北京市6种癌症住院费用回顾性分析

目的 研究北京市2009—2012年6种癌症患者的一般情况、诊疗费用及费用影响因素,为将来开展更大范围的癌症筛查和早诊早治项目的卫生决策提供依据。方法 运用描述性统计分析对患者的一般人口特征和诊疗费用等进行归纳;在此基础上,运用多元线性回归模型对各癌种次均住院费用的影响因素进行分析。结果 （1）北京市2009—2011年癌症病例的次均住院费用分别为24 982元、23 501元、24 528元;（2）6种恶性肿瘤次均住院费用的主要影响因素有住院日、医院类型、治疗方案等。结论 加快恶性肿瘤防治工作、缩短住院时间是控制住院费用的有效手段。     

恶性肿瘤化疗所致院内感染31例分析

目的探讨恶性肿瘤患者化疗后发生院内感染的相关因素及防治措施。方法对31例恶性肿瘤患者化疗后发生的院内感染作回顾性分析。结果恶性肿瘤患者化疗后发生院内感染与中性粒细胞减少程度及持续时间有关,感染的部位以呼吸道为主,主要采用粒细胞集落刺激因子（G-CSF）及抗生素治疗。结论恶性肿瘤患者化疗所致院内感染与中性粒细胞减少程度及持续时间密切相关,合理使用G—CSF及抗生素是预防和控制感染的重要措施。     

β2GPI及其抗体与血栓形成的相关性研究

血栓形成是临床疾病中常见的一种病理过程,以血栓形成为基本病理特征的心、脑血管疾病已超过恶性肿瘤,成为威胁人类生命的第一杀手。如何有效防治血栓,也是临床治疗中比较棘手的一个问题。目前对血栓形成的机理还有待进一步阐明。β2糖蛋白I(β2GPI)及其抗体是血栓形成发生发展的重要因素之一,可影响内皮细胞、单核细胞、血小板和纤溶系统,促进血液凝固,导致血栓发生。如果能对β2GPI及其抗体进行有效控制,将有助于防治血栓性疾病。本文就近年来β2GPI及其抗体与血栓形成的相关性研究予以综述,希望能为寻找一种安全有效防治血栓性疾病的新途径提供可能。     

恶性肿瘤干性及其量化分析方法的研究进展

一直以来,肿瘤干细胞一直是恶性肿瘤研究领域的重要研究靶点之一,其干性特征影响了癌症的发生、治疗抵抗和复发。传统的肿瘤干性机制研究需要实验流式技术对肿瘤干细胞进行分选和提取。二代测序技术在肿瘤研究领域的普及产生了大量的肿瘤组织测序数据并提供了丰富的恶性肿瘤遗传和分子图谱。随着计算方法的不断革新,研究人员基于分子特征或机器学习原理,通过改良算法和组合策略对恶性肿瘤组织中的干性水平进行评估,并使用干性指数对其描述和定义。对干性的量化计算,可以为恶性肿瘤中干性调控机制提供帮助,基于干性指数等指标进行建模预测,能够指导临床对癌症患者的治疗和预后进行评估。     

阻止癌症发展

癌细胞不幸地装备了它们扩散所需的一整套工具。恶性肿瘤的细胞快速分裂只是其危险性的一部分。另一部分原因则是其在新地方制造生存空间的奇异能力。美国每年确诊的100万癌症患者中,半数病人的主要死亡原因是癌症转移。内科医师难以完全阻止癌症转移。事实上,几乎所有结肠癌和乳房癌患者死亡的主要原因不在于肿瘤本身,而在于它转移到身体其它部位。 癌症的这种特殊能力还使病人虚弱。能转移的几百种癌症类型几乎都遵循着相同的机理发生转移。弄     

继发性PICC导管异位使用观察及护理体会

目的观察继发性PICC导管异位的并发症情况。方法对15例继发性导管异位鼻咽癌患者使用PICC情况进行观察分析。结果发生有症状血栓2例,穿刺口渗液1例,导管堵塞1例。结论发生继发性PICC导管异位患者,要做好患者血栓形成的风险评估,根据病人情况采取护理干预措施,有效的护理该类导管部份可以保留使用,可达到减轻病人痛苦、降低医疗费用和保护外周血管的目的。但血液流变学异常、D-二聚体增高、纤维蛋白原增高、血小板增高等血栓高危人群慎用。     

中医药干预癌症免疫逃逸的研究进展

免疫逃逸是指恶性肿瘤细胞通过免疫编辑过程后具备浸润、转移等恶性生物学行为,并逃脱免疫系统的监视和清除,最终促进恶性肿瘤病情发生发展的过程。除其他因素外,免疫细胞还积极影响肿瘤发展的每一步,决定了癌细胞在受威胁的微环境中生存的机会。一旦发现第一个癌细胞,抗肿瘤免疫机制就会被激活,并在原发肿瘤形成和转移过程中发挥作用。然而,免疫功能受损时,肿瘤细胞就会通过逃避或者阻挠免疫反应的机制来促进自身的增殖,就会导致肿瘤的持续性发展。而中医药干预癌症免疫逃逸机制需以“扶正”为基本原则,补益正气以治其本,增强免疫细胞对癌细胞的杀伤力,阻止癌症免疫逃逸,从而抑制癌症的发展。根据现有文献分析可知,目前通过免疫逃逸治疗癌症多用补益类药物,这可能是因为机体免疫调节功能与中医“扶正”观点相符合。因此,研究癌症免疫逃逸机制不仅能够提高治疗癌症的效率,而且通过对中医药的开发利用,能够延缓疾病的发展进程,更好的改善患者的生存质量。     

肿瘤转移研究的现状与趋势

肿瘤转移是恶性肿瘤的主要特征,是引起癌症患者死亡的首要因素．肿瘤转移的发生涉及到肿瘤细胞及其所处的微环境中复杂的信号通路,这些信号通路的激活及相互作用介导了肿瘤的转移、侵袭和在血液/淋巴循环系统中存活,以及在转移靶部位的生长过程．肿瘤转移是一个复杂的、多因素调控的动态过程,对于肿瘤转移机制的研究将有助于深入了解转移过程,并可以鉴定到有意义的治疗靶标,为临床诊断和治疗奠定基础．     

胃癌发生及其耐药性形成中的相关信号通路

胃癌是常见的消化道恶性肿瘤,而化疗药物的耐药性严重影响晚期胃癌患者的化疗效果。本文总结了多种与胃癌的发生及耐药性产生相关的信号通路,包括rnTOR、Nrf2-ARE、Notch、Hedgehog和Wnt。这些信号通路不仅决定着胃癌等恶性肿瘤的发生、分化与转移,更影响着恶性肿瘤耐药性的产生,而耐药性正是目前肿瘤化疗的最大障碍。研究这些信号通路可以从分子水平研究癌症发生的机理从而阻断肿瘤的生长,从这些肿瘤相关信号通路中亦能了解到肿瘤耐药性产生的机制,为胃癌等恶性肿瘤研究和治疗提供新的思路。     

影响妇科腹腔镜术后下肢深静脉血栓形成的相关因素分析

目的:探讨妇科腹腔镜手术后下肢深静脉血栓形成(DVT)的危险因素。方法:回顾性分析339例行妇科腹腔镜手术患者的临床资料,对患者的一般临床资料、术前实验室检查指标、手术类型、术中治疗及术后干预措施等进行单因素及多因素Logistic回归分析。结果:339例行妇科腹腔镜手术患者中30例术后发生DVT(发生率约8.8%),年龄(OR=1.438)、手术类型(腹腔镜妇科恶性肿瘤手术)(OR=3.153、血浆D-二聚体水平≥0.5 mg/L(OR=2.531)、术前合并症(OR=2.885)、术中气腹压(OR=2.835)、手术时间≥1h(OR=1.397)、术后卧床天数(OR=1.498)与妇科腹腔镜手术后发生DVT呈正相关(P0.05)。结论:年龄、手术类型、血浆D-二聚体水平、术前合并症、术中气腹压、手术时间及术后卧床天数是妇科腹腔镜术后发生VDT的独立危险因素。     

脂联素及其受体抗肿瘤的研究进展

目前大量的研究已表明循环系统的脂联素浓度与恶性肿瘤的发病风险呈负相关。这些恶性肿瘤包括绝经后乳腺癌、子宫内膜癌、大肠癌、前列腺癌等。脂联素是在其受体(AdipoR1和AdipoR2)的介导下发挥其生物学作用。相关实验发现,AdipoR1/R2在乳腺癌、子宫内膜癌、结直肠癌等肿瘤组织中有表达。因此针对脂联素的研究可能揭示其与恶性肿瘤的发生、发展的相关性。     

PRDM基因与非小细胞肺癌关系的研究现状

肺癌是当今世界上严重威胁人类健康的恶性肿瘤,具有高发病率和高死亡率。目前缺乏理想的早期诊断手段。PRDM基因家族是近年来新发现的与人类肿瘤形成相关的转录调节因子家族,通过启动子区高甲基化参与多种肿瘤形成,并在细胞分化和恶变中发挥重要作用。目前,对于PRDM基因在非小细胞肺癌中作用的研究多集中在PRDM1、PRDM5和PRDM14。本文主要综述了PRDM1、PRDM5和PRDM14在非小细胞肺癌中的表达及其与非小细胞肺癌患者临床特征关系的研究现状。PRDM基因有望成为肺癌的早期诊断和预后评估的新靶点。     

炎症-肿瘤转化在眼部相关疾病中的研究进展

炎症向癌症转化的机制一直是癌症研究中的重点。作为炎症-肿瘤转化起始时所处的环境，炎性微环境是一个多种调控因子、细胞的大集合，其中包含的肿瘤干细胞、肿瘤相关巨噬细胞以及细胞因子（如趋化因子、生长因子）等在常见的眼部肿瘤中对肿瘤的起始、发生、演进乃至恶性转化和转移的过程起到了至关重要的调控作用。基于此，主要讨论了在炎性微环境中的肿瘤相关细胞、细胞因子以及细胞外基质等对肿瘤细胞的增殖、转移、浸润、侵袭过程的影响，着重探讨了眼部炎症-肿瘤转化相关的分子机制；并综述了视网膜母细胞瘤、腺样囊性癌等常见眼部肿瘤的特征及其由炎症到肿瘤发生过程中起重要调控作用的分子；最后，针对这些眼部肿瘤普遍存在的信号通路和分子靶点做出了对未来诊断及治疗方法的展望，以期在今后对眼科肿瘤的诊治过程中，能够针对提及的炎性成分设计思路，最大化防止炎症-肿瘤转化和恶性转归出现。     

Application of the Macrophage Migration Inhibition Test to Screen Patients with Early Cancer and Obtain Prognostic Determinations of Cancer Treatment

A modified direct method of the macrophage migration inhibition test (MMIT) was attempted on a large number of patients with malignant or benign tumors. Results of the MMIT in almost all patients with benign tumors were negative except for those with hydatidiform moles, dermoid cysts and viral benign tumors such as verruca plana which were positive. The number of cases determined as false positives were exceptionally few. Conversely, about the half of the patients with malignant tumors were positive. The majority of negative cancer patients were confirmed pathologically to be advanced cases and, therefore, were postulated to have been immunologically unresponsive. The remaining false negative patients were diagnosed to be very early cases with their malignant foci too small to be effective antigenic stimuli. The MMIT was also performed postoperatively on some of the patients using autologous antigens, which had been preserved by freezing, for examination of changes in the per cent migration index. The results led the authors to conclude that postoperative repetitions of the test permitted them to tell that cancer cells had been completely eradicated or that a relapse might occur in the near future. Examinations of cross reactivity between tumor antigens revealed that such reactivity exists between cancer antigens and antigens originating in hydatidiform moles and that there is also a very strong cross reactivity between allogeneic cancer antigens regardless of differences in the organs of origin. This fact suggests that the present test is effective for the screening of preoperative patients with early cancer.     

miR-137 inhibits glutamine catabolism and growth of malignant melanoma by targeting glutaminase

Glutamine catabolism is considered to be an important metabolic pathway for cancer cells. Glutaminase (GLS) is the important rate-limiting enzyme of glutamine catabolism. miR-137 functions as a tumor suppressor in many human malignant tumors. However, the role and molecular mechanism of miR-137 and GLS in malignant melanoma has not been reported. In this study, we showed that miR-137 was decreased in melanoma tissue, and the low miR-137 level and high GLS expression are independent risk factor in melanoma. miR-137 suppressed the proliferation and glutamine catabolism of melanoma cells. GLS is crucial for glutamine catabolism and growth of malignant melanoma. We also demonstrated that miR-137 acts as a tumor suppressor in melanoma by targeting GLS. This result elucidates a new mechanism for miR-137 in melanoma development and provides a survival indicator and potential therapeutic target for melanoma patients.     

Antiangiogenic activity of chemopreventive drugs

Tumors growing within the host form dynamic aberrant tissue that consists of host components, including the stroma, an expanding vasculature and often chronic inflammation, in addition to the tumor cells themselves. These host components can contribute to, rather than limit, tumor expansion, whereas deprivation of vessel formation has the potential to confine tumors in small, clinically silent foci. Therapeutic inhibition of vessel formation could be best suited to preventive strategies aimed at the suppression of angiogenesis in primary tumors in subjects at risk, or of micrometastases after surgical removal of a primary tumor. Our analysis of potential cancer chemopreventive molecules including N-acetylcysteine, green tea flavonoids and 4-hydroxyphenyl-retinamide has identified antiangiogenic activities that could account--at least in part--for the tumor prevention effects observed with these compounds. These drugs appear to target common mechanisms of tumor angiogenesis that may permit identification of critical targets for antiangiogenic therapy and antiangiogenic chemoprevention.     

Long-term follow-up of patients treated with radical surgery for rectal cancer

In developed societies colorectal cancer (CRC) is the second most frequent malignant tumor which causes more than 5000 deaths yearly in Hungary. We have attempted to answer the question how to improve the above mentioned data by the long-term follow-up of patients operated upon for rectal cancer at our department. Of the patients operated on for rectal cancer at our department between March 1990 and April 2006, we have conducted regular follow-up of 297 patients according to a protocol developed by us. We have examined the length of time between the rectum operation and the diagnosis and the number of local recurrences, distant metastases, tumor progression in more than one organ as well as second tumors (independent of the rectal cancer). During this period we found 24 local recurrences, 32 distant metastases, 43 tumor progressions in more than one organ, and 21 second tumors. In two patients, in addition to distant metastases, we found a second CRC independent of the original rectal cancer, and in one patient with tumor progression in more than one organ we also detected breast cancer. In one patient we found 3 second tumors (CR, lung and urinary bladder) independent of the original rectal cancer. Altogether we found tumors in 117 out of 297 patients. During the same period, we performed 69/117 operations and 31/117 patients were alive at the end of our study with a median survival of 60.4 (3-184) months. In summary, we can state that this work is beneficial for curing the recurrence of rectal cancer, making the patients' life longer or making the quality of life better for the patients operated on for rectal cancer.     

Soluble AXL: A Possible Circulating Biomarker for Neurofibromatosis Type 1 Related Tumor Burden

Neurofibromatosis type 1 (NF1) is the most common tumor predisposition disorder affecting 1/3500 worldwide. Patients are at risk of developing benign (neurofibromas) and malignant peripheral nerve sheath tumors (MPNST). The AXL receptor tyrosine kinase has been implicated in several kinds of cancers, but so far no studies have investigated the role of AXL in NF1 related tumorigenesis. Recently, the soluble fraction from the extracellular domain of AXL (sAXL) has been found in human plasma, and its level was correlated to poor prognosis in patients with renal cancer. Compared to normal human Schwann cells, a significantly high expression level of AXL was found in three of the four MPNST cell lines and two of the three primary MPNST tissues. Similarly, the level of sAXL in conditioned media corresponded to the protein and mRNA levels of AXL in the MPNST cell lines. Furthermore, in two different human MPNST xenograft models, the human sAXL could be detected in the mouse plasma. Its level was proportionate to the size of the xenograft tumors, while no human sAXL was detect prior to the formation of the tumors. Treatment with a newly developed photodynamic therapy, prevented further tumor growth and resulted in drastically reduced the levels of sAXL compared to that of the control group. Finally, the level of sAXL was significantly increased in patients with plexiform tumors compared to patients with only dermal neurofibromas, further supporting the role of sAXL as a marker for NF1 related tumor burden.     

Mice deficient in tumor necrosis factor-alpha are resistant to skin carcinogenesis.

Given the associations between chronic inflammation and epithelial cancer, we studied susceptibility to skin carcinogenesis in mice deficient for the pro-inflammatory cytokine TNF-alpha (refs. 5,6). TNF-alpha(-/-) mice were resistant to development of benign and malignant skin tumors, whether induced by initiation with DMBA and promotion with TPA or by repeated dosing with DMBA. TNF-alpha(-/-) mice developed 5-10% the number of tumors developed by wild-type mice during initiation/promotion and 25% of those in wild-type mice after repeated carcinogen treatment. TNF-alpha could influence tumor and stromal cells during tumor development. The early stages of TPA promotion are characterized by keratinocyte hyperproliferation and inflammation. These were diminished in TNF-alpha(-/-) mice. TNF-alpha was extensively induced in the epidermis, but not the dermis, in TPA-treated wild-type skin, indicating that dermal inflammation is controlled by keratinocyte TNF-alpha production. Deletion of a TNF-alpha inducible chemokine also conferred some resistance to skin tumor development. TNF-alpha has little influence on later stages of carcinogenesis, as tumors in wild-type and TNF-alpha(-/-) mice had similar rates of malignant progression. These data provide evidence that a pro-inflammatory cytokine is required for de novo carcinogenesis and that TNF-alpha is important to the early stages of tumor promotion. Strategies that neutralize TNF-alpha production may be useful in cancer treatment and prevention.