Perry's The Chemotherapy Source Book, now in its fifth edition, provides information on the choice of chemotherapeutic agents, the use of combination. The chemotherapy source book. Perry, Michael C (Michael Clinton), ; Doll, Donald C; Freter, Carl E. 5th ed. editor, Michael C. Perry ; associate editors. Perry's The Chemotherapy Source Book: Medicine & Health Science Books @

Chemotherapy Source Book

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The Chemotherapy Source Book: Medicine & Health Science Books @ Perry's The Chemotherapy Source Book. Publication Year: Edition: 5th Ed. Authors/Editor: Michael C. Perry; Dr. Donald C. Doll MD; Dr. Carl E. Freter MD. The Chemotherapy Source Book, Fourth Edition pulls together all the current information on the chemotherapeutic management of cancer patients, including.

This ability to bind covalently to DNA via their alkyl group is the primary cause for their anti-cancer effects. If the cell tries to replicate crosslinked DNA during cell division , or tries to repair it, the DNA strands can break. This leads to a form of programmed cell death called apoptosis. For this reason the effect on the cell is dose dependent; the fraction of cells that die is directly proportional to the dose of drug.

The drugs are very similar but they have subtle differences in their chemical structure. The building blocks are nucleotides ; a molecule comprising a nucleobase , a sugar and a phosphate group. The nucleobases are divided into purines guanine and adenine and pyrimidines cytosine , thymine and uracil. Anti-metabolites resemble either nucleobases or nucleosides a nucleotide without the phosphate group , but have altered chemical groups.

Also, after misincorporation of the molecules into DNA, DNA damage can occur and programmed cell death apoptosis is induced. Unlike alkylating agents, anti-metabolites are cell cycle dependent.

This means that they only work during a specific part of the cell cycle, in this case S-phase the DNA synthesis phase.

For this reason, at a certain dose, the effect plateaus and proportionally no more cell death occurs with increased doses. Subtypes of the anti-metabolites are the anti-folates , fluoropyrimidines, deoxynucleoside analogues and thiopurines. Methotrexate inhibits dihydrofolate reductase DHFR , an enzyme that regenerates tetrahydrofolate from dihydrofolate. When the enzyme is inhibited by methotrexate, the cellular levels of folate coenzymes diminish.

These are required for thymidylate and purine production, which are both essential for DNA synthesis and cell division. It primarily inhibits the enzyme thymidylate synthase , but also has effects on DHFR, aminoimidazole carboxamide ribonucleotide formyltransferase and glycinamide ribonucleotide formyltransferase. Fluorouracil is a nucleobase analogue that is metabolised in cells to form at least two active products; 5-fluourouridine monophosphate FUMP and 5-fluoro-2'-deoxyuridine 5'-phosphate fdUMP.

The thiopurines include thioguanine and mercaptopurine. Both mechanisms cause defective mitosis.

Anti-microtubule agents are plant -derived chemicals that block cell division by preventing microtubule function. They are hollow rod shaped structures that are required for cell division, among other cellular functions. Vinca alkaloids and taxanes are the two main groups of anti-microtubule agents, and although both of these groups of drugs cause microtubule dysfunction, their mechanisms of action are completely opposite.

The vinca alkaloids prevent the formation of the microtubules, whereas the taxanes prevent the microtubule disassembly.

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By doing so, they prevent the cancer cells from completing mitosis. Following this, cell cycle arrest occurs, which induces programmed cell death apoptosis.

They bind to specific sites on tubulin, inhibiting the assembly of tubulin into microtubules. The original vinca alkaloids are natural products that include vincristine and vinblastine.

They bind to the tubulin molecules in S-phase and prevent proper microtubule formation required for M-phase.

The Chemotherapy Source Book

The first drug of their class, paclitaxel , was originally extracted from the Pacific Yew tree, Taxus brevifolia. Now this drug and another in this class, docetaxel , are produced semi-synthetically from a chemical found in the bark of another Yew tree; Taxus baccata.

These drugs promote microtubule stability, preventing their disassembly. Paclitaxel prevents the cell cycle at the boundary of G2-M, whereas docetaxel exerts its effect during S-phase. Taxanes present difficulties in formulation as medicines because they are poorly soluble in water.

It has anti-microtubule activity, and its mechanism is similar to that of vinca alkaloids in that they bind to tubulin, inhibiting microtubule formation. Podophyllotoxin is used to produce two other drugs with different mechanisms of action: etoposide and teniposide. When the DNA double-strand helix is unwound, during DNA replication or transcription , for example, the adjacent unopened DNA winds tighter supercoils , like opening the middle of a twisted rope.

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The stress caused by this effect is in part aided by the topoisomerase enzymes. This allows the normal unwinding of DNA to occur during replication or transcription. Inhibition of topoisomerase I or II interferes with both of these processes.

This prevents DNA replication and transcription , causes DNA strand breaks, and leads to programmed cell death apoptosis. These agents include etoposide , doxorubicin , mitoxantrone and teniposide.

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The second group, catalytic inhibitors, are drugs that block the activity of topoisomerase II, and therefore prevent DNA synthesis and translation because the DNA cannot unwind properly. This group includes novobiocin , merbarone, and aclarubicin , which also have other significant mechanisms of action.

The common theme that they share in their chemotherapy indication is that they interrupt cell division. The most important subgroup is the anthracyclines and the bleomycins ; other prominent examples include mitomycin C , mitoxantrone , and actinomycin.

Other clinically used drugs in the anthracyline group are pirarubicin , aclarubicin , and mitoxantrone. The mechanisms of anthracyclines include DNA intercalation molecules insert between the two strands of DNA , generation of highly reactive free radicals that damage intercellular molecules and topoisomerase inhibition. This occurs when bleomycin binds to a metal ion , becomes chemically reduced and reacts with oxygen. The girl at left has a central venous catheter inserted in her neck.

The Chemotherapy Sourcebook

The girl at right has a peripheral venous catheter. The arm board stabilizes the arm during needle insertion.

Anti-cancer IV drip is seen at top right. Most chemotherapy is delivered intravenously , although a number of agents can be administered orally e.

There are many intravenous methods of drug delivery, known as vascular access devices. These include the winged infusion device , peripheral venous catheter , midline catheter, peripherally inserted central catheter PICC , central venous catheter and implantable port.

The devices have different applications regarding duration of chemotherapy treatment, method of delivery and types of chemotherapeutic agent. For continuous, frequent or prolonged intravenous chemotherapy administration, various systems may be surgically inserted into the vasculature to maintain access.

Drug Resistance. Principles of Chemotherapy. Clinical Trials. Hematopoietic Growth Factors. Principles of Biotherapy. Gonadal Complications and Teratogenicity of Cancer Therapy.

Perry's The Chemotherapy Source Book , 5/e

General Issues in Brain Tumor Chemotherapy. Chemotherapy of Head and Neck Cancer. Chemotherapy of Lung Cancer.

Gastrointestinal Cancer. Intraperitoneal Chemotherapy. Intraarterial Chemotherapy. Isolated Regional Therapy. Hematopoietic Stem Cell Transplantation. Dermatologic Toxicity. Ocular Side Effects of Chemotherapy.

Pulmonary Toxicity of Antineoplastic Therapy. Gastrointestinal Complications of Chemotherapy. Hepatotoxicity of Chemotherapeutic Agents. Renal and Electrolyte Abnormalities Due to Chemotherapy. ChemotherapyInduced Peripheral Neuropathy.

Vascular Toxicity of Antineoplastic Agents.The Siege of Ladysmith goes developed. Renal and Electrolyte Abnormalities Due to Chemotherapy. Anti-microtubule agents are plant -derived chemicals that block cell division by preventing microtubule function. Kenya, of map, has the Obama lasting quantum. Organized by site, this is the only book of its kind to focus strictly on the clinical practice of chemotherapy. They bind to specific sites on tubulin, inhibiting the assembly of tubulin into microtubules.

The nitrogen mustards most commonly alkylate the N7 nitrogen of guanine as shown here but other atoms can be alkylated.

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