细胞凋亡与肿瘤治疗

细胞凋亡与许多疾病特别是肿瘤的发生发展有关，许多癌基因与抑癌基因参与细胞凋亡过程。对细胞凋亡以及在肿瘤治疗中的有关系进行了综述。     

卵巢环状小管性索瘤的临床病理分析

对38例（本院2周及国内文献36例）卵巢太小管性索瘤从临床、病理和激素分泌等方面进行分析，年龄4－60岁，平均23岁。主要临床表现为：内分泌功能紊乱（性早熟，月经不规则及绝经后出血）和腹部肿块，仅1例伴有口唇粘膜黑色素沉着－－胃肠道息肉综合征；特征性组织学结构为：单层或复层环状小管，管周有基底膜样结构。此病属于低度恶性肿瘤，并对此病的组织来源进行了讨论。     

中药对肿瘤组织血管生成的影响

恶性肿瘤的无限制侵袭性生长及其转移依赖于血管生成（angiogenesis)抑制血管生成是不同于常规的肿瘤治疗新策略，肿瘤血管生成的过程是个多步骤过程，目前已进入临床的肿瘤血管生成抑制剂有数十种，许多有抗肿瘤活性的中药的有效成分，如：人参皂苷Rg^3、鲨鱼软骨生成抑因子（SCAIF）等可抑制肿瘤血管生成。     

蝙蝠葛碱增强博莱霉素A5对肿瘤细胞的毒性

应用增殖抑制方法发现,无生长抑制作用的0.5mg ·L~(-1)的蝙蝠葛碱(Dau)使博莱霉素A_5单独对小鼠肉瘤S-180V细胞作用的I_(C50)值从2.1mg·L~(-1)降低到1.3mg·L~(-1),无抑制作用的1 mg·L~(-1) Dau使博莱霉素A_5单独对人喉癌HEP2细胞作用的I_(C50) 值从0.33 mg·L~(-1)降低到0.1 mg·L~(-1).克隆形成法证明:无细胞毒性的10 mg·L~(-1)的Dau明显增强博莱霉素A_5对HEP2细胞毒性.TFP法证实,有一定生长抑制作用的Dau对HEP2细胞内活化钙调素有影响.结果表明:蝙蝠葛碱有一定的增强博莱霉素A_5对肿瘤细胞的毒性.     

Immunotherapy against antigenic tumors: a game with a lot of players

Our understanding of how immune responses are generated and regulated drives the design of possible immunotherapies for cancer patients. For that reason, we first describe briefly the actual immunological theories and their common perspectives about cancer vaccine development. Second, we describe cancer vaccines that are able to induce tumor-specific immune responses in cancer patients. However, these responses are not always followed by tumor rejection. At the end of the review, we discuss two possible reasons that might explain this dichotomy of cancer immunology. First, the immune response generated, although detectable, may not be quantitatively sufficient to reject the tumor. Second, the tumor microenvironment may modulate tumor cell susceptibility to the systemic immune response induced by the immunization. Finally, we discuss what, in our opinion, might be the best way to improve cancer vaccine strategies and how the relationship between the tumor and its surroundings might be studied in more details. Received 21 June 2001; received after revision 15 August 2001; accepted 15 August 2001     

Initiation of cancer and other diseases by catechol ortho-quinones: a unifying mechanism

Exposure to estrogens is a risk factor for breast and other human cancers. Initiation of breast, prostate and other cancers has been hypothesized to result from reaction of specific estrogen metabolites, catechol estrogen-3,4-quinones, with DNA to form depurinating adducts at the N-7 of guanine and N-3 of adenine by 1,4-Michael addition. The catechol of the carcinogenic synthetic estrogen hexestrol, a hydrogenated derivative of diethylstilbestrol, is metabolized to its quinone, which reacts with DNA to form depurinating adducts at the N-7 of guanine and N-3 of adenine. The catecholamine dopamine and the metabolite catechol (1,2-dihydroxybenzene) of the leukemogen benzene can also be oxidized to their quinones, which react with DNA to form predominantly analogous depurinating adducts. Apurinic sites formed by depurinating adducts are converted into tumor-initiating mutations by error-prone repair. These mutations could initiate cancer by estrogens and benzene, and Parkinson's disease by the neurotransmitter dopamine. These data suggest a unifying molecular mechanism of initiation for many cancers and neurodegenerative diseases and lay the groundwork for designing strategies to assess risk and prevent these diseases. Received 4 September 2001; received after revision 28 November 2001; accepted 2 December 2001     

Role of FGF-2／FGFR signaling pathway in cancer and its signification in breast cancer

Fibroblast growth factor-2 (FGF-2) is a member of a large family of proteins that bind heparin and heparan sulfate and modulate the function of a wide range of cell types. It has been proved that FGF-2 stimulates the growth and development of new blood vessels (angiogenesis) that contribute to the pathogenesis of several diseases (i.e. cancer, atherosclerosis). However, many of the biological activities of FGF-2 have been found to depend on its receptor抯 intrinsic tyrosine kinase activity and second messengers such as the mitogen activated protein kinases. This review will focus on the mechanism of FGF-2/FGFR induced signaling pathway in tumor and human breast cancer.     

Viewpoints on the proinflammation state of leukemia

Proinflammation represents a pathophysiological state on the early stage of a number of diseases, especially the infectious and immunological ones. In recent years, proinflammation has attracted much attention, and the term 損roinflammation factors?appears frequently in the literature. While investigating leukemia and leukemic cells from the angle of 損roinflammation state? we got some intriguing findings, e.g. we detected the significantly elevated expression of proinflammation factor IL-18 in patients with acute myeloid leukemia (AML), which could up-regulate matrix metalloproteinases (MMP) and specific tissue inhibitors (TIMPs). The increased MMP may play a role in the aggressiveness of myeloid leukemic cells, and be associated with a poor prognosis. This phenomenon reflects an ignored aspect of leukemia. Investigations from the angle of 損roinflammation state?have broaden the fields of tumor and leukemia study.     

The Ras family of GTPases in cancer cell invasion

The ability of tumoral cells to invade surrounding tissues is a prerequisite for metastasis. This is the most life-threatening event of tumor progression, and so research is intensely focused on elucidating the mechanisms responsible for invasion and metastasis. The Ras superfamily of GTPases comprises several subfamilies of small GTP-binding proteins whose functions include the control of proliferation, differentiation, and apoptosis, as well as cytoskeleton organization. The development of metastasis is a multistep process that requires coordinated activation of proliferation, motility, changes in normal cell-to-cell and cell-to-substrate contacts, degradation of extracellular matrix, inhibition of apoptosis, and adaptation to an inappropriate tissue environment. Several members of the Ras superfamily of proteins have been implicated in these processes. The present review summarizes the current knowledge in this field.     

海萝多糖抗突变与抗肿瘤作用的研究

用海萝多糖粗提物灌胃昆明种小鼠,观察海萝多糖粗提物对环磷酰胺(CP)诱发小鼠染色体突变和精子畸变的抑制作用和对荷S180肉瘤小鼠的抑瘤作用.实验结果显示:海萝多糖粗提物可使环磷酰胺诱发的小鼠骨髓嗜多染红细胞(PCE)微核率和精子畸形率明显降低,具有显著的抗突变作用,且呈现一定的剂量效应关系;海萝粗多糖对S180肉瘤也有明显的抑制作用,并有一定的剂量关系.结果表明,海萝多糖粗提物有明显的抗突变、抗肿瘤作用.