视黄酸对肿瘤血管形成影响的研究进展

血管形成是肿瘤增殖及转移所依赖的基础。多种因素影响肿瘤血管形成，视黄酸在此方面有其独特的作用及机制，在多种实验模型中，视典酸均表明有明显的抑制肿瘤血管形成的作用，其作用机制可能与影响细胞因子活性、抑制内皮细胞增殖及迁移、调节细胞外基质成分及诱导相应抑制因子有关。     

视黄酸与肿瘤转移

癌转移是肿瘤细胞从原发部位进入体液循环,最后穿过管壁在靶器官定位,并在该处增殖成转移癌.已经发现癌转移是一个多步骤、多阶段、多基因的复杂过程,是癌症患者死亡的主要原因.因此如何控制癌转移是决定预后的关键因素.对癌转移机制研究也成为当今国内外的研究热点之一.     

抑制肿瘤血管形成的研究进展

抑制肿瘤血管形成的研究进展陶厚权（综述）王瑞年林言箴（审校）关键词血管形成肿瘤中图号Ｒ７３５．２１９７１年，Ｆｏｌｋｍａｎ首先发现了肿瘤血管形成因子（Ｔｕｍｏｒａｎｇｉｏｇｅｎｅｓｉｓｆａｃｔｏｒ，ＴＡＦ），并据此提出抗血管形成可作为肿瘤治疗的一个途...     

肿瘤血管形成因子的研究进展

肿瘤血管形成因子的研究进展王贵齐（综述）徐光炜（审阅血管形成即新的毛细血管芽发展过程是胚胎发育、肾脏、脑及其它器官血管化所必需的生理过程。成年人女性经期及伤口愈合时所发生的血管形成是短暂的且受机体严格的调节。与之相反，病理性血管形成则是以内皮细胞的持...     

肿瘤血管形成调节剂

血管形成即一个微血管床的发展是许多重要的生理过程所必需的，正常的生长与分化等过程均伴有血管形成。在某些病理性疾病中常发生无控制的血管形成，如实体瘤等组织中血管明显增殖，肿瘤细胞分泌血管形成调节因子，这些因子能够诱导宿毛细胞管新生并长入肿瘤组织。     

肿瘤血管形成及其抑制因子研究进展

血管新生是从已形成的血管网络芽生出新的血管.肿瘤的生长、浸润和转移是一个依赖于血管的过程抑制新生血管的生成可使肿瘤细胞进入休眠状态并诱导死亡.     

肿瘤血管形成诱导和抑制因子研究进展

1肿瘤发生发展与血管形成肿瘤发生后生长过程大致可分为以下几个时期：第一时期为无血管期或称为血管前期。该期的肿瘤细胞主要靠弥散获得营养c如动物和人体内原位癌,浅表的皮肤黑色素瘤以及腹膜面小肿瘤,早期移植性小瘤灶等。第二时期为血管期也称为血管浸润性生长期。该时期瘤组织有新血管形成,这些血管不断地为痛组织提供营养和排除代谢产物,使肿瘤得以迅速增长。第三时期为转移期。当肿瘤生长到一定程度就向周围组织侵袭及发生转移,但转移灶形成过程,也会出现第一、二期的发展阶段。1．1肿瘤血管形成的实验研究一般利用不同移植物…     

三氧化二砷抑制肿瘤血管形成的研究进展

三氧化二砷(As2O3)是一种致癌剂,其适当剂量对肿瘤疗效明显.近年来,越来越多的证据表明三氧化二砷可通过各种机制抑制新生血管形成,使肿瘤细胞生长受到抑制,渐被广泛用于治疗血液系统肿瘤和实体瘤.现就As2O3抑制肿瘤新生血管形成的研究进展作一综述.     

基质金属蛋白酶与肿瘤血管形成关系的研究进展

基质金属蛋白酶(MMP)家族的主要作用是降解细胞外基质，促进肿瘤侵袭和转移。近来研究发现MMP除了降解基质外，还与肿瘤血管形成有密切关系，现对此研究现状作一综述。     

Combination of phenylbutyrate and 13-cis retinoic acid inhibits prostate tumor growth and angiogenesis

Differentiation-inducing agents, such as retinoids and short-chain fatty acids, have an inhibitory effect on tumor cell proliferation and tumor growth in preclinical studies. Clinical trials involving these compounds as single agents have been suboptimal in terms of clinical benefit. Our study evaluated the combination of phenylbutyrate (PB) and 13-cis retinoic acid (CRA) as a differentiation and antiangiogenesis strategy for prostate cancer. On the basis of previous evidence, common signal transduction pathways and possible modulation of retinoid receptors and retinoid response elements by PB could be responsible for such activities. We assessed the effect of the combination of PB and CRA on human and rodent prostate carcinoma cell lines. The combination of PB and CRA inhibited cell proliferation and increased apoptosis in vitro in an additive fashion as compared with single agents (P < 0.014). Prostate tumor cells treated with both PB and CRA revealed an increased expression of a subtype of retinoic acid receptor (retinoic acid receptor-beta), suggesting a molecular mechanism for the biological additive effect. The combination of PB and CRA also inhibited prostate tumor growth in vivo (up to 82-92%) as compared with single agents (P < 0.025). Histological examination of tumor xenografts revealed decreased in vivo tumor cell proliferation, an increased apoptosis rate, and a reduced microvessel density in the animals treated with combined drugs, suggesting an antiangiogenesis effect of this combination. Thus, endothelial cell treatment with both PB and CRA resulted in reduced in vitro cell proliferation. In vivo testing using the Matrigel angiogenesis assay showed an additive inhibitory effect in the animals treated with a combination of PB + CRA (P < 0.004 versus single agents). In summary, this study showed an additive inhibitory effect of combination of differentiation agents PB and CRA on prostate tumor growth through a direct effect on both tumor and endothelial cells.     

Endoglin与肿瘤血管生成及在肿瘤研究中的意义

Endoglin是内皮细胞表面与增殖相关的膜抗原,主要表达于肿瘤新生血管内皮细胞,可作为肿瘤诊断、转移、复发和判断预后的早期指标,是治疗人体恶性肿瘤的理想的分子靶位.     

Dominant negative retinoic acid receptor initiates tumor formation in mice

Background  

Retinoic acid suppresses cell growth and promotes cell differentiation, and pharmacological retinoic acid receptor (RAR) activation is anti-tumorigenic. This begs the question of whether chronic physiological RAR activation by endogenous retinoids is likewise anti-tumorigenic.     

Growth-promoting effect of retinoic acid in transplantable pituitary tumor of rat

MtT/F84 grew well in Fischer rats (F344), but tumor growth was promoted in hyperestrogenized rats. Effects of dietary retinoic acid (RA) on tumor growth, estrogen receptor (ER) and serum growth hormone (GH) level were examined. Tumor latency became shortened, and tumor take and weight were promoted by all-trans RA at dosages of 50 and 200 mg/kg basal diet, but not dose-dependently. ER level was elevated in tumor of RA-treated rats, whereas the retinoic acid-binding protein level remained unchanged. RA also elevated incorporation of 5-bromo-2'-deoxyuridine, a thymidine analogue, into DNA of tumor cells. Average serum GH level was increased in tumor-bearing rats treated with RA and was well correlated with tumor weight. RA may directly affect ER level and enhance estrogenic action, resulting in promotion of tumor growth, or it may act independently for tumor growth and elevation of serum GH level.     

放疗对荷瘤鼠肿瘤血管生成的抑制作用

目的:观察荷瘤鼠肿瘤放疗后肿瘤组织内微血管密度(microvesseldensity,MVD)及肿瘤细胞血管内皮生长因子(vascularendothelialgrowthfactor,VEGF)表达阳性率的变化,分析放疗对肿瘤血管生成的抑制作用。方法:24只荷B16黑色素瘤的C57BL/6小鼠随机分为对照组和放疗组(30Gy/10次/10天),放疗结束后第5天处死小鼠,免疫组化法测定肿瘤组织内MVD值和肿瘤细胞VEGF表达阳性率,比较两组间的差异。结果:两组肿瘤组织内MVD值分别为52.7±9.1和26.4±5.5(t=8.52,P<0.001),两组肿瘤细胞VEGF表达阳性率分别为31.4%±6.5%和10.6%±3.0%(对照组VS放疗组)(t=10.1,P<0.001),均有明显显著性差异。结论:放疗可明显抑制荷瘤鼠肿瘤的血管生成过程。     

The role of integrins in tumor angiogenesis

Integrins are cell adhesion molecules that play an important role in the regulation of angiogenesis. In this overview, the vascular integrins and their mechanisms of action are outlined. Integrins have been evaluated in preclinical and clinical studies for the treatment of cancer and as diagnostic markers of angiogenesis. Furthermore, integrins are the basis for targeted therapy for solid tumors and novel imaging techniques to assess the angiogenic response of tumors.     

The effects of retinoic acid and a tumor promoter, 12-O-tetra-decanoylphorbol-13-acetate, on lymphocyte proliferation

The tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA)inhibits DNA synthesis in allogenic, mixed cultures of bovinelymphocytes. Retinoic acid, an antagonist of TPA in in vivoskin promotion, was tested for its ability to counteract theeffect of TPA on lymphocyte proliferation. Retinoic acid orrelated compounds, retinol or retinol actetate, did not reverseor prevent the inhibitory effect of TPA. Instead retinoic acidalso inhibited DNA synthesis in mixed lymphocyte cultures. Onthe average, about 8 µM retinoic acid inhibited the mixedlymphocyte response by 50%. The mitogenic response of lymphocytesto phytohemagglutinin (PHA) was also inhibited by retinoic acid.The degree of inhibition depended both on the concentrationof PHA and of retinoic acid. Therefore, in regard to bovinelymphocytes, retinoic acid depresses DNA synthesis in both allogenicand lectin stimulated responses. Such suppression should betaken into account in the use of retinoic acid in chemotherapy.     

肿瘤血管形成的转基因鼠模型

RIP-Tag转基因鼠、BPV1.69转基因鼠以及K14-HPV16转基因鼠,是目前用于肿瘤血管形成研究常见的3种动物模型.在实体瘤形成前各个阶段的组织学、细胞生物学、分子生物学变化均可检测到,且能够反映VEGF、FGF等血管形成刺激因子的相应变化.已开始用于验证AGM1470(TNP470)、α干扰素、米诺环素等抗肿瘤血管形成药物前临床试验,结果满意,具有良好的应用价值与前景.     

N-乙酰氨基葡萄糖转移酶V对肿瘤血管生成的影响

N-乙酰氨基葡萄糖转移酶V(N-acetylglucosaminyltransferase-V,GnT-V)是与肿瘤相关的一种重要的糖基化酶.而肿瘤的发生、发展、转移与新生血管有着密切的联系.研究发现GnT-V与肿瘤血管生成有关,其主要通过血管生成因子的异常糖基化及分泌型GnT-V调节肿瘤血管生成.