Cancer surveys最新文献_第5页

Antisense therapy for B cell lymphomas. B细胞淋巴瘤的反义治疗。

Cancer surveys Pub Date : 1997-01-01

F E Cotter

引用次数: 0

Apoptosis and cancer mechanisms. 细胞凋亡和癌症机制。

Cancer surveys Pub Date : 1997-01-01

H Pan, C Yin, T Van Dyke

引用次数: 0

The DNA replication licensing system. DNA复制许可制度。

Cancer surveys Pub Date : 1997-01-01

P Thömmes, J J Blow

{"title":"The DNA replication licensing system.","authors":"P Thömmes, J J Blow","doi":"","DOIUrl":"","url":null,"abstract":"The Xenopus cell free system has proved a good model system to study in vitro DNA replication and the mechanism preventing rereplication in a single cell cycle. Studies using this system resulted in the development of a model postulating the existence of a replication licensing factor (RLF), which binds to the chromatin before the G1-S transition of the cell cycle and is displaced during replication. The nuclear envelope prevents rebinding of RLF and hence relicensing. Nuclear envelope breakdown at mitosis is required to allow another round of replication. Protein kinase inhibitors block licensing factor activity and arrest Xenopus extracts in a G2 like state. These kinase inhibitors have allowed the development of an in vitro assay leading to the biochemical purification of RLF components. RLF can be separated into RLF-B and RLF-M, the latter consisting of several members of the MCM/P1 class of replication proteins. In Xenopus as well as in many other eukaryotes, the binding of MCM/P1 proteins to chromatin before S phase is essential for replication to occur. The proteins are then displaced as replication proceeds. These changes in subnuclear distribution are reflected by changes in the phosphorylation status. MCM/P1 proteins do not bind to the DNA on their own but need RLF-B to be loaded onto the chromatin. Their cycling behaviour is reminiscent of the existence of a prereplicative complex at the origins of replication in yeast, suggesting that the licensing mechanism is ubiquitous in eukaryotes.","PeriodicalId":77062,"journal":{"name":"Cancer surveys","volume":"29 ","pages":"75-90"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20271511","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: 0

The anaphase promoting complex. 后期促进复合体。

Cancer surveys Pub Date : 1997-01-01

A M Page, P Hieter

{"title":"The anaphase promoting complex.","authors":"A M Page, P Hieter","doi":"","DOIUrl":"","url":null,"abstract":"We have proposed a preliminary model of how the anaphase promoting complex functions throughout the cell cycle, but despite the flurry of recent publications characterizing the APC--its components, regulation and substrate specificity--many fundamental questions remain to be answered. Firstly, the remaining components of the APC need to be identified and characterized. We do not know if all cyclosome components are conserved in all eukaryotes, or if higher eukaryotes, having a more complicated cell cycle machinery, maintain additional subunits for more sophisticated functional and regulatory control. In addition, we need to determine the identity of the various kinases and phosphatases that regulate the APC itself. The biochemistry of individual APC components is also a mystery, and a specific biochemical function has not been assigned to any known members of the complex. It is not at all clear which subunit(s) of the complex actually recognizes the E2 enzyme and which subunit(s) recognizes the cyclin destruction box. It is likely that many cyclosome substrates remain to be identified, and it will be interesting to determine whether all cyclosome substrates require a destruction box for their degradation or whether the APC recognizes other determinants of protein instability. Finally, we assume that the APC degrades mitotic cyclins in all proliferating cells, but whether it degrades unique cell cycle related substrates in specific tissues is unclear. Furthermore, nothing is known about APC function during meiosis, or whether the APC degrades other substrates that are not related to the cell cycle. This is an exciting and rapidly developing field in the exciting world of cell cycle biology. We expect that new findings will surely reveal many interesting surprises about this essential protein complex.","PeriodicalId":77062,"journal":{"name":"Cancer surveys","volume":"29 ","pages":"133-50"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20271514","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: 0

Lymphomatoid granulomatosis: pathogenesis, pathology and clinical implications. 类淋巴瘤肉芽肿病:发病机制、病理及临床意义。

Cancer surveys Pub Date : 1997-01-01

E S Jaffe, W H Wilson

{"title":"Lymphomatoid granulomatosis: pathogenesis, pathology and clinical implications.","authors":"E S Jaffe, W H Wilson","doi":"","DOIUrl":"","url":null,"abstract":"Lymphomatoid granulomatosis (LG) exhibits many similarities both clinically and pathologically to angiocentric T/NK cell lymphoma and was until recently considered to be part of the same disease spectrum. However, recent data indicate that LG is an EBV positive B cell proliferation associated with an exuberant T cell reaction. LG presents in extranodal sites, most commonly the lung (Katzenstein and Peiper, 1990). Other frequent sites of involvement include kidney, skin, central nervous system and liver. The pattern of necrosis in both LG and T/NK cell lymphoma is very similar, emphasizing the probable importance of EBV in mediating the vascular damage. Recent studies implicate the chemokines IP-10 and Mig in the pathogenesis of the vascular damage. Although the predominant infiltrating cells are T cells, the T cell receptor genes are not clonally rearranged. However, by VDJ polymerase chain reaction, approximately 60% of cases contain clonal rearrangements. EBV sequences can be localized to B cells and are clonal in most cases. Most patients with LG when carefully evaluated clinically have defects in cytotoxic T cell function and reduced levels of CD8+ T cells. LG is also common in many immunodeficiency states, such as AIDS, Wiskott-Aldrich syndrome and post-transplantation immunodeficiency. Thus, in many respects, LG resembles an EBV driven lymphoproliferative disorder. Some cases of LG regress spontaneously, but most patients require therapy. Treatment approaches have included cyclophosphamide and prednisone, aggressive combination chemotherapy and interferon alpha 2b, because of its antiviral, antiproliferative and immunomodulatory effects.","PeriodicalId":77062,"journal":{"name":"Cancer surveys","volume":"30 ","pages":"233-48"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20470295","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: 0

Lymphoma. Introduction. 淋巴瘤。介绍。

Cancer surveys Pub Date : 1997-01-01

A C Wotherspoon

引用次数: 0

Telomerase, checkpoints and cancer. 端粒酶，检查点和癌症。

Cancer surveys Pub Date : 1997-01-01

C B Harley, S W Sherwood

{"title":"Telomerase, checkpoints and cancer.","authors":"C B Harley, S W Sherwood","doi":"","DOIUrl":"","url":null,"abstract":"Telomere dynamics and changes in telomerase activity are consistent elements of cellular alterations associated with changes in proliferative state. In particular, the highly specific correlations and early causal relationships between telomere loss in the absence of telomerase activity and replicative senescence or crisis, on the one hand, and telomerase reactivation and cell immortality, on the other, point to a new and important paradigm in the complementary fields of ageing and cancer. Although the signalling pathways between telomeres and transcriptional and cell cycle machinery remain undefined, recently described homologies between telomeric proteins and lipid/protein kinase activities important in chromosome stability provide evidence for the existence of pathways transducing signals originating in chromosome structure to cell cycle regulatory processes. Similarities between cell cycle arrest at senescence and the response of mortal cells to DNA/oxidative damage suggest overlap in the signal transduction mechanisms culminating in irreversible and stable cell cycle arrest. The feasibility of targeting telomeres/telomerase as a strategy for antiproliferative therapeutics has been shown in studies in yeast, in which mutations in specific telomere associated genes result in delayed cell death. Similarly, antisense oligonucleotide inhibition of telomerase activity in human tumour cells (HeLa) results in delayed cell death. The mechanism of cell death and possible escape from this fate require further study. In human cells, however, it would seem reasonable to predict that in these circumstances, apoptosis is induced in the vast majority of cells either directly in response to a DNA damage signal arising from critically shortened telomeres or as a secondary consequence of genetic instability.","PeriodicalId":77062,"journal":{"name":"Cancer surveys","volume":"29 ","pages":"263-84"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20271395","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: 0

S phase damage sensing checkpoints in mammalian cells. 哺乳动物细胞S期损伤传感检查点。

Cancer surveys Pub Date : 1997-01-01

J M Larner, H Lee, J L Hamlin

{"title":"S phase damage sensing checkpoints in mammalian cells.","authors":"J M Larner, H Lee, J L Hamlin","doi":"","DOIUrl":"","url":null,"abstract":"Mammalian cells have evolved multiple responses for dealing with DNA damage. One response is to acutely downregulate DNA synthesis at the initiation step. Essentially nothing is known about the initial signal that activates this SDS pathway or the macromolecules involved in transducing the signal into the final inhibitory step at origins. Determining whether any radiation induced changes in known proteins involved in cell cycle regulation or in other signal transduction pathways are primary or secondary responses to DNA damage constitutes a major challenge to identifying members of the pathway. It may turn out to be easier to identify the final mediator in the pathway, namely the protein(s) whose interaction with origins is ultimately affected by radiation. Hopefully, mutations in SDS genes in genetically tractable systems such as S cerevisiae or Schizosaccharomyces pombe will allow the identification of homologous genes in mammals. Most tumour cells are TP53 negative, and yet it is not clear that TP53 status influences radiation sensitivity. The SDS pathway may therefore represent an important protective mechanism that stands in the way of effective tumour cell killing by radiation therapy. It is hoped that an understanding of this pathway will provide opportunities for developing novel antineoplastic targets and/or radiation sensitizers.","PeriodicalId":77062,"journal":{"name":"Cancer surveys","volume":"29 ","pages":"25-45"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20271509","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: 0

Molecular single cell studies of normal and transformed lymphocytes. 正常和转化淋巴细胞的分子单细胞研究。

Cancer surveys Pub Date : 1997-01-01

R Küppers, A Roers, H Kanzler

引用次数: 0

Clonality in lymphocyte predominance Hodgkin's disease. 淋巴细胞显性霍奇金病的克隆性。

Cancer surveys Pub Date : 1997-01-01

L M Weiss, D A Arber, K L Chang

{"title":"Clonality in lymphocyte predominance Hodgkin's disease.","authors":"L M Weiss, D A Arber, K L Chang","doi":"","DOIUrl":"","url":null,"abstract":"Abundant evidence has led to the clinical and biological separation of lymphocyte predominance from other types of Hodgkin's disease. However, it is still not clear whether lymphocyte predominance represents a polyclonal reactive lesion (possibly representing an abnormal immune disorder), a polyclonal or oligoclonal preneoplastic disorder or a monoclonal neoplastic disorder. The clinical and histological features are distinctive, but they do not provide clear indications of the nature of lymphocyte predominance. Some immunohistochemical and in situ hybridization studies have shown monotypic light chain restriction in the L&H cells, almost always of kappa type, implying a monoclonal process. Southern blotting studies are of limited utility, given their relatively low sensitivity and the rarity of L&H cells within involved tissues. Polymerase chain reaction studies have yielded conflicting results. Some, but not all, have demonstrated monoclonal populations in tissue extracts. Single cell PCR studies have generally not found monoclonal populations, although one case stands as an exception. Cases of large cell lymphoma complicating lymphocyte predominance have been monoclonal by polymerase chain reaction and clonospecific primers derived from these clones have demonstrated similar populations in the corresponding lymphocyte predominance tissues in some, but not all, studies.","PeriodicalId":77062,"journal":{"name":"Cancer surveys","volume":"30 ","pages":"125-41"},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20469767","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: 0