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Khác biệt giữa bản sửa đổi của “Hóa trị liệu”

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Dòng 19:
{{Main|Lịch sử hóa trị liệu ung thư}}
[[File:Sidney Farber nci-vol-1926-300.jpg|thumb|150px|[[Sidney Farber]] được xem là cha đẻ của hóa trị ung thư hiện đại.]]
Thuốc đầu tiên được sử dụng điều trị ung thư vào đầu thế kỷ 20, mặc dù ban đầu nó không được sửu dụng cho mục đích này. [[khí mustard]] được sử dụng như là vũ khí [[hoá học]] trong [[thế chiến thứ I]] và được khám phá có khả năng chống [[tạo huyết]].<ref>{{cite journal |author=Krumbhaar EB |title=tole of the blood and the bone marrow in certain forms of gas poisoning |journal=JAMA |volume=72 |pages=39–41 |year=1919 |doi=10.1001/jama.1919.26110010018009f }}</ref> Một hợp chất cấu trúc tương tự là [[nitrogen mustards]] được nghiên cứu thêm trong [[chiến tranh thế giới thứ II]] tại đại học Yale University.<ref name="gilman">{{cite journal |author=Gilman A |title=The initial clinical trial of nitrogen mustard|journal=Am. J. Surg. |volume=105 |pages=574–8 |year=1963 |month=May |pmid=13947966 |doi=10.1016/0002-9610(63)90232-0|issue=5 }}</ref> chúng tiêu diệt các tế bào phát triển nhanh như tế bào bạch cầu ,do đó nó có tác dụng tương tự trên tế bào ung thư.Do đó , tháng 12 năm 1942, một số bệnh nhân mắc [[lymphomas]] (ung thư tế bào máu) đưa thuốc vào cơ thể qua tĩnh mạch.<ref name="gilman" /> Their improvement, although temporary, was remarkable.<ref>{{cite journal | author =Goodman LS, Wintrobe MM, Dameshek W, Goodman MJ, Gilman A, McLennan MT. | title = Nitrogen mustard therapy | journal = JAMA| volume = 132 | issue = 3 |pages = 126–132 | year = 1946 | doi = 10.1001/jama.1946.02870380008004 }}</ref><ref>{{cite journal | author =Goodman LS, Wintrobe MM, Dameshek W, Goodman MJ, Gilman A, McLennan MT. | title = Landmark article Sept. 21, 1946: Nitrogen mustard therapy. Use of methyl-bis(beta-chloroethyl)amine hydrochloride and tris(beta-chloroethyl)amine hydrochloride for Hodgkin's disease, lymphosarcoma, leukemia and certain allied and miscellaneous disorders. By Louis S. Goodman, Maxwell M. Wintrobe, William Dameshek, Morton J. Goodman, Alfred Gilman and Margaret T. McLennan| journal = JAMA|volume = 251 | issue = 17 | pages = 2255–61 | year = 1984 | pmid=6368885 | doi=10.1001/jama.251.17.2255}}</ref> Đồng thời, during a military operation in World War II, following a German [[Air raid on Bari|air raid]] on the Italian harbour of Bari, several hundred people were accidentally exposed to mustard gas, which had been transported there by the [[Allies of World War II|Allied forces]] to prepare for possible retaliation in the event of German use of chemical warfare. The survivors were later found to have very low white blood cell counts.<ref>Faguet, p. 71</ref> Sau chiến tranh thế giới thứ II was over and the reports declassified, the experiences converged and led researchers to look for other substances that might have similar effects against cancer. The first chemotherapy drug to be developed from this line of research was [[mustine]]. Since then, many other drugs have been developed to treat cancer, and drug development has exploded into a multibillion-dollar industry, although the principles and limitations of chemotherapy discovered by the early researchers still apply.<ref>{{cite journal | author =Joensuu H. | title = Systemic chemotherapy for cancer: from weapon to treatment| journal = Lancet Oncol.| volume = 9| issue = 3 | page = 304 | year = 2008| pmid=18308256 | doi = 10.1016/S1470-2045(08)70075-5}}</ref>
 
==Phân loại==
Dòng 27:
===Alkylating===
{{Main|Thuốc chống ung thư Alkylating}}
Alkylating là nhóm hóa trị liệu đầu tiên còn được sử dụng. Nguồn gốc là dẫn chất từ [[khí mustard]] sử dụng trong chiến tranh, hiện nay có nhiều loại alkylating được sử dụng.<ref name=Corrie/> They are so named because of their ability to [[alkylation|alkylate]] nhiều phân tử, bao gồm [[protein]], [[RNA]] và [[DNA]]. This ability to bind [[covalent bond|covalently]] to DNA via their [[alkyl group]] is the primary cause for their anti-cancer effects.<ref name=lind>{{cite journal|last=Lind M.J.|title=Principles of cytotoxic chemotherapy|journal=Medicine|year=2008|volume=36|issue=1|pages=19–23|doi=10.1016/j.mpmed.2007.10.003|first1=M.J.}}</ref> DNA is made of two strands and the molecules may either bind twice to one strand of DNA (intrastrand crosslink) or may bind once to both strands (interstrand crosslink). 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]].<ref name =Siddik>{{citechú bookthích sách|last=Siddik ZH|title=Mechanisms of Action of Cancer Chemotherapeutic Agents: DNA-Interactive Alkylating Agents and Antitumour Platinum-Based Drugs|year=2005|publisher=John Wiley & Sons, Ltd|doi=10.1002/0470025077.chap84b}}</ref><ref name="pmid19002790"/> Alkylating agents will work at any point in the cell cycle and thus are known as cell cycle-independent drugs. 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.<ref name="pmid14508075"/>
 
The subtypes of alkylating agents are the [[nitrogen mustard]]s, [[nitrosoureas]], [[tetrazine]]s, [[aziridine]]s, [[cisplatin]]s and derivatives, and non-classical alkylating agents. Nitrogen mustards include [[mechlorethamine]], [[cyclophosphamide]], [[melphalan]], [[chlorambucil]], [[ifosfamide]] and [[busulfan]]. Nitrosoureas include [[N-Nitroso-N-methylurea]] (MNU), [[carmustine]] (BCNU), [[lomustine]] (CCNU) and [[semustine]] (MeCCNU), [[fotemustine]] and [[streptozotocin]]. Tetrazines include [[dacarbazine]], [[mitozolomide]] and [[temozolomide]]. Aziridines include [[thiotepa]], [[mytomycin]] and diaziquone (AZQ). Cisplatin and derivatives include [[cisplatin]], [[carboplatin]] and [[oxaliplatin]].<ref name=lind/><ref name="pmid19002790">{{cite journal |author=Damia G, D'Incalci M |title=Mechanisms of resistance to alkylating agents |journal=Cytotechnology |volume=27 |issue=1–3 |pages=165–73 |year=1998 |month=September |pmid=19002790 |pmc=3449574 |doi=10.1023/A:1008060720608 |url=}}</ref> They impair cell function by forming [[covalent bond]]s with the [[amino group|amino]], [[carboxyl group|carboxyl]], [[sulfhydryl group|sulfhydryl]], and [[phosphate group]]s in biologically important molecules.<ref name=takimoto>Takimoto CH, Calvo E.[http://www.cancernetwork.com/cancer-management-11/chapter03/article/10165/1402628 "Principles of Oncologic Pharmacotherapy"] in Pazdur R, Wagman LD, Camphausen KA, Hoskins WJ (Eds) [http://www.cancernetwork.com/cancer-management-11/ Cancer Management: A Multidisciplinary Approach]. 11 ed. 2008.</ref> Non-classical alkylating agents include [[procarbazine]] and hexamethylmelamine.<ref name=lind/><ref name="pmid19002790"/>
Dòng 50:
===Topoisomerase inhibitors===
[[File:Topoisomerase Inhibitor.JPG|thumb|Topoisomerase I and II Inhibitors]]
[[Topoisomerase inhibitor]]s are drugs that affect the activity of two enzymes; [[topoisomerase I]] and [[topoisomerase II]]. When the DNA double stranded helix is unwound, during DNA replication or [[translation (biology)|translation]] for example, the adjacent unopened DNA winds tighter (supercoils), like opening the middle of a twisted rope. The stress caused by this effect is in part aided by the topoisomerase enzymes. They produce single or double strand breaks into DNA, reducing the tension in the DNA strand. This allows the normal unwinding of DNA to occur during [[DNA replication|replication]] or [[translation (biology)|translation]]. Inhibition of topoisomerase I or II interferes with both of these processes.<ref>{{citechú bookthích sách|last=Lodish H, Berk A, Zipursky SL, et al.|title=Molecular Cell Biology. 4th edition. The Role of Topoisomerases in DNA Replication|year=2000|publisher=New York: W. H. Freeman|url=http://www.ncbi.nlm.nih.gov/books/NBK21703/}}</ref><ref name="pmid12351817">{{cite journal |author=Goodsell DS |title=The molecular perspective: DNA topoisomerases |journal=Stem Cells |volume=20 |issue=5 |pages=470–1 |year=2002 |pmid=12351817 |doi=10.1634/stemcells.20-5-470 |url=}}</ref>
 
Two topoisomerase I inhibitors, [[irinotecan]] and [[topotecan]], are semi-synthetically derived from [[camptothecin]], which is obtained from the Chinese ornamental tree ''[[Camptotheca acuminata]]''.<ref name="pmid14508075"/> Drugs that target topoisomerase II can be divided into two groups. The topoisomerase II poisons cause increased levels enzymes bound to DNA. This prevents DNA replication and [[translation (biology)|translation]], causes DNA strand breaks, and leads to programmed cell death ([[apoptosis]]). These agents include [[etoposide]], [[doxorubicin]], [[mitoxantrone]] and [[teniposide]]. 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.<ref name="pmid19377506">{{cite journal |author=Nitiss JL |title=Targeting DNA topoisomerase II in cancer chemotherapy |journal=Nature Reviews Cancer |volume=9 |issue=5 |pages=338–50 |year=2009 |month=May |pmid=19377506 |pmc=2748742 |doi=10.1038/nrc2607 |url=}}</ref>
Dòng 57:
The cytotoxic antibiotics are a varied group of drugs that have various mechanisms of action. The group includes the [[anthracycline]]s and other drugs including [[actinomycin]], [[bleomycin]], [[plicamycin]] and [[mitomycin]]. [[Doxorubicin]] and [[daunorubicin]] were the first two anthracyclines, and were obtained from the [[bacterium]] ''[[Streptomyces peucetius]]''. Derivatives of these compounds include [[epirubicin]] and [[idarubicin]]. 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.<ref name="pmid15169927">{{cite journal |author=Minotti G, Menna P, Salvatorelli E, Cairo G, Gianni L |title=Anthracyclines: molecular advances and pharmacologic developments in antitumor activity and cardiotoxicity |journal=Pharmacol. Rev. |volume=56 |issue=2 |pages=185–229 |year=2004 |month=June |pmid=15169927 |doi=10.1124/pr.56.2.6 |url=}}</ref> Actinomycin is a complex molecule that intercalates DNA and prevents [[RNA synthesis]].<ref name="pmid2410919">{{cite journal |author=Sobell HM |title=Actinomycin and DNA transcription |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=82 |issue=16 |pages=5328–31 |year=1985 |month=August |pmid=2410919 |pmc=390561 |doi= 10.1073/pnas.82.16.5328|url=}}</ref> Bleomycin, a [[glycopeptide]] isolated from ''Streptomyces verticillus'', also intercalates DNA, but produces [[free radical]]s that damage DNA. This occurs when bleomycin binds to a [[metal ion]], becomes [[reduction (chemistry)|chemically reduced]] and reacts with [[oxygen]].<ref name="pmid1384141">{{cite journal |author=Dorr RT |title=Bleomycin pharmacology: mechanism of action and resistance, and clinical pharmacokinetics |journal=Semin. Oncol. |volume=19 |issue=2 Suppl 5 |pages=3–8 |year=1992 |month=April |pmid=1384141 |doi= |url=}}</ref><ref name="isbn0-470-09254-8 3">Airley, p. 87</ref> Mitomycin is a cytotoxic antibiotic with the ability to alkylate DNA.<ref name="pmid2131038">{{cite journal |author=Verweij J, Pinedo HM |title=Mitomycin C: mechanism of action, usefulness and limitations |journal=Anticancer Drugs |volume=1 |issue=1 |pages=5–13 |year=1990 |month=October |pmid=2131038 |doi= 10.1097/00001813-199010000-00002|url=}}</ref>
== Tham khảo ==
{{Reflisttham khảo|2}}
 
[[Thể loại:Thuốc chống ung thư]]
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