\n\n -IT hydrocortisone is often given at the same time to reduce inflammation<\/p>\n\n\n\n -MUST be preservative free to avoid CNS irritation<\/p>\n\n\n\n Chemotherapy-Induced N\/V (CINV) Risk factors Types of CINV -Delayed: from 24 hour – 5 days after<\/p>\n\n\n\n -Breakthrough: Occurring despite treatment<\/p>\n\n\n\n -Anticipatory: triggered by taste, odor, memories, visions, anxiety r\/t chemo<\/p>\n\n\n\n -Refractory: occurring despite subsequent cycles when treatment failed in earlier cycles<\/p>\n\n\n\n Prevention\/Treatment of hand foot syndrome -take cool showers<\/p>\n\n\n\n -avoid exposure to sources of heat, such as using saunas or sitting in the sun<\/p>\n\n\n\n -avoid activities that cause unnecessary force or friction on the hands or feet, such as running or aerobics<\/p>\n\n\n\n -avoid contact with harsh chemicals used in detergents and household cleaning products<\/p>\n\n\n\n -avoid activities that require you to press your hand against a hard surface<\/p>\n\n\n\n -elevate your hands and feet when sitting or lying down<\/p>\n\n\n\n -gently apply skin care creams to keep hands moist<\/p>\n\n\n\n -wear loose-fitting, well ventilated shoes<\/p>\n\n\n\n Nadir -typically, but not always, occurs 7-10 days after the cycle is administered<\/p>\n\n\n\n Neutropenia -less than 1000\/mm3 with the expectation that the count will drop below 500 in the next 48 hours<\/p>\n\n\n\n Neutopenia RF -hx of neutropenia with previous chemo<\/p>\n\n\n\n -previous chemo or radiation<\/p>\n\n\n\n -hematologic malignancy, uncontrolled or advanced cancer, or lung cancer<\/p>\n\n\n\n Neutropenic Fever -temp of 38 lasting 1 hour<\/p>\n\n\n\n Absolute Neutrophil Count<\/p>\n\n\n\n Mucositis -affects 40-100% of pts<\/p>\n\n\n\n Stomatitis Xerostomia Hypersensitivity Reaction (HSR) IgE-mediated T-Cell–Mediated Type 1 HSR early S\/SX Type IV HSR Lesson 7: Cumulative Dose<\/p>\n\n\n\n Cumulative dose Cumulative lifetime dose -total amount of specific antineoplastic agents that can be safely given over the course of a pt’s lifetime<\/p>\n\n\n\n Extravasation Irritant Vesicants Vesicants in PIVs -Do NOT place the IV below a recent ventipuncture site used (<24 hours)<\/p>\n\n\n\n -Use a flexible IV catheter<\/p>\n\n\n\n When a vesicant extravasation occurs or is suspected, take the following steps:<\/p>\n\n\n\n Managing Non-DNA Binding Vesicant Extravasation -Do not bind to DNA in healthy cells when they extravasate into tissue. Indirect effect on healthy tissue<\/p>\n\n\n\n -Treat with heat, elevation, and hyaluronidase local injection (spreads the vesicant through the tissue for faster metabolism of the vesicant agent)<\/p>\n\n\n\n -Usually results in less tissue damage<\/p>\n\n\n\n -Improves over a short period of time (days to weeks(<\/p>\n\n\n\n Management of DNA-Binding Vesicant Extravasation -Binds to DNA in healthy cells when they extravasate into tissue<\/p>\n\n\n\n -When not immediately treated with dexrazoxane, the vesicant remains in the tissue and invades adjacent healthy tissue<\/p>\n\n\n\n -Likely to result in more tissue damage<\/p>\n\n\n\n -Left untreated, extravasations become larger and deeper, worsening over time (weeks to months)<\/p>\n\n\n\n Lesson 11: Targeted Therapy<\/p>\n\n\n\n How targeted therapy and chemo differ -chemo has more SEs<\/p>\n\n\n\n -targeted therapy ae chosen and designed to interact with their target on or within the cells, whereas chemo were IDed becaused they kill cells<\/p>\n\n\n\n -targeted therapies are often cytostatic (they block tumor cell proliferation) whereas chemo agents are cytotoxic (kill tumor cells)<\/p>\n\n\n\n Goals of targeted therapy -improving overall response or increase disease-free survival when used in combination with conventional therapies<\/p>\n\n\n\n -controlling or stabilizing disease<\/p>\n\n\n\n -maintaining or enhancing quality of life<\/p>\n\n\n\n -decreasing the severity of toxicities from other therapies<\/p>\n\n\n\n Receptor Monomer Ligand Ligand Binding Dimerization Kinase phosphorylation targeted therapies work by doing the following<\/p>\n\n\n\n BCR\/ABL -gene abnormality called the Philadelphia chromosome seen in CML and ALL<\/p>\n\n\n\n VEGF mTOR -a protein that tells cells when to grow, divide, and survive<\/p>\n\n\n\n Two ways that angiogenesis inhibitors work<\/p>\n\n\n\n Small Molecule Compound Targeted Therapies -targets located inside the cell because these gents are able to enter cells more easily<\/p>\n\n\n\n -intracellular<\/p>\n\n\n\n -most given orally<\/p>\n\n\n\n Monoclonal Antibody Targeted Therapy<\/p>\n\n\n\n -relatively large in size and therefore usually cannot enter cells<\/p>\n\n\n\n -extracellular or transmembrane<\/p>\n\n\n\n -man made version of antibodies that are designed to attack a very specific target on cancer cells<\/p>\n\n\n\n -usually from mice<\/p>\n\n\n\n Lesson 12: Immunotherapy<\/p>\n\n\n\n Immunotherapy works by -stopping cancer from spreading to other parts of the body<\/p>\n\n\n\n -helping the immune system recognize cancer cells and increase its effectiveness at eliminating cancer cells<\/p>\n\n\n\n Passive Immunotherapy -require repeated administration to be effective<\/p>\n\n\n\n -includes monoclonal antibodies and cytokines<\/p>\n\n\n\n Active Immunotherapy -mount an immune response against the tumor and hopefully remember the cancer cells long after treatment has stopped<\/p>\n\n\n\n -includes cancer vaccines<\/p>\n\n\n\n Specific Immunotherapy -examples are mAbs and cancer vaccines<\/p>\n\n\n\n Nonspecific Immunotherapy -given adjuvantly to other anticancer treatment drugs<\/p>\n\n\n\n -examples are cytokines, interleukins, and checkpoint inhibitors<\/p>\n\n\n\n Lesson 13: Safe Handling<\/p>\n\n\n\n Hierarchy of Hazard Controls aimed at reducing worker exposure<\/p>\n\n\n\n -substitute a less toxic substance for the hazardous material<\/p>\n\n\n\n -not feasible with drug therapy<\/p>\n\n\n\n -use of machines or equipment that isolate or contain the hazard to reduce worker exposure<\/p>\n\n\n\n -Examples: biosafety cabinets and closed-system drug-transfer devices<\/p>\n\n\n\n -safe handling policies<\/p>\n\n\n\n -procedures<\/p>\n\n\n\n -work practices<\/p>\n\n\n\n -education and training of those responsible for HD handling<\/p>\n\n\n\n -consisting of garments that provide barriers to protect workers from HDs<\/p>\n\n\n\n -places the primary responsibility for protection on the worker<\/p>\n\n\n\n Donning PPE<\/p>\n\n\n\n Doffing PPE<\/p>\n\n\n\n 5.remove inner gloves<\/p>\n\n\n\n True statements related to drug dose calculation and administration -Pts who have had previous radiation therapy or chemo are considered special populations with regard to a potential need for dose modification<\/p>\n\n\n\n -The AUC calculation is used for carboplatin dosing<\/p>\n\n\n\n -Children may metabolize drugs differently than adults; dose modifications are possible<\/p>\n\n\n\n What is a monoclonal antibody, and how is it different from chemo? -mAbs search out proteins on the cells surface<\/p>\n\n\n\n -mAbs recognize and bind to specific anatigens on the cells surface<\/p>\n\n\n\n -natural killer cells and\/or cytotoxic proteins of the immune system recognize and destroy the marked tumor cells<\/p>\n\n\n\n -mAbs can also directly induce cell death as well<\/p>\n\n\n\n -One of the biggest differences is that mAbs cause harm only to those cells that are marked or binded<\/p>\n\n\n\n –<\/p>\n\n\n\n Should I avoid my grandchildren and other family members when I am getting treatment? -Hugging, kissing, and spending time together while eating are all safe activities<\/p>\n\n\n\n -Safety with bodily fluids is necessary for the first 48 hours after receiving chemo<\/p>\n\n\n\n Can I be intimate with my partner during treatment? -traces of chemo may be present in vaginal fluid for up to 48 hours after treatment<\/p>\n\n\n\n -use of a barrier is recommended for this reason for at least the first 48 hours<\/p>\n\n\n\n 3 major phases of cell division: 3 steps of interphase: 4 phases of mitosis: Innate immunity: Adaptive immunity: Define mutations 3 main goals of treatment: Define neoadjuvant therapy Define adjuvant therapy Define conditioning\/preparative therapy 2 types of conditioning therapies: Define dose density Define dose intensity How is relative dose intensity (RDI) calculated? How do alkylating agents work? 3 subcategories of alkylating agents:<\/p>\n\n\n\n Most common subcategory of alkylating agents: Common alkylating agents: Common platinum-based agents: What is unique about nitrosoureas agents? Common nitrosoureas agents: Hypersensitivity can occur with late doses of: These agents are typically categorized as highly emetogenic:<\/p>\n\n\n\n Pre-administration labs for alkylating agents and nitrosoureas: What is the medication Mesna used for? Instruct pts receiving __<\/em><\/strong> to avoid exposure to cold air and consuming cold fluids for 3-4 days following treatment How do antimetabolites function? Antimetabolites work in the _<\/em> phase. What types of cells are best affected by antimetabolites? Common side effects of antimetabolites: Common antimetabolite drugs: The institute for Safe Medication Practices recommends what route of administration for vincristine? Anthracycline antitumor abx work by: The two major classifications of antitumor antibiotics are: Common anthracycline antitumor abx: The antitumor abx _<\/strong><\/em><\/strong> is not an anthracycline, but has anthracycline-type properties. Common non-anthracycline antitumor abx: Monitoring necessary with doxorubicin: Lifetime dose of doxorubicin should not exceed: What cardiac protectant medication can be administered prior to doxorubicin? Significant side effects of doxorubicin are: Monitoring necessary with bleomycin: Pulmonary fibrosis is possible when the lifetime dose of bleomycin exceeds: What 6 patient characteristics make CINV more likely?<\/p>\n\n\n\n Types of CINV: Define acute CINV Define delayed CINV Define breakthrough CINV Define anticipatory CINV Define refractory CINV Highly emetogenic chemo (HEC) causes CINV in more than _<\/em>% of patients Moderately emetogenic chemo (MEC) causes CINV in patients % to <\/em><\/strong>% of the time Patients on low-potential emetogenic chemo develop CINV % to <\/em><\/strong>% of the time Minimal-risk emetogenic chemo causes CINV less than _<\/em>% of the time Common IV HEC drugs include: Common IV MEC drugs include: Common low-potential IV emetogenic chemo drugs include: Common minimal-risk IV emetogenic chemo drugs include: The 2 most important neurotransmitters involved in vomiting are:<\/p>\n\n\n\n Describe the peripheral pathway of CINV Describe the central pathway of CINV Common serotonin 5-HT3 antagonists used for CINV: Common neurokinin-1 antagonists used for CINV: Common steroids used for CINV: 2 types of therapies that commonly have cutaneous reactions:<\/p>\n\n\n\n Most-common cutaneous reaction seen with 5-FU and Capecitabine: Antimetabolites that commonly cause cutaneous reactions: Define myelosuppression If severe: myeloablation<\/p>\n\n\n\n The most common dose-limiting toxicity of chemotherapy Define nadir, and when does it occur? Typically occurs 7-10 days following cycle<\/p>\n\n\n\n NCCN defines neutropenia as an ANC < _<\/em><\/strong>\/mm^3 Risk factors for developing neutropenia include:<\/p>\n\n\n\n 65 years old Define neutropenic fever ANC calculation Normal WBC count Normal neutrophil count An ANC of less that _<\/strong> is considered a risk for infection Define thrombocytopenia Symptoms of thrombocytopenia Define anemia Symptoms of anemia Acute diarrhea lasts: Persistent diarrhea lasts: Chronic diarrhea lasts:<\/p>\n\n\n\n 4 weeks<\/p>\n<\/blockquote>\n\n\n\n Common constipation-causing agents: Define mucositis Define stomatitis AKA oral mucositis<\/p>\n\n\n\n Define xerostomia Common diarrhea-causing agents: Hypersensitivity reaction (HSR) versus anaphylaxis Anaphylaxis- severe inflammatory response; systemic; caused by histamine release<\/p>\n\n\n\n Immediate HSR can occur: Delayed HSR can occur: Risk factors for HSR and anaphylaxis: First thing to do if a HSR occurs: Define cumulative dose Define single dose Define course dose (AKA divided dose) Define extravasation Agents classified as irritants can cause: Agents classified as vesicants can cause: Define infiltration Common plant alkaloids: Vinca alkaloids are ALL administered (1)<\/em> and should NEVER be administered (2)<\/em>, as this will result in patient death<\/p>\n\n\n\n How does hormone therapy work? LHRH agonists MOA *Prostate cancer LHRH antagonists MOA *No tumor flare<\/p>\n\n\n\n Most common type of breast cancer Aromatase inhibitors MOA **Less estrogen is available to stimulate growth of HR-positive breast cancer cells<\/p>\n\n\n\n 2 types of aromatase inhibitors<\/p>\n\n\n\n 3 aromatase inhibitors Common side effects of aromatase inhibitors (AI): Selective ER downregulators (SERDs) MOA Common SERD Selective ER modulators (SERMs) MOA *Can function as ER agonists, antagonists, or mixed agonist-antagonists Common SERMs Antiandrogens MOA Androgen synthesis inhibitors MOA Common androgen synthesis inhibitors CYP17 inhibitors MOA Common CYP17 inhibitors Adrenolytic agents MOA Define receptor Define monomer Define ligand Define ligand bonding Define dimerization Define kinase Define phosphorylation Targeted therapies work by:<\/p>\n\n\n\n __<\/em><\/strong> has been described as a way to “fire up the immune system’s response to cancer” Immunotherapy works by the following 3 ways:<\/p>\n\n\n\n What sets immunotherapy apart from traditional chemotherapy? Immunotherapy categories: Passive immunotherapy MOA Examples of passive immunotherapy Active immunotherapy MOA Examples of active immunotherapy Specific immunotherapy MOA Examples of specific immunotherapy Nonspecific immunotherapy MOA *Given adjuvantly to other anticancer treatment drugs<\/p>\n\n\n\n Examples of nonspecific immunotherapy 2 different ways that immunotherapies work against cancer:<\/p>\n\n\n\n 6 main types of immunotherapy<\/p>\n\n\n\n mAbs MOA Different types of mAbs used in treatment of cancer mAbs ending in “-ximab” source mAbs ending in “-zumab” source mAbs ending in “-umab” source mAbs ending in “-omab” source Immune checkpoint inhibitors MOA Immune checkpoint inhibitors initially cause tumors to swell, making it appear as if the tumor is growing. This is called _<\/em><\/strong><\/em><\/strong> 2 main types of cancer vaccines Nonspecific immunotherapies MOA Adoptive cell therapy MOA Oncolytic virus therapy MOA Common side effects of immunotherapies Common treatment for immunotherapy side effects Results of immunotherapy agents most commonly occur between __<\/strong><\/em><\/strong> after starting therapy Hierarchy of controls when controlling workplace hazards 4 different types of medication dosing:<\/p>\n\n\n\n G1 2 mitosis interphase G1 cell division Chemotherapy and immunotherapy cyclins and cyclin-dependent kinases pluripotent undifferentiated myeloid, lymphoid myeolid lymphoid immunotherapy B, T Alkylating agents Altretamine (Hexalen) Bendamustine (Treanda\/Bendeka) Irritant and vesicant properties<\/p>\n\n\n\n infusion reactions likely to occur in 2nd or subsequent infusions<\/p>\n\n\n\n Busulfan (IV busulfex: PO Myleran) seizure prophylaxis Carboplatin Irritant Chlorambucil (Leukeran) empty stomach Cisplatin Mannitol and hydration to prevent nephrotoxicity Cyclophosphamide (Cytoxan) Lesson 1: Foundations to Set the Stage Focusing on Cellular Structure and Function The Normal Cell Cycle-The cell cycle refers to the ordered seres of processes of DNA replication and mitosis, or cell division -Cell nucleus regulates these processes by gathering and processing complexes molecular information Interphase and Mitotic PhaseCell division produces two identical cells 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-The cells of the immune system are created in the bome marrow from what is know as a _<\/em><\/p>\n\n\n\n
Mature into:
-RBCS
-Plts
-WBCs (Granulocytes)<\/p>\n\n\n\n
Mature into:
-Specialized WBCs called lymphocytes (Agranulocytes)<\/p>\n\n\n\n
Consists of 2 types of immunity:<\/p>\n\n\n\n
2: Adaptive<\/p>\n\n\n\n
-First line of defense against a pathogen<\/p>\n\n\n\n
(skin, mucous membranes, and normal flora of the skin and gut)
(Cellular components such as phagocytes, natural killer cells, granulocytes, and macrophages)<\/p>\n\n\n\n\n
1.Cells that engulf and destroy invader<\/li>\n\n\n\n
Eosinophils – parasites
Basophils – release histamine to stimulate immune response)<\/li>\n\n\n\n
-Stimulated if innate immunity is insufficient<\/p>\n\n\n\n
-B-Cells
-Memory B-Cells
-Plasma act to produce immunoglobulins (Igs) or antibodies<\/p>\n\n\n\n
-each one is programmed to make one specific antibody<\/p>\n\n\n\n
-some plasma cells will undergo apoptosis<\/p>\n\n\n\n
Depends upon cytotoxic T cells and helper T cells and their cyokinds<\/p>\n\n\n\n
regulate the immune response to prevent autoimmune reactions and limit inflammatory responses<\/p>\n\n\n\n
-Can only recognize antigens when they are presented to them by “presenting cells”<\/p>\n\n\n\n
-help other T-Cells by secreting chemicals<\/p>\n\n\n\n
-Directly kill cells for which they are activated to kill<\/p>\n\n\n\n
-Secreted by lymphocytes<\/p>\n\n\n\n
-Interferons (IFNs)<\/p>\n\n\n\n
-encapsulated and grow in an orderly manner with smooth edges<\/p>\n\n\n\n
-Malignant tumors are not encapsulated<\/p>\n\n\n\n
-regulate normal cell growth and division<\/p>\n\n\n\n
when mistakes in copies of DNA can occur, if a mutation occurs next to a proto-oncogene, it can “turn on” and become a __<\/strong><\/p>\n\n\n\n\n
\n
-act like brakes in a car, slowing down or stopping cell growth and division<\/p>\n\n\n\n
-“sucidie gene”<\/p>\n\n\n\n
-cancer cells are able to find their own growth signals making them self-sufficient<\/p>\n\n\n\n
-the communication or passage of a message telling the cell to do a biologic process, such as make a protein, divide, or make new blood vessels<\/p>\n\n\n\n\n
\n
-turned on by giving up a phosphate molecule<\/p>\n\n\n\n
many pathways and crossalks signaling btw and among the different pathways, and they all have the power to control cell behavior in one way or another<\/p>\n\n\n\n
-shown to decrease the benefits of some cancer drugs<\/p>\n\n\n\n
-play a role in resistance to some chemotherapy agents in certain pts by keeping cells that have been exposed to chemotherapy from undergoing apoptosis<\/p>\n\n\n\n
-transduction enzymes that activate Akt, leading to cell survival, increased cell proliferation, and growith<\/p>\n\n\n\n
-treatment given as a first step to shrink a tumor before the main treatment, usually surgery<\/p>\n\n\n\n
-additonal cancer treatment given after the primary treatment to lower the risk that the cancer can recur<\/p>\n\n\n\n
-refers to the drug dose per unit of time<\/p>\n\n\n\n
-amount of drug delivered over time<\/p>\n\n\n\n
-calculated by comparing the dose that the pt received to the planned dose of the standard regimen<\/p>\n\n\n\n
-greater challenge to adherence because the responsibility falls on the pt and caregiver<\/p>\n\n\n\n
-pt takes too few or too many pills<\/p>\n\n\n\n
-when a pt believes a dose was missed or that “more is better”, too much medication may be taken, leading to increased toxicity<\/p>\n\n\n\n
-provider relationship
-side effects
-necessity
-routinization
-support
-lifestyle fit
-cost
-medication knowledge
-pill burden
-regiment complexity<\/p>\n\n\n\n
-function by causing a break in the DNA helix strand, causing interference with DNA replication, which results in cell death<\/p>\n\n\n\n
-Nitrogen mustards (cyclophosphamide{Cytoxin}, ifosfamide{Ifex}, bendamustine{Treanda})<\/p>\n\n\n\n
-subgroup of alkylating agents<\/p>\n\n\n\n
-Lomustine (CeeNu)
-Streptozocin (Zanosar)<\/p>\n\n\n\n
-Alkylazing agent<\/p>\n\n\n\n
-Alkylating agent<\/p>\n\n\n\n
-severe N\/V<\/p>\n\n\n\n
-Alkylating agent)<\/p>\n\n\n\n
-Alkylating agent<\/p>\n\n\n\n
-injects chemo directly into the subarachnoid space so it reaches the CNS<\/p>\n\n\n\n
-younger
-have a hx of low or no alcohol consumption
-are female
-hx of morning sickness
-prone to motion sickness
-have had chemo previously<\/p>\n\n\n\n
-Acute: occurring within 24 hours<\/p>\n\n\n\n
-limit exposure of hands and feet to hot water<\/p>\n\n\n\n
-point at which blood cell counts are at their lowest following treatment<\/p>\n\n\n\n
-ANC of less than 500\/mm3 or<\/p>\n\n\n\n
-older than 65<\/p>\n\n\n\n
-temp of 38.3 or greater one time<\/p>\n\n\n\n\n
-inflammation of the mucous membrane lining the digestive tract from mouth to anus<\/p>\n\n\n\n
-specifically inflammatory conditions of the mouth<\/p>\n\n\n\n
-dryness of the mouth caused by damage to or dysfunction of the salivary glands<\/p>\n\n\n\n
-body mounts an immunologic response to a foreign substance or antigen, resulting in local tissue injury<\/p>\n\n\n\n
-immediate (within 5 minute) HSR, present like classic allergic reactions<\/p>\n\n\n\n
-Delayed hypersensitivity reactions, can occur any time after the immediate hypersensitivity window, even days or weeks<\/p>\n\n\n\n
-pruritus
-restlessness, agitation, anxiety, feeling of impending doom
-fever, flushing, chills
-urticaria (hives)
-maculopapular rash
-edema of hands, face, and feet
-N\/V
-dyspnea, wheezing, bronchospasm
-hypotension, cyanosis
-circulatory and respiratory collapse<\/p>\n\n\n\n
-pneumonitis
-mucositis
-contact dermatitis
-granulomas
-Graph vs host disease<\/p>\n\n\n\n
total amount of one antineoplastic agent given to the pt, adding up each time that the pt has received it<\/p>\n\n\n\n
-“cumulative dose should not exceed\u2026”<\/p>\n\n\n\n
-leak of a drug capable of causing tissue damage from the vessel in which it is being administered into the surround tissue<\/p>\n\n\n\n
-causes inflammation, pain, and burning but rarely causes tissue necrosis<\/p>\n\n\n\n
-causes blistering and significant pain and tissue damage and destruction, leading to tissue death<\/p>\n\n\n\n
-Do not use IV in hand, wrist, AC areas<\/p>\n\n\n\n\n
-Vinca Alkaloids (vincristine, vinblastine)<\/p>\n\n\n\n
–Anthracyclines (doxorubicin, epirubicin, daunorubicin, idarubicin)<\/p>\n\n\n\n
-targeted therapies act on specific molecular targets on or within the cells that are associated with cancer, whereas standard chemo act on all rapidly dividing cells<\/p>\n\n\n\n
-disease cure when used as primary or adjuvant therapy<\/p>\n\n\n\n
-molecule inside or on the surface of a cell that binds to a specific substance causes a specific effect in that cell<\/p>\n\n\n\n
molecule that can join with other identical monomers to form a structure called a polymer<\/p>\n\n\n\n
a substance that forms a complex with another biomolecule to exert a biologic effect<\/p>\n\n\n\n
process by which the ligand attaches to a specific receptor site and activates that receptor, activating the signaling pathway<\/p>\n\n\n\n
two monomers that are side-by-side on the surface of the cell are paired and activated by a ligand, which causes a series of signals<\/p>\n\n\n\n
type of enzyme that adds chemicals called phosphates to other molecules such as sugars or proteins causing other molecules in the cell to become either active or inactive<\/p>\n\n\n\n
activation of a chemical process to initiate signaling<\/p>\n\n\n\n\n
-fusion protein tyrosine kinase formed with a gene translocation occurs between gene 9 and 22<\/p>\n\n\n\n
this is the primary angiogenic factor produced by cells<\/p>\n\n\n\n
-target of rapamycin<\/p>\n\n\n\n\n
-end in -ib<\/p>\n\n\n\n\n
-stopping or slowing the growth of cancer cells<\/p>\n\n\n\n
-initate an antitumor effect but do not result in any immunologic memory<\/p>\n\n\n\n
-capitalize on the immune system’s ability to remember a foreign invade<\/p>\n\n\n\n
-capitalize on tumor markers to specifically target and kill cancer cells<\/p>\n\n\n\n
-do no target cancer cells alone but rather stimulate a large immune response<\/p>\n\n\n\n\n
-highest level of protection from a hazardous exposure<\/li>\n<\/ol>\n\n\n\n\n
-second highest level of protection<\/li>\n<\/ol>\n\n\n\n\n
-third level of protection<\/li>\n<\/ol>\n\n\n\n\n
-lowest form of protection<\/li>\n<\/ol>\n\n\n\n\n
\n
\n
-the AUC calculation incorporates renal function as part of the equation<\/p>\n\n\n\n
-mAbs are agents that are derived from human or mouse antibodies or a combination of the two<\/p>\n\n\n\n
-it is perfectly safe for you to have contact with your loved ones while getting treatment<\/p>\n\n\n\n
-you should definiely check with your HCP first to be sure<\/p>\n\n\n\n
Interphase
Mitotic phase
Cytokinesis<\/p>\n\n\n\n
First growth phase (G1)
Synthesis phase (S phase)
Second growth phase (G2)<\/p>\n\n\n\n
Prophase
Metaphase
Anaphase
Telophase<\/p>\n\n\n\n
Non-specific response, either:<\/p>\n\n\n\n\n
Follows innate immunity if unsuccessful. Memory immunity, including:<\/p>\n\n\n\n\n
Variations in the nucleotide sequence of a gene<\/p>\n\n\n\n
Cure
Control
Palliation<\/p>\n\n\n\n
Treatment is given prior to surgery to shrink the tumor<\/p>\n\n\n\n
Additional cancer treatment given after the primary treatment to lower the risk that the cancer reoccur<\/p>\n\n\n\n
Treatments used to prepare a patient for stem cell transplantation<\/p>\n\n\n\n
Myeloablative
Nonmyeloablative<\/p>\n\n\n\n
Drug dose per unit of time<\/p>\n\n\n\n
Amount of drug delivered over time<\/p>\n\n\n\n
By comparing the dose that the patient ACTUALLY received to the planned dose of the standard regimen<\/p>\n\n\n\n
By causing a break in the DNA helix strand, interfering with DNA replication and causing cell death<\/p>\n\n\n\n\n
Nitrogen mustards<\/p>\n\n\n\n
Cyclophosphamide (Cytoxan)
Ifosfamide (Ifex)
Bendamustine (Treanda)<\/p>\n\n\n\n
Cisplatin (Platinol)
Carboplatin (Paraplatin)<\/p>\n\n\n\n
Able to cross the blood-brain barrier; can be effective in treating some brain tumors<\/p>\n\n\n\n
Carmustine (BiCNU)
Lomustine (CeeNu)
Streptozocin (Zanosar)<\/p>\n\n\n\n
Carboplatin<\/p>\n\n\n\n\n
BUN
Creatinine
CBC w\/ diff<\/p>\n\n\n\n
Bladder protectant with administration of cyclophosphamide or ifosfamide<\/p>\n\n\n\n
Oxaliplatin<\/p>\n\n\n\n
By blocking DNA and RNA growth by interfering with enzymes needed for normal cell metabolism<\/p>\n\n\n\n
S<\/p>\n\n\n\n
Cells with high division rates<\/p>\n\n\n\n
Myelosuppression
GI toxicities
Photosensitivity
Hand-foot syndrome<\/p>\n\n\n\n
Azacitidine
Capecitabine
5-FU
Cytarabine
Decitabine
Methotrexate<\/p>\n\n\n\n
IV piggyback via gravity<\/p>\n\n\n\n
Interfering with enzymes necessary for DNA to replicate in ALL phases of the cell cycle<\/p>\n\n\n\n
Anthracyclines
Non-anthracyclines<\/p>\n\n\n\n
Daunorubicin
Doxorubicin
Epirubicin
Idarubicin<\/p>\n\n\n\n
Mitoxantrone<\/p>\n\n\n\n
Actinomycin D
Mitomycin C
Bleomycin<\/p>\n\n\n\n
Vesicant –> extravasation
Cardiac function
Lifetime dose tracking (cardiotoxicity)<\/p>\n\n\n\n
550 mg\/m^2<\/p>\n\n\n\n
Dexrazoxane<\/p>\n\n\n\n
Cardiotoxicity
N\/V
Mucositis
Diarrhea
Severe myelosuppression
Hepatic impairment
Secondary cancers<\/p>\n\n\n\n
Pulmonary toxicity
Hypersensitivity reactions (esp. in lymphoma patients)
Cutaneous reactions
Lifetime dose tracking (pulmonary toxicity)<\/p>\n\n\n\n
400 units<\/p>\n\n\n\n\n
Acute
Delayed
Breakthrough
Anticipatory
Refractory<\/p>\n\n\n\n
Occurring within 24 hours of chemotherapy<\/p>\n\n\n\n
Occurring from 24 hours to 5 days after treatment<\/p>\n\n\n\n
Occurring despite treatment<\/p>\n\n\n\n
Triggered by taste, odor, memories, visions, or anxiety related to chemotherapy<\/p>\n\n\n\n
Occurring during subsequent cycles when treatment failed in earlier cycles<\/p>\n\n\n\n
90<\/p>\n\n\n\n
30-90<\/p>\n\n\n\n
10-30<\/p>\n\n\n\n
10<\/p>\n\n\n\n
Carmustine
Cisplatin
Cyclophosphamide
Dacarbazine
Mechlorethamine
Streptozosin<\/p>\n\n\n\n
Carboplatin
Cytarabine
Daunorubicin
Doxorubicin
Epirubicin
Idarubicin
Ifosfamide
Irinotecan
Oxaliplatin<\/p>\n\n\n\n
5-FU
Cytarabine
Docetaxel
Etoposide
Gemcitabine
Methotrexate
Mitomycin C
Mitoxantrone
Paclitaxel
Pemetrexed<\/p>\n\n\n\n
Bleomycin
Bevacizumab
Bortezomib
Busulfan
Cetuximab
Fludarabine
Trastuzumab
Vinca alkaloids<\/p>\n\n\n\n\n
Primarily occurs in the GI tract
Associated with acute CINV
Neurotransmitter –> serotonin<\/p>\n\n\n\n
Primarily occurs in the brain
Associated with delayed CINV
Neurotransmitter –> Substance P<\/p>\n\n\n\n
Dolasetron
Granisetron
Ondansetron
Palonosetron<\/p>\n\n\n\n
Aprepitant
Fosaprepitant<\/p>\n\n\n\n
Dexamethasone<\/p>\n\n\n\n\n
Palmar-plantar erythrodysesthesia AKA hand-foot syndrome<\/p>\n\n\n\n
5-FU
Capecitabine (Xeloda)<\/p>\n\n\n\n
Bone marrow activity is decreased, resulting in fewer RBCs, WBCs and platelets<\/p>\n\n\n\n
Myelosuppression<\/p>\n\n\n\n
The point at which blood cell counts are at their lowest following a treatment cycle.<\/p>\n\n\n\n
500<\/p>\n\n\n\n\n
Hx of neutropenia with previous chemotherapy
Hx of chemotherapy or radiation treatment
Hematologic malignancy
Uncontrolled\/advanced cancer
Lung cancer<\/p>\n<\/blockquote>\n\n\n\n
Fever of 101 F or greater one time
OR
Fever of 100.4 F lasting one hour or longer<\/p>\n\n\n\n
(% polys + % bands) x (WBC)\/100<\/p>\n\n\n\n
4,500-10,000<\/p>\n\n\n\n
54%-62% of WBC<\/p>\n\n\n\n
1,000<\/p>\n\n\n\n
Low platelet count<\/p>\n\n\n\n
Petechiae or easily bruising
Headaches
Hypotension and tachycardia
Prolonged bleeding (gums, menstruation)<\/p>\n\n\n\n
Deficiency of RBC or hemoglobin in the blood<\/p>\n\n\n\n
Dyspnea
Fatigue
Dizziness
Headaches<\/p>\n\n\n\n
1-2 days and resolves on its own<\/p>\n\n\n\n
2-4 weeks<\/p>\n\n\n\n\n
Vinca alkaloids (vincristine and vinorelbine)
Thalidomide
Lenalidomide
Bortezomib<\/p>\n\n\n\n
Inflammation of the mucous membranes lining the digestive tract from mouth to anus<\/p>\n\n\n\n
Inflammatory conditions of the mouth specifically<\/p>\n\n\n\n
Dryness of the mouth caused by damage to or dysfunction of the salivary glands<\/p>\n\n\n\n
Irinotecan
5-FU
Paclitaxel
Dactinomycin
Capecitabine<\/p>\n\n\n\n
HSR- localized tissue injury; generalized<\/p>\n\n\n\n
Within 5 minutes of start of infusion to 6 hours following infusion<\/p>\n\n\n\n
Days or weeks after immediate HSR window<\/p>\n\n\n\n
Administration of a known HSR causing agent
Hx of allergies
Hx of hypersensitivity or anaphylaxis
Premedications not ordered\/administered<\/p>\n\n\n\n
STOP THE INFUSION IMMEDIATELY<\/p>\n\n\n\n
Total dose of an antineoplastic agent or radiation after repeated exposure to the treatment<\/p>\n\n\n\n
Recommended dose of one antineoplastic agent given at a single point in time<\/p>\n\n\n\n
Recommended dose of one antineoplastic agent given over a defined period of time<\/p>\n\n\n\n
Leak of a drug capable of causing tissue damage from the intended vessel into the surrounding tissue or unintended sites<\/p>\n\n\n\n
Inflammation
Pain
Burning
** Rarely cause tissue necrosis comparable to vesicants<\/p>\n\n\n\n
Blistering
Significant pain
Tissue damage and destruction
**Lead to tissue death<\/p>\n\n\n\n
Leakage of non-vesicant\/non-irritant solutions into surrounding tissue<\/p>\n\n\n\n
Etoposide
Docetaxel
Paclitaxel
Vinblastine
Vinorelbine<\/p>\n\n\n\n\n
Attempts to add, block, or remove hormones from the body to interrupt cancer cell division<\/p>\n\n\n\n
Produce an initial increase in LH and FSH, which can cause a flare. Then lower testosterone made by testicles and estrogen & progesterone made by ovaries<\/p>\n\n\n\n
*Estrogen receptor-positive, premenopausal metastatic breat cancer<\/p>\n\n\n\n
Directly inhibits pituitary from releasing LH and FSH<\/p>\n\n\n\n
Hormone receptor (HR)-positive breast cancer<\/p>\n\n\n\n
Block the enzyme aromatase, which turns the hormone androgen into small amounts of estrogen in the body<\/p>\n\n\n\n\n
Anastrozole
Letrozole
Exemestane<\/p>\n\n\n\n
Fatigue
N\/V*
Weakness
HA*
Insomnia
Dizziness
Hot flashes*
Weight gain*
Higher cholesterol
Increased sweating*
Bone\/joint pain*<\/p>\n\n\n\n
Binding to and degrading ER<\/p>\n\n\n\n
Fulvestrant<\/p>\n\n\n\n
Blocking and downregulating ERs<\/p>\n\n\n\n
*Can activate or block estrogen<\/p>\n\n\n\n
Tamoxifen
Raloxifine
Bazedoxifine<\/p>\n\n\n\n
Keeps androgens from binding to androgen receptors found in prostate cancer cells (and in some other tissue cells)<\/p>\n\n\n\n
Stop the adrenal glands from producing androgens<\/p>\n\n\n\n
Ketoconazole
Aminoglutethimide
Abiraterone acetate<\/p>\n\n\n\n
Inhibit the key enzyme that catalyzes biosynthesis of androgens from all sources<\/p>\n\n\n\n
Abiraterone
Orteronel<\/p>\n\n\n\n
Suppress testicular and adrenal steroidogenesis, rapidly reducing testosterone levels<\/p>\n\n\n\n
Molecule inside\/on surface of a cell that binds to a specific substance and causes a specific effect in that cell<\/p>\n\n\n\n
Molecule that can be bonded to other identical molecules to form a polymer<\/p>\n\n\n\n
Molecule that binds to a receptor to exert a biologic effect<\/p>\n\n\n\n
Process by which ligand attaches to specific receptor site and activates receptor, activating the signaling pathway<\/p>\n\n\n\n
2 monomers that are side-by-side on cell surface are paired and activated by a ligand, which causes a series of signals<\/p>\n\n\n\n
Enzyme that adds phosphates to other molecules, causing other molecules in the cell to become either active or inactive<\/p>\n\n\n\n
Activation of a chemical process to initiate signaling<\/p>\n\n\n\n\n
Immunotherapy<\/p>\n\n\n\n\n
Highly specific
Trained to remember cancer cells<\/p>\n\n\n\n
Passive
Aggressive
Specific
Nonspecific<\/p>\n\n\n\n
Administered to initiate an antitumor effect
*Do not result in any immunologic memory<\/p>\n\n\n\n
Monoclonal antibodies
Cytokines<\/p>\n\n\n\n
Mount an immune response against tumor
*Should remember cancer cells long after treatment has stopped<\/p>\n\n\n\n
Cancer vaccines<\/p>\n\n\n\n
Target tumor markers or tumor-associated antigens (TAAs) to kill cancer cells<\/p>\n\n\n\n
mAbs
Cancer vaccines<\/p>\n\n\n\n
Stimulate a large immune response<\/p>\n\n\n\n
Cytokines, interleukins, checkpoint inhibitors<\/p>\n\n\n\n\n
\n
Mark cancer cell surface receptor\/antigen to make the cell visible to the immune system to destroy<\/p>\n\n\n\n
Naked mAbs
Conjugated monoclonal antibodies
Bispecific monoclonal antibodies<\/p>\n\n\n\n
Chimeric human-mouse<\/p>\n\n\n\n
Humanized mouse<\/p>\n\n\n\n
Fully human<\/p>\n\n\n\n
Murine mouse<\/p>\n\n\n\n
Prevent cancer cells from turning off T cells –> allows T cells to infiltrate a tumor and stop it from growing<\/p>\n\n\n\n
Pseudoprogression<\/p>\n\n\n\n
Preventative\/prophylactic
Treatment\/therapeutic<\/p>\n\n\n\n
Stimulating the immune system in a general way, hopefully leading to a better immune response against cancer cells<\/p>\n\n\n\n
T cells collected from patient
T cells grown in laboratory
This increases amount of T cells able to kill cancer cells or fight infections
T cells given back to patient to help immune system<\/p>\n\n\n\n
Naturally occurring or genetically engineered virus that can infect and kill a cancer call without harming normal cells<\/p>\n\n\n\n
Fatigue
Diarrhea
Colitis
Musculoskeletal pain
Dermatitis<\/p>\n\n\n\n
Corticosteroids<\/p>\n\n\n\n
12-16 weeks<\/p>\n\n\n\n
Elimination
Substitution
Engineering controls
Administrative controls
PPE<\/p>\n\n\n\n\n
first growth phase (or first gap)<\/p>\n\n\n\n
How many cells are produced each time a cell divides?<\/p>\n\n\n\n
the process of cell division<\/p>\n\n\n\n
The time when a cells grows and replicates DNA in preparation for cell division.<\/p>\n\n\n\n
most important checkpoint in cell division<\/p>\n\n\n\n
Phases of include synthesis phase, G1, G2, M phase<\/p>\n\n\n\n
These treatments are ALL developed to target specific points in the cell division process.<\/p>\n\n\n\n
Progression through the cell cycle is controlled by these two proteins:<\/p>\n\n\n\n
_____<\/em><\/strong><\/em><\/strong> stem cells are created in the bone marrow and can differentiate into any type of cell (except embryonic tissue).<\/p>\n\n\n\n
Is a pluripotent stem cell differentiated or undifferentiated?<\/p>\n\n\n\n
for hematology a pluripotent stem cell divides producing cells from either _<\/em><\/strong><\/em><\/strong> or _<\/em><\/strong><\/em><\/strong> lineage<\/p>\n\n\n\n
This type of precuros or pre-cell matures into red blood cells, platelets, and white blood cells.<\/p>\n\n\n\n
this type of stem cell or pre-cell matures into specialized WBCs called lymphocytes.<\/p>\n\n\n\n
the use of the body’s own immune system to treat cancer<\/p>\n\n\n\n
These two letters make up the two types of lymphocyte cells.<\/p>\n\n\n\n
Classification
Break DNA helix strand, thereby interfering with DNA replication<\/p>\n\n\n\n
Alkylating Agent
PO
Ovarian CA
Side effects- nausea, vomiting, skin rash, hypersensitivity reaction, diarrhea
Dose limiting – neuro-toxicity, peripheral neuropathy, myelosuppression<\/p>\n\n\n\n
Alkylating agent
IV
CLL or Indolent NHL
Side effects- pyrexia, nausea, vomiting, skin reactions, TLS, hepatotoxicity, vein irritation
Dose limiting – myelosuppression<\/p>\n\n\n\n
Alkylating Agent
IV or PO
CML and Stem cell prep
Side effects – profound tachycardia, HTN, chest pain, hyperpigmentation, alopecia, infertility, confusion, suizures, mucositis, nausea, vomiting, insomnia, hyperglycemia, blurred vision, secondary malignancy, VOD (now sinusoidal obstruction syndrome)<\/p>\n\n\n\n
central line only for IV<\/p>\n\n\n\n
Alkylating agent
IV
Ovarian CA
Side effects – neutropenia, nausea, vomiting, hypersensitivity, mild alopecia, skin rash
Dose Limiting – thrombocytopenia<\/p>\n\n\n\n
AUC dosing<\/p>\n\n\n\n
Alkylating agent
PO
CLL, HL, NHL
Side effects – infertility, nausea, vomiting, secondary malignancy, hyperuricemia, pulmonary fibrosis, seizure
Dose Limiting – myelosuppression, skin reactions<\/p>\n\n\n\n
caution in pts with seisure history and within 1 month of radiation or other cytotoxic therapy<\/p>\n\n\n\n
Alkylating agent
IV
Ovarian, Testicular, Bladder
Side Effects – severe acute and delayed CINV, ototoxicity, hyperuricemia, hypersensitivity, electrolyte abnormalities, peripheral neuropathy
Dose Limiting – nephrotoxicity, myelosupression<\/p>\n\n\n\n
check creatinine prior to dose
nausea up to 6 days after dose<\/p>\n\n\n\n
Alkylating agent
IV, PO<\/p>\n","protected":false},"excerpt":{"rendered":"