肿瘤内注射^32P—玻璃微球后注射后剂量与生物效应的关系

目的：为了解小鼠内直接注射不同剂量＾３２Ｐ－玻璃微球（＾３２Ｐ－ＧＴＭＳ）后,不同时间肿瘤组织的生物效应。方法：采用昆明作为实验动物,腹部皮下接种Ｓ１８０肿瘤细胞,７－１０天后在注射部位长出实体瘤块。将３６只带瘤鼠分成三个剂量组,分别向各组鼠瘤块中心注射没剂量的＾３２Ｐ－玻璃微球碘油悬浮液５０μｌ,在注射后不同时间（７天,１４天,２１天,２８天）分批杀死各剂量组小鼠,取出瘤块,观察瘤体大步及病理变     

^32P玻璃微球直接注入法治疗肿瘤的动物研究

３２Ｐ玻璃微球直接注入法治疗肿瘤的动物研究袁志斌高克加朱瑞森朱继芳马寄晓关键词肿瘤，动物实验／放射性核素治疗３２Ｐ－玻璃微球作者单位：上海市第六人民医院核医学科（上海，２００２３３）用核素标记的玻璃微球（ＧＴＭＳ）来治疗肿瘤已被人们所注意，ＹａｎＺＰ...     

钇－90玻璃微球内辐射治疗小鼠移植性肝癌的实验研究

为了配合临床对肿瘤内注射钇－９０玻璃微球治疗肝癌，作者研究观察了钇－９０玻璃微球瘤内注射对小鼠移植性肝癌的疗效及其与剂量的关系。７０只载瘤ＢＡＬＢ／Ｃ小鼠随机分为７组（Ａ、Ｂ、Ｃ、Ｄ、Ｅ、Ｆ、Ｇ），每组１０只按下列分组给药：Ａ组３７ＭＢｑ／ｃｍ￣３（１ｍＣｉ＝３７ＭＢｑ）、Ｂ组１８．５ＭＢｑ／ｃｍ￣３，Ｃ组１４．８ＭＢｑ／ｃｍ￣３、Ｄ组１１．１ＭＢｑ／ｃｍ￣３、Ｅ组７．４ＭＢｑ／ｃｍ￣３，Ｆ组３．７ＭＢｑ／ｃｍ￣３，对照组Ｇ组０ＭＢｑ／ｃｍ￣３Ｍ。结果显示：Ａ、Ｂ组大部分小鼠肿瘤结节从逐渐缩小到不能触及，Ｃ、Ｄ、Ｅ、Ｆ各组肿瘤生长趋势均受到抑制，并随剂量增大，肿瘤生长率明显缩小，各治疗组与对照组肿瘤生长率经统计学处理差异均有显著意义。病理切片显示：Ａ、Ｂ组大部分小鼠肿瘤完全坏死，无存活的肿瘤细胞，Ｃ、Ｄ、Ｅ、Ｆ各组镜下显示片状坏死，均不同程度地见到存活的肿瘤细胞，Ｇ组见大片存活的肿瘤组织，仅表现为点、小片状坏死。实验表明：钇－９０直接注入肿瘤内治疗肝癌疗效肯定，其剂量达１８．５ＭＢｑ／ｃｍ￣３以上时，对于直径１ｃｍ的肝瘤可造成完全性坏死，获得较好的疗效。     

立体定向间质照射治疗生殖细胞瘤

ＣＴ引导立体定向间质照射治疗生殖细胞瘤１５例。瘤内注射＾３２Ｐ或＾９０Ｙ同位素胶体共２１次，每次肿瘤吸收剂量为４００ＧＹ。无手术死亡者及颅内出血、感染等严重并发症。随访３－１８个月，手术有效率１００％。作者认为该法治疗生殖细胞瘤安全简便、疗效可靠、副损伤小，值得推广应用。     

肿瘤内注射32P-玻璃微球后注射剂量与生物效应的关系

目的 :为了解小鼠肿瘤内直接注射不同剂量 32P -玻璃微球(32P -GTMS)后 ,不同时间肿瘤组织的生物效应。方法 :采用昆明鼠作为实验动物 ,腋部皮下接种S180肿瘤细胞 ,7～10天后在注射部位长出实体瘤块。将36只带瘤鼠分成三个剂量组 ,分别向各组鼠瘤块中心注射不同剂量(37MBq,74MBq,148MBq)的 32P -玻璃微球碘油悬浮液50μl ,在注射后不同时间(7天 ,14天 ,21天 ,28天)分批杀死各剂量组小鼠 ,取出瘤块 ,观察瘤体大小及病理变化。结果 :32P -玻璃微球具有明显的肿瘤抑制和杀伤作用 ,它的有效杀伤半径约为3.5～4mm ,有效杀伤半径不随剂量的增加而增大。结论 :32P -玻璃微球是一种有应用前景的肿瘤治疗药物     

全甲注参胶囊对环磷酰胺致畸和抑瘤作用

目的 观察全甲洋参胶囊（ＱＪＹＳ）对环磷酰胺（ＣＰ）引起的荷瘤小鼠骨髓嗜多工细胞微核形成（ＭＮＦ）和对ＣＰ抑瘤作用的影响，探讨其临床应用的合理性。方法 以荷瘤（Ｓ１８０）小鼠为动物模型，分别观察单纯给予不同剂量的ＱＪＹＳ，单纯给予ＣＰ，同时给予ＱＪＹＳ和ＣＰ对小鼠肿瘤生长和骨髓嗜多工细胞ＭＮＦ的影响，并与对照组进行比较。结果 单纯给予ＱＪＹＳ各剂量组小鼠肿瘤平均重量及ＮＭＦ均略低于对照组，但无显著     

帕米膦酸二钠和^153Sm—EDTMP治疗骨继发性恶性肿瘤疗效对比 …

帕米膦酸二钠（ＡＰＤ）与＾１５３钐－乙二胺四甲基膦酸（１５３Ｓｍ－ＥＤＴＭＰ）皆为治疗骨继发性恶性肿瘤的较新药物，为比较两者的治疗效果，将４２例骨继发性患者随机分为ＡＰＤ组和＾１５３Ｓｍ－ＥＤＴＭＰ组每组各２１例，结果显示：ＡＰＤ和＾１５３Ｓｍ－ＥＤＴＭＰ组对患者骨痛缓解率分别为７６．１９％，９０．４８％（Ｐ〉０．０５），ＡＰＤ与＾１５３Ｓｍ－ＥＤＴＭＰ对骨转移灶控制率分别为４７．６２％，２３．８     

^125I标记的免疫毒素（TCS—Hepama—1）在荷人肝癌裸鼠体内分布及…

＾１２５Ｉ标记的免疫毒素ＴＣＳ－Ｈｅｐａｍａ－１及对照用ＴＣＳ－ＮＭＩｇＧ在荷瘤裸鼠体内分布及肿瘤显像结果表明：实验组裸鼠尾静脉注入＾１２５Ｉ－ＴＣＳ－Ｈｅｐａｍａ－１后第２天，血的放射性提高，随着时间延长，血各组织宫官的放射量逐渐减少。而肿瘤组织的每克放射剂量逐渐增多，第６起Ｔ／ＮＴ值均〉１，第８天达最高，瘤／血，瘤／肝比为１．４５及２．０。５     

放射性微球治疗晚期肝癌内照射剂量与疗效关系的探讨

目的探讨核素微球治疗晚期肝癌的量效关系。材料与方法３２磷一玻璃微球（Ｐｈｏｓｐｈｏｒｕｓ－３２ｇｌａｓｓｍｉｃｒｏｓｐｈｅｒｅｓ，３２Ｐ－ＧＭＳ）肝动脉灌注治疗２８例晚期肝癌患者，动脉血酮体比率（Ａｒｔｅｒｙｋｅｔｏｎｅｂｏｄｙｒａｔｉｏ，ＡＫＢＲ）等监测术后肝脏能量代谢变化，ＣＴ、ＥＣＴ、Ｂ超、ＡＦＰ等观察疗效，平均随访２８个月。结果６１μ的３２Ｐ－ＧＭＳ是治疗晚期肝癌安全有效的放射性栓塞材料，当靶肝组织吸收放射剂量＞５０Ｇｙ及微球量＞３ｇ时近期疗效满意，但有严重消化道反应和明显肝代谢功能损害，而２８～３７Ｇｙ组术后肝功能恢复良好，各种术后并发症明显减少，远期疗效较好。结论放疗性栓塞治疗肝硬变肝癌患者的合理靶肝吸收剂量应在３０Ｇｙ左右。     

^153Sm—EDTMP治疗肿瘤骨转移止痛效果相关因素分析

目的 分析影响＾１５３Ｓｍ－ＥＤＴＭＰ对肿瘤转移性骨痛治疗效果的相关因素，方法 对我院近两年使用＾１５３Ｓｍ－ＥＤＴＭＰ行内照射治疗的５９例肿瘤转移性骨病人进行回顾性分析，按年龄，病灶数量，不同肿瘤分组，单次剂量给予＾１５３Ｓｍ－ＥＤＴＭＰ１８．５－３７ＭＢｑ／ｋｇ静脉注射，第２天行全身骨显像现查放射分布情况，建立随访。结果 总有效率为９３．６％，在年龄组中，以老年组效果最好，止痛有效率为９６．９     

Religiosity and Physical and Emotional Functioning Among African American and White Colorectal and Lung Cancer Patients

The literature suggests that religiosity helps cope with illness. The present study examined the role of religiosity in functioning among African Americans and Whites with a cancer diagnosis. Patients were recruited from an existing study and mailed a religiosity survey. Participants (N = 269; 36% African American, 56% women) completed the mail survey, and interview data from the larger cohort was utilized in the analysis. Multivariate analyses indicated that in the overall sample religious behaviors were marginally and positively associated with mental health and negatively with depressive symptoms. Among women, religious behaviors were positively associated with mental health and negatively with depressive symptoms. Religiosity was not a predictor of study outcomes for men. Among African Americans, religious behaviors were positively associated with mental health and vitality. Among Whites, religious behaviors were negatively associated with depressive symptoms. These findings suggest a mixed role of religious involvement in cancer outcomes. The current findings may have applied potential in the areas of emotional functioning and depression.     

Occupational and environmental radiation and cancer

Epidemiologic evidence on the relation between occupational and environmental radiation and cancer is reviewed. Studies of pioneering radiation workers, underground miners, and radium dial painters revealed excess cancer deaths and contributed to the setting of radiation protection standards and to theories of carcinogenesis. Occupational exposures today are generally much lower than in the past, thus any associated increases in cancer will be difficult to detect. Pooling investigations of these more recently exposed workers, however, has the potential to validate current estimates of risk used in radiation protection. New information on the effects of chronic radiation exposure also may come from studies in the former Soviet Union of Chernobyl clean-up workers and of workers at the Mayak nuclear facilities. Studies of environmental radiation exposures, other than radon, are largely inconclusive, due mainly to the difficulties in detecting the low risks associated with low dose exposures. Thyroid cancer, however, has been linked to environmental radiation from the Chernobyl accident and from nuclear weapons tests. Low-level radiation released during normal operations at nuclear plants has not been found to increase cancer rates in surrounding populations. Radon, a human carcinogen, is the most ubiquitous exposure to human populations; remediating high residential-radon levels is recommended, recognizing that the exposure can never be removed completely because it occurs naturally.     

Vitamin D and melanoma and non-melanoma skin cancer risk and prognosis: A comprehensive review and meta-analysis

Vitamin D is formed mainly in the skin upon exposure to sunlight and can as well be taken orally with food or through supplements. While sun exposure is a known risk factor for skin cancer development, vitamin D exerts anti-proliferative and pro-apoptotic effects on melanocytes and keratinocytes in vitro. To clarify the role of vitamin D in skin carcinogenesis, we performed a review of the literature and meta-analysis to evaluate the association of vitamin D serum levels and dietary intake with cutaneous melanoma (CM) and non-melanoma skin cancer (NMSC) risk and melanoma prognostic factors. Twenty papers were included for an overall 1420 CM and 2317 NMSC. The summary relative risks (SRRs) from random effects models for the association of highest versus lowest vitamin D serum levels was 1.46 (95% confidence interval (CI) 0.60–3.53) and 1.64 (95% CI 1.02–2.65) for CM and NMSC, respectively. The SRR for the highest versus lowest quintile of vitamin D intake was 0.86 (95% CI 0.63–1.13) for CM and 1.03 (95% CI 0.95–1.13) for NMSC. Data were suggestive of an inverse association between vitamin D blood levels and CM thickness at diagnosis. Further research is needed to investigate the effect of vitamin D on skin cancer risk in populations with different exposure to sunlight and dietary habits, and to evaluate whether vitamin D supplementation is effective in improving CM survival.     

New and emerging radiosensitizers and radioprotectors

The combination of chemotherapy and radiation has led to clinical breakthroughs in several disease sites, and current work continues to define optimum combinations of proven chemotherapy as well as more recently available, noncytotoxic agents. Administration of systemic therapies allows modulation of radiation response to improve tumor control (radiosensitization) or to prevent normal tissue toxicity (radioprotection). Substantial progress has been made in identifying the targets of standard chemotherapeutic radiation sensitizers and protectors as well as in the introduction of a new generation of molecularly targeted therapies in combination with radiation. We have reviewed the most recent, predominantly early phase clinical trials combining systemic agents with radiation. Although the proof of an improved schedule ultimately needs to come from well-run Phase III trials, the search among schedules could be shortened by the use of surrogate endpoints such as presence of active drug metabolites in the tumor. This has been accomplished only in a few cases and needs to become a more standard part of radiation sensitizer and protector trials.     

Fruit and vegetables and cancer risk

The possibility that fruit and vegetables may help to reduce the risk of cancer has been studied for over 30 years, but no protective effects have been firmly established. For cancers of the upper gastrointestinal tract, epidemiological studies have generally observed that people with a relatively high intake of fruit and vegetables have a moderately reduced risk, but these observations must be interpreted cautiously because of potential confounding by smoking and alcohol. For lung cancer, recent large prospective analyses with detailed adjustment for smoking have not shown a convincing association between fruit and vegetable intake and reduced risk. For other common cancers, including colorectal, breast and prostate cancer, epidemiological studies suggest little or no association between total fruit and vegetable consumption and risk. It is still possible that there are benefits to be identified: there could be benefits in populations with low average intakes of fruit and vegetables, such that those eating moderate amounts have a lower cancer risk than those eating very low amounts, and there could also be effects of particular nutrients in certain fruits and vegetables, as fruit and vegetables have very varied composition. Nutritional principles indicate that healthy diets should include at least moderate amounts of fruit and vegetables, but the available data suggest that general increases in fruit and vegetable intake would not have much effect on cancer rates, at least in well-nourished populations. Current advice in relation to diet and cancer should include the recommendation to consume adequate amounts of fruit and vegetables, but should put most emphasis on the well-established adverse effects of obesity and high alcohol intakes.     

肾上腺素能β受体与肿瘤生长及转移

大量研究表明肿瘤细胞可表达β受体，而一些神经递质、药物和社会心理因素可能通过β受体影响肿瘤的生长和转移，β受体激动剂、β受体阻滞剂以及抑郁等社会心理因素可加强或削弱这种作用。这为表达β受体肿瘤的治疗开辟了新的道路，提供了新的治疗靶点。     

VEGF及KDR在大肠腺瘤和腺癌中的表达及意义

目的：探讨VEGF和KDR在大肠腺瘤和大肠腺癌中的表达及临床病理特征的关系。方法：大肠腺瘤和大肠腺癌组织标本各100例,采用免疫组织化学染色法检测VEGF和KDR在标本中的表达情况。结果：VEGF和KDR在大肠腺癌组中的阳性表达明显高于大肠腺瘤组（P〈0.05）;在正常大肠黏膜均未见VEGF和KDR表达的阳性染色;VEGF阳性表达组中KDR的阳性表达率为70%,显著高于VEGF阴性表达组中KDR的阳性表达率16%,两组比较有统计学意义（P〈0.01）。结论：大肠腺癌组织中KDR的表达与肿瘤大小、转移情况、浸润深度密切相关;VEGF和KDR在大肠腺瘤中的表达与患者的年龄、性别及分型均无相关性,而与增生程度相关（P〈0.05）。在大肠腺癌患者中VEGF及KDR表达更高,二者具有协同效应。     

Cell and tissue interactions in carcinogenesis and metastasis and their clinical significance

This review describes a new vision for future directions in the study of metastatic cancer biology and pathology. It is based upon clinical and experimental observations on the constituent cell lineages within a neoplasm and on tumour-host interactions. The vision incorporates information from studies in population biology, developmental biology and experimental pathology as well as investigations upon human malignant disease. The assembled information reveals that invasion and metastasis are supra-cellular manifestations of "emergent behavior" among combinations of normal and malignant cell lineages in vivo. Emergent behavior is a combinatorial interactive process in which a population displays new traits which cannot be achieved by individuals acting separately and which subside when the specific population mix disaggregates. Disruption of such pathological interactions in the field of a developing primary or secondary tumour is, therefore, required to disable the malignant population and arrest progression without tissue destruction. These conclusions originate, in part, from principles which govern the sociobiology and group behavior of bees, ants, fish, birds and human societies. In all these social organisms, external factors can disrupt signaling mechanisms and induce expanding self-perpetuating rogue behavior, leading to social disintegration. These principles also apply to cellular societies composing higher animals, which likewise need intrinsic rules to maintain social order and avoid anarchy, and recognition of this is essential for advancing future research on the mechanisms involved in carcinogenesis and metastasis. Summarised evidence is presented here to support the conclusion that miscommunications between cells and tissues in the region of the developing tumour and its metastases are the main direct perpetrators of malignant disease. Genetic lesions (mutations, deletions, translocations, reduplications, etc.), commonly seen in cancers, can significantly disrupt important molecular pathways in the networks of communications needed to sustain orderly tissue/organ structure and function. However, genetic lesions can also, themselves, be induced by abnormal cell interactions initiated by extrinsic carcinogenic agents such as chemicals, viruses, hormones and radiation. The evidence shows that, irrespective of the initiating cause, it is this miscommunication in the region of a developing tumour and its metastases that is ultimately responsible for the emergence and progression of the disease. The article describes how this information collectively, provides a framework for designing specific novel therapeutic approaches targeting the cell and tissue interactions driving tumour metastasis and its manifold effects on the whole body.