Update on cancer therapeutics最新文献_第10页

Plasma cell dyscrasias and leukemias 浆细胞异常和白血病

Update on cancer therapeutics Pub Date : 2006-12-01 DOI: 10.1016/j.uct.2006.05.007

Peter H. Wiernik

{"title":"Plasma cell dyscrasias and leukemias","authors":"Peter H. Wiernik","doi":"10.1016/j.uct.2006.05.007","DOIUrl":"10.1016/j.uct.2006.05.007","url":null,"abstract":"<div>There has been remarkable progress in our understanding of plasma cell dyscrasias and leukemias in recent years. New prognostic factors have come to light. Del(1)(p12) and t(4;14) confer poor prognoses on patients with myeloma. COX-2 positivity is associated with poorer progression-free and overall survival in myeloma patients and a role for COX-2 inhibitors in myeloma has been suggested. Thalidomide (400 mg/day) and dexamethasone (20 <!-->mg/m2 daily for 4 days) has emerged as first-line treatment for myelomas. Serious toxicities have been recognized, however. The thalidomide derivative, lenalidomide may be more active and less toxic than the parent compound and may replace it. Lenolidomide is also highly active against 5q-syndrome. Bortezomib is at least as active as thalidomide and less toxic, and the two drugs are not cross-resistant. Although marrow transplantation was the standard of care for newly diagnosed myeloma patients, recent prospective randomized studies cast doubt on its role.ZAP-70 and CD38 expression have major prognostic impact on outcome of chronic lymphocytic leukemia (CLL). The former may be a stronger predictor of the need for treatment than the presence of an unmutated IgV(H) gene. Although fludarabine is highly active in CLL, it may be associated with a higher number of second malignancies than are other treatments. Rituximab has major activity against CLL. However, at standard dose its effectiveness is limited by the fact that CD20 density is relatively low on CLL cells and circulating CD20 binds a significant fraction of administered drug. Either combining rituximab with other agents, or giving it in mega doses, which are safe and highly effective, can overcome these impediments.Imatinib has revolutionized the treatment of chronic phase chronic myelocytic leukemia (CML) and markedly decreased the number of allogeneic bone marrow transplants done for this neoplasm. However, the development of rapid resistance to the agent in blast crisis of CML or Philadelphia chromosome-positive acute lymphocytic leukemia gives the agent only a minor role in those diseases. More effective tyrosine kinase inhibitors currently under development may prove to be more useful in acute leukemias with the Philadelphia chromosome.Clofarabine is a successful new drug for acute myeloid leukemias of childhood and juvenile myelomonocytic leukemia. Drugs such as gemtuzumab ozogamicin, FLT3 inhibitors and farnesyl transferase inhibitors have been disappointing in acute leukemia. Histone deacetylase inhibition, especially in combination with proteasome inhibition, may be effective acute leukemia treatment.</","PeriodicalId":87487,"journal":{"name":"Update on cancer therapeutics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2006-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.uct.2006.05.007","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"55737633","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

Contents of Volume 1 第一卷内容

Update on cancer therapeutics Pub Date : 2006-12-01 DOI: 10.1016/S1872-115X(06)00077-6

引用次数: 0

Recent advances in the use of antigen-specific T cells for the treatment of cancer 利用抗原特异性T细胞治疗癌症的最新进展

Update on cancer therapeutics Pub Date : 2006-09-01 DOI: 10.1016/j.uct.2006.06.002

Cassian Yee , Herschel Wallen , Naomi Hunder , John A. Thompson , David Byrd , J. Zachary Reilly , Deborah Hendricks , Karla Kenyon , Lisa Schirmer

引用次数: 3

Soft tissue sarcoma 软组织肉瘤

Update on cancer therapeutics Pub Date : 2006-09-01 DOI: 10.1007/978-3-662-48590-3_20

M. Austin, R. Andrassy

引用次数: 5

NSC-Numbers

Update on cancer therapeutics Pub Date : 2006-09-01 DOI: 10.1016/S1872-115X(06)00064-8

引用次数: 0

Abbreviations of drugs 药物简写

Update on cancer therapeutics Pub Date : 2006-09-01 DOI: 10.1016/S1872-115X(06)00061-2

引用次数: 0

Biological Abbreviations 生物的缩写

Update on cancer therapeutics Pub Date : 2006-09-01 DOI: 10.1016/S1872-115X(06)00063-6

引用次数: 0

Copyright text 版权文本

Update on cancer therapeutics Pub Date : 2006-09-01 DOI: 10.1016/S1872-115X(06)00060-0

引用次数: 0

Biology and therapy of solid tumors in childhood 儿童实体瘤的生物学和治疗

Update on cancer therapeutics Pub Date : 2006-09-01 DOI: 10.1016/j.uct.2006.05.004

Henk van den Berg

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引用次数: 4

Cyclin dependent kinases as targets for cancer therapy 细胞周期蛋白依赖激酶作为癌症治疗的靶点

Update on cancer therapeutics Pub Date : 2006-09-01 DOI: 10.1016/j.uct.2006.08.001

Manish A. Shah, Gary K. Schwartz

{"title":"Cyclin dependent kinases as targets for cancer therapy","authors":"Manish A. Shah, Gary K. Schwartz","doi":"10.1016/j.uct.2006.08.001","DOIUrl":"10.1016/j.uct.2006.08.001","url":null,"abstract":"<div>The cell cycle represents a series of tightly integrated events that allow the cell to grow and proliferate. Critical parts of the cell cycle machinery are the cyclin dependent kinases (CDKs) which, when activated, provide a means for the cell to move from one phase of the cell cycle to the next. The CDKs are positively regulated by cyclins and negatively regulated by naturally occurring cyclin dependent kinase inhibitors (CDKIs). Cancer represents a dysregulation of the cell cycle such that cells that over-express cyclins or do not express the CDKIs continue to undergo unregulated cell growth. The cell cycle also serves to protect the cell from DNA damage. Thus, cell cycle arrest represents a survival mechanism that provides the tumor cell the opportunity to repair damaged DNA. Abrogation of cell cycle checkpoints before DNA repair is complete can activate the apoptotic cascade leading to cell death. Over the past several years a series of targeted agents have been developed that directly inhibit the CDKs, inhibit unrestricted cell growth, and induce a growth arrest. In addition, there are now agents that abrogate the cell cycle checkpoints at critical time points and make the tumor cell susceptible to apoptosis. Many of these agents are now in clinical trials and represent a new direction in cancer treatment. An understanding of the cell cycle is critical to learning how best to clinically develop these agents, both when administered as single agents or in combination with chemotherapy.</div>","PeriodicalId":87487,"journal":{"name":"Update on cancer therapeutics","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2006-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.uct.2006.08.001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"55737894","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 52