表皮生长因子受体在喉癌及癌前病变中的表达

目的：探讨表皮生长因子受体的表达在喉癌和癌前病变中的作用。方法：应用免疫组化ＡＢＣ法检测喉鳞癌３１例，喉上皮非典型增生１６例，正常喉粘膜１０例的表皮生长因子受体（ＥＧＦＲ）的表达。结果：发现正常喉粘膜组织全部阴性，喉癌的ＥＧＦＲ阳性率为４８％，非典型增生ＥＧＦＲ的阳性率为５６％，并随异型增生程度的增高ＥＧＦＲ表达增加，其差异有显著性（Ｐ〈０．０５）。但ＥＧＦＲ的表达与喉癌发生部位、肿瘤分期、组织分     

nm23H1蛋白及DNA倍体状态与食管癌区域淋巴结转移相关性研究

目的：研究ｎｍ２３Ｈ１蛋白、ＤＮＡ倍体状态与食管癌区域淋巴结转移的相关性及临床意义。方法：应用流式细胞荧光免疫技术检测食管癌新鲜手术标本食管癌组织（癌）、食管癌旁１ｃｍ粘膜（癌旁）、食管正常粘膜（切缘）及食管癌区域淋巴管（淋巴结）组织中ｎｍ２３Ｈ１蛋白表达及ＤＮＡ倍体状态。结果：ｎｍ２３Ｈ１蛋白表达阳性率在食管癌旁、切缘、癌及淋巴结组织中依次降低，在有转移组分别为１６．６５％、９．４４％、４．９９％和８．３０％，在无转移组分别为２４．７７％、１４．４９％、７．０９％和３．８１％。在无转移组内，切缘与癌及淋巴结组织间差异显著（Ｐ〈０．０５）。在有转移组央差异无显著性（Ｐ〉０．０５）；食管癌组织中异倍体发生率为８９．５８％（４３／４８），异倍体发生与淋巴结转移及ｎｍ２３Ｈ１蛋白表达之间无显著相关性。结论：ｎｍ２３Ｈ     

表皮生长因子受体在宫颈癌及宫颈癌前病变组织中的表达

表皮生长因子受体（ＥＧＦ－Ｒ）是原癌基因。ｃ－ｅｒｂＢ－１（也称ＨＥＲ－１）的表达产物,它与肿瘤形成的关系日渐受到人们的重视。本研究采用免疫组化方法检测正常宫颈粘膜。宫颈上皮异型增生及宫颈鳞癌组织中ＥＧＦ－Ｒ的表达,探讨ＥＧＦ－Ｒ与宫颈癌发生及生物学行为的关系。１材料与方法１．１材料收集宫颈活检及子宫切除标本１３６例,其中正常宫颈粘膜１０例,宫颈上皮轻度异型增生２２例,中度异型增生１８例,重度异型增生１５例,原位癌８例,早期浸润癌（癌组织浸润间质深度为距基底膜５ｍｍ之内）１５例,浸润癌（癌组织浸…     

表皮生长因子受体在颊粘膜上皮良性和恶性病变中的表达及…

目的：研究表皮生长因子受体（ＥＧＦＲ）在颊粘膜上皮良性和性病变中的表达，探讨其在颊粘膜上皮细胞恶变中关系及意义。方法：采用免疫组化ＡＢＣ法检测ＥＧＦＲ在正常颊粘膜上皮、慢性非特异性炎症病变、鳞状细胞癌和癌旁组织中的表达。结果：ＥＧＦＲ在恶性病变和部分癌旁组织中的表达明显高于正常颊粘膜上皮和良性病变。结论：ＥＧＦＲ与颊粘膜上皮恶变具有相关性。部分癌旁组织因有恶变倾向，ＥＧＦＲ也呈高表达。     

c－erbB－2和EGFR在胃癌中表达的研究

应用ＡＢＣ和ＬＳＡＢ法对７５例胃癌及癌旁组织进行了ｃ－ｅｒｂＢ－２和ＥＧＦＲ表达的研究。结果：１）７５例胃癌ｃ－ｅｒｂＢ－２表达阳性率为１８．７％，阳性表达只限于癌灶，而癌旁组织均为阴性。ｃｅｒｂＢ－２在高分化胃癌、大体局限型胃癌中的阳性率较高（Ｐ＜０．０５）。２）ＥＧＦＲ表达阳性率为６１．３％，癌旁组织、新生血管有阳性表达。ＥＧＦＲ表达与胃癌的大体类型、生长方式、分化程度、淋巴结受累和远处转移至正相关（Ｐ＜０．０５）。３）ｃ－ｅｒｂＢ－２表达与ＥＧＦＲ表达无明显关系。结果说明：ｃ－ｅｒｂＢ－２表达出现于胃粘膜癌变的后期，是恶性细胞的标志；ＥＧＦＲ表达与胃癌的恶性程度有明显关系；ｃ－ｅｒｂＢ－２和ＥＧＦＲ在胃癌中的表达是互相独立的。     

c—erbB—2和EGFR在胃癌中表达的研究

应用ＡＢＣ和ＬＳＡＢ法对７５例胃癌及癌旁组织进行了ｃ－ｅｒｂＢ－２和ＥＧＦＲ表达的研究。结果：１）７５例胃癌ｃ－ｅｒｂＢ－２表达阳性率为１８．７％，阳性表达只限于癌灶，而癌旁组织均为阴性。ｃ－ｅｒｂＢ－２在高分化胃癌，大体局限型胃癌中的阳性率较高。２）ＥＧＦＲ表达阳性为６１．３％，癌旁组织，新生血管有阳性表达。ＥＧＦＲ表达与胃癌的大体类型，生长方式，分化程度，淋巴结受累和远外转移呈正相关。     

nm23和p53蛋白在喉鳞癌组织中表达的意义

应用免疫组化技术，了３２例喉鳞癌组织及１２社异型增生组织的ｎｍ２３和ｐ６３蛋白的表达情况。结果发现：ｎｍ２３与ｐ５３在喉鳞癌组织的阳性一表达率分别为８７．５０％及８４．３８％。在癌旁异型增生组织阳性表达率分别为１００％和２０％。ｎｍ２３的表达与喉鳞癌的组织学分级有关，Ｐ５３的表达与喉鳞癌组织学分级无关，但Ｐ５３的强阳性表达预示预后不良。     

胃癌多基因表达的同步检测

应用ＬＳＡＢ和ＡＢＣ法对７５例胃癌及癌旁组织进行了ｐ５３、ｃ－ｅｒｂＢ－２、ＥＧＦＲ和ｒａｓ表达的研究。结果显示：（１）７５例胃癌ｐ５３、ｃ－ｅｒｂＢ－２、ＥＧＦＲ和ｒａｓ表达阳性率分别为４１．３％、１８．７％、６１．３％和４６．７％。ｐ５３在肠型胃癌中阳性率为５２．６％，高于弥漫型胃癌的２９．７％（Ｐ＜０．０５）；在早期胃癌中阳性率较高（６０．０％），癌旁重度异型增生亦有阳性表达（２／４）。ｃ－ｅｒｂＢ－２阳性表达只限于癌灶，而癌旁组织均为阴性。ｃ－ｅｒｂＢ－２在高分化胃癌中阳性率较高（Ｐ＜０．０５）。ＥＧＦＲ表达与胃癌的大体类型、生长方式、分化程度、淋巴结受累和远处转移呈正相关（Ｐ＜０．０５）。（２）ｃ－ｅｒｂＢ－２和ＥＧＦＲ在胃癌中的表达互相独立。（３）ｒａｓ表达与ＥＧＦＲ表达呈正相关，而与ｃ－ｅｒｂＢ－２呈负相关。（４）ｐ５３表达与其它基因表达无明显关系。上述结果表明，胃癌发生发展过程中伴有多种癌基因的变化，其出现时间不同，意义也不一样。     

肺鳞癌中MDR1基因产物P-gp、p53及nm23蛋白的表达及临床意义

研究肺鳞癌中Ｐ５３蛋白、ｎｍ２３蛋白以及药基因ＭＤＲ１产物Ｐ－糖蛋白（Ｐ－ｇｌｙｃｏｐｒｏｔｅｉｎＰ－ｇｐ）的表达及相互关系,探讨它们在肺鳞癌发展,预后耐药中的作用。方法：采用免疫组化ＳＰ法,对４０例肺鳞癌及其癌旁正常肺组织中Ｐ５３蛋白ｎｍ２３和Ｐ－ｇｐ进行检测。     

膀胱癌中nm23-H1基因突变及表达的意义

目的：探讨ｎｍ２３－Ｈ１基因在膀胱癌中突变及表达的意义。方法：应用半定量逆转录聚合酶链反应（ＲＴ－ＰＣＲ）和银染单链构象多态性（ＳＳＣＰ）方法检测ｎｍ２３－Ｈ１基因在２５例膀胱癌组织及１５例对照组织中突变和表达情况。结果：对照粘膜中未检测出ｎｍ２３－Ｈ１基因突变,而在２５例膀胱癌组织中发现６例出现ＰＣＲ产物单链泳动状态异常,异常率为２４％。癌组织和对照组织均有ｎｍ２３－Ｈ１基因ｍＲＮＡ的表达,８８     

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.     

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.     

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。     

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。     

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.     

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.