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44 Cards in this Set
- Front
- Back
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True or False:
In order to optimally target only cancerous tissue, it is imperative to understand not only how normal cells function, but also how cancer cells differ from normal cells. |
TRUE
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The cell cycle consists of four phases. What stage do RNA and protein synthesis, cell growth, and DNA repair take place?
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During the G1 phase (postmitotic phase)
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Once the processes of the G1 phase are complete, the cell enters the S phase (synthesis phase). What happens during the S-Phase?
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DNA is completely replicated
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What happens during the G2 phase of the cell cycle?
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The G2 phase is a period of additional synthesis of RNA, protein, and specialized DNA
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Cell division occurs during which stage of the cell cycle?
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M Phase (Mitosis)
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After the M phase of the cell cycle, cells have 2 options for where they can go next. What are these 2 options?
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After mitosis, cells can again enter the G1 phase, or can “drop out” of the cell cycle and enter a resting phase (G0).
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True or False:
Cells in the G0 phase are vulnerable to therapies aimed at actively growing and dividing cells. |
FALSE:
Cells in G0 do not engage in the synthetic activities characteristic of the cell cycle and are not vulnerable to therapies aimed at actively growing and dividing cells. |
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What is the "GROWTH FRACTION"?
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The growth fraction is the proportion of cells in a tumor that are actively involved in cell division (i.e., not in the G0 phase). The growth fraction of tumors decreases as they enlarge, because vascular supply and oxygen levels are decreased.
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Why might Surgical removal of tumor tissue (cytoreductive debulking surgery) make them more vulnerable to chemotherapy and radiation therapy?
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Surgical removal of tumor tissue (cytoreductive debulking surgery) can result in G0 cells reentering the cell cycle, thus making them more vulnerable to chemotherapy and radiation therapy.
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What is the "Generation time" of the cell cycle?
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The generation time is the length of the cell cycle, from one M phase to the next M phase.
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For a given cell type, the lengths of the S and M phases are relatively constant, whereas G2 and especially G1 vary. Why does G1 vary so much?
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The variable length of G1 can be explained by cells entering the resting phase (G0) for a period and then reentering the cycle. The length of G1 has a profound effect on the cell's susceptibility to treatment.
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Why are several intermittent doses of Chemotherapy more likely to be curative than a single large dose?
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Chemotherapeutic agents and radiation kill cancer cells by first-order kinetics. This means that each dose kills a constant fraction of tumor cells, instead of a constant number. The resulting clinical implication is that several intermittent doses are more likely to be curative than a single large dose.
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Chemotherapeutic agents can be (1) cell cycle (phase)-nonspecific or or (2) cell cycle (phase)-specific. When would you choose one over the other?
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(1) cell cycle (phase)-nonspecific, which means that they can kill in all phases of the cell cycle and are useful in tumors with a low growth index, or
(2) cell cycle (phase)-specific, which means that they kill in a specific phase of the cell cycle and are most useful in tumors that have a large proportion of actively dividing cells. |
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What is the major side effect of the alkylating agents?
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Myelosuppression
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Name the class of Chemotherapuetics and list the major toxicites:
Bind and cross-link DNA either interstrand, intrastrand, or to proteins; prevents replication and transcription |
Alkylating agents: Cyclophosphamide, ifosfamide, melphalan
Hemorrhagic cystitis, alopecia, nephrotoxicity |
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What class of drugs are Cisplatin and carboplatin?
What is the MOA? Tox? |
Alkylating-like agents
Cross-link DNA strands (interstrand) Nephrotoxicity, neurotoxicity, myelosuppression |
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How might antibiotics be useful in treating cancer?
What antibiotic agents are used in cancer therapy? |
Interfere with DNA replication through free radical formation and intercalation between bases
Bleomycin, actinomycin D |
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What class of drugs are Methotrexate and 5-fluorouracil?
MOA? Toxicity? |
Antimetabolites
Block enzymes required for DNA synthesis Gastrointestinal, myelosuppression, dermatologic, hepatotoxicity |
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What class of chemotheraputics are Vincristine, vinblastine, & paclitaxel?
MOA? Tox? |
Plant (vinca) alkaloids
Inhibit microtubule assembly Myelosuppression |
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What class of chemotheraputics are Etoposide & Topotecan?
MOA? Tox? |
Topoisomerase inhibitors
Inhibit topoisomerase, resulting in DNA strand breaks Myelosuppression, alopecia, gastrointestinal |
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Which of the following works by inhibit DNA-directed RNA synthesis and also are involved in the formation of free radicals, causing strand breakage. They are phase-nonspecific. Their general side effects are similar to those of the alkylating agents; however, each individual drug has its own individual toxicity.
A) Antitumor antibiotics B) Antimetbolites C) Plant (Vinca) Alkloids D) Topoisomerase Inhibitors |
A) Antitumor antibiotics
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Which of the following re are structural analogs of normal molecules necessary for cell function? They competitively interfere with the enzymes involved with normal synthesis of nucleic acids and, therefore, are most active during the S phase of cell division. They may cause bone marrow suppression or gastrointestinal mucositis when given in a bolus.
A) Antitumor antibiotics B) Antimetbolites C) Plant (Vinca) Alkloids D) Topoisomerase Inhibitors |
B) Antimetbolites
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Which of the following interfere with the M phase of cell division by preventing the assembly of microtubules? They may cause bone marrow suppression or an anaphylactoid reaction.
A) Antitumor antibiotics B) Antimetbolites C) Plant (Vinca) Alkloids D) Topoisomerase Inhibitors |
C) Plant (Vinca) Alkloids
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Which of the following result in cell death by inhibiting an enzyme required for DNA replication.
A) Antitumor antibiotics B) Antimetbolites C) Plant (Vinca) Alkloids D) Topoisomerase Inhibitors |
In a normally replicating cell, TOPO-I induces reversible single-strand breaks in the DNA.
TOPO-I inhibitors complex with the DNA and TOPO-I and prevent repair of the breaks in the single strand of DNA, thus resulting in cellular death. |
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What is the MOA of SERMs, relating to their effect on breast tumors?
(Raloxifene & Tamoxifen are MC) |
Acts in estrogen-sensitive breast tumors to block the interaction of estrogen with estrogen receptors (ERs).
The therapeutic importance of cellular ERs has been well established in breast cancers. ER-positive tumors are responsive to endocrine therapy. SERMs act as competitive inhibitors of estrogen binding; the SERM-ER complex binds to chromosomes, but does not activate cell metabolism. The subsequent decrease in cellular activity and cell division results in reduced tumor growth. |
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What type of cancer are patients taking SERMs at risk for?
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Although relatively nontoxic, this class of drugs is related to an increased risk of endometrial cancer and uterine sarcomas and an increase in benign endometrial pathology.
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Which class of drugs suppress intratumor and plasma estrogen levels & are being used in postmenopausal patients for treatment of advanced breast cancer that has progressed beyond tamoxifen therapy
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Aromatase inhibitors (AIs)
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Which class of drugs has been found to be useful in the treatment of early-stage endometrial cancer when sugery is either not feasible, unsafe, or not desired?
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Progestational agents have been found to be useful in the treatment of early-stage endometrial cancer when surgery is either not feasible, unsafe, or not desired. Progestational therapy is also useful for some patients with recurrent disease. The most common progestational agents used are medroxyprogesterone and megestrol.
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Why are antineoplastic drugs considered toxic?
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Antineoplastic drugs are toxic because they act on normal as well as cancer cells.
Rapidly dividing cell types of the erythroid, myeloid, and megakaryocytic lineages are most sensitive to damage by common neoplastic drugs. Anemia, granulocytopenia (neutropenia), and thrombocytopenia are predictable side effects. |
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Why are fractionated doses of radiation are more likely to be effective than a single dose?
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Because dividing cells are more sensitive to radiation damage and because not all cells in a given tumor are dividing at any one time, fractionated doses of radiation are more likely to be effective than a single dose.
Providing multiple lower doses of radiation also reduces the deleterious effects on normal tissues. |
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The basis of fractionated dosage comes from the “four Rs” of radiobiology. What are the 4 R's?
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1. Repair of sublethal injury. When a dose is divided, the number of normal cells that survive is greater than if the dose were given at one time (higher total amounts of radiation can be tolerated in fractionated as opposed to single doses).
2. Repopulation. Reactivation of stem cells occurs when radiation is stopped; thus regenerative capacity depends on the number of available stem cells. 3. Reoxygenation. Cells are more vulnerable to radiation damage with oxygen present; as tumor cells are killed, surviving tumor cells are brought into contact with capillaries, making them radiosensitive. 4. Redistribution in the cell cycle. Because tumor cells are in various phases of the cell cycle, fractionated doses make it more likely that a given cell is irradiated when it is most vulnerable. |
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Major Application and Side Effects of Chemotherapeutic Agents on page 356
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If we need to know all these. I will make more cards later.
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What is a rad?
What is a Gray? How are they related? |
The rad has been used as a measure of the amount of energy absorbed per unit mass of tissue.
A standard measure of absorbed dose is the Gray, which is defined as 1 joule per kilogram; 1 Gray is equal to 100 rad. |
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Radiation is delivered in two general ways: external irradiation (teletherapy) and local irradiation (brachytherapy). What is the difference?
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Teletherapy depends on the use of high-energy (>1 million eV) beams, because this spares the skin and delivers less toxic radiation to the bone. Tolerance for external radiation depends on the vulnerability of surrounding normal tissues. Teletherapy usually is used to shrink tumors before localized radiation.
Brachytherapy depends on the inverse square law: the dose of radiation at a given point is inversely proportional to the square of the distance from the radiation source. |
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To put the radioactive material at the closest possible distance, brachytherapy uses encapsulated sources of ionizing radiation implanted directly into tissues (interstitial) or placed in natural body cavities (intracavitary). Where in the female reproductive tract can Intracavitary devices be placed?
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uterus, cervix, or vagina
Intracavitary devices can be placed within the uterus, cervix, or vagina, P.357 and then (after) loaded with radioactive sources as either low-dose radiotherapy (cesium-137), high-dose radiotherapy (iridium-192, cobalt-60), or as interstitial implants. This method protects health personnel from radiation exposure. |
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Interstitial Implants use which Isotopes?
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Interstitial implants use isotopes (iridium-192, iodine-125) formulated as wires or seeds. These implants are usually temporary, but permanent seed implants are being investigated.
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Complications associated with radiation therapy can be acute or late (chronic). What are the acute? What are the chronic?
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Acute reactions affect rapidly dividing tissues, such as epithelia (skin, gastrointestinal mucosa, bone marrow, and reproductive cells). Manifestations are cessation of mitotic activity, cellular swelling, tissue edema, and tissue necrosis. Early problems associated with irradiation of gynecologic cancers include enteritis, acute cystitis, vulvitis, proctosigmoiditis, topical skin desquamation, and, occasionally, bone marrow depression.
Chronic complications occur months to years after completion of radiation therapy. These include obliteration of small blood vessels or thickening of the vessel wall, fibrosis, and reductions in epithelial and parenchymal cell populations. Chronic proctitis, hemorrhagic cystitis, formation of ureterovaginal or vesicovaginal fistula, rectal or sigmoid stenosis, and bowel obstructions, as well as gastrointestinal fistulae may result. |
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Name the drug:
DNA-derived monoclonal antibody to the human epidermal growth factor receptor 2 protein (HER-2). |
Trastuzamab
Treatment with trastuzumab is currently indicated in patients with metastatic breast cancer whose tumors overexpress HER-2. |
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Tumor vaccines are also currently being investigated for the treatment of ovarian cancer. What is the theory behind this?
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The underlying principle behind these therapeutic vaccines is to inoculate the patient with a modified cancer cell line in an attempt to stimulate the patient's immune system to recognize and eliminate the tumor.
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Because half of ovarian cancers exhibit deleterious mutations in the p53 gene, research has focused on delivering a normal p53 gene product to the tumor using a variety of viral vectors. The hope is that the wild-type gene product would then be expressed by the tumor and the growth would then be inhibited.
What is the name of this type of therapy? |
GENE THERAPY
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What is adjuvant chemotherapy?
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Adjuvant chemotherapy is usually a set course of combination chemotherapy that is given in a high dose to patients who have no evidence of residual cancer after radiotherapy or surgery. The purpose is to eliminate any residual cancer cells, typically with the intent to cure disease.
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What is neoadjuvant chemo?
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Neoadjuvant chemotherapy aims to eradicate micrometastases or reduce inoperable disease in order to prepare patients for surgery and/or radiotherapy.
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What is meant by "Induction Chemotherapy?"
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Induction chemotherapy is usually a combination chemotherapy given in a high dose to cause a remission.
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What is maintenance Chemotherapy?
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Maintenance chemotherapy (consolidation chemotherapy) is a long-term and low-dose regimen that is given to a patient in remission to maintain the remission by inhibiting the growth of remaining cancer cells.
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