2016年陕西省恶性肿瘤发病与死亡分析

目的 研究2016年陕西省肿瘤登记地区恶性肿瘤的发病和死亡情况.方法 收集陕西省23个肿瘤登记地区的恶性肿瘤发病和死亡数据,计算发病(死亡)率、标化发病(死亡)率以及累积发病(死亡)率(0～74岁).结果 2016年陕西省肿瘤登记地区恶性肿瘤发病率为212.40/10万,中标率为142.42/10万,世标率为152.2...     

脂代谢通路及脂代谢异常在癌症中的研究现状

脂质具有多种重要的生物功能,在生物体内具有复杂的代谢通路及多种脂质间的相互转化。脂质代谢异常可引发诸多人类疾病,包括糖尿病、肥胖症、癌症以及神经退行性疾病等。肿瘤的发生发展是一个多机制多因素的复杂的生物学过程,近年来,能量代谢异常在多种癌症研究中日益受到关注。随着脂质组学技术的发展,越来越多的研究表明脂质谱系变化及脂代谢异常在癌症的发生发展过程中扮演着十分重要的作用。本文从脂代谢通路、不同脂类在癌症中的异常代谢及其研究进展这几个方面对脂代谢在癌症发生发展中的作用与研究现状作一综述。     

Antibody ligation of CD9 modifies production of myeloid cells in long- term cultures

The KMC8.8 monoclonal antibody was made by immunizing rats with the BMS2 stromal cell clone, and was selected for further study because its ability to inhibit production of myeloid cells in Dexter cultures but not that of lymphoid cells in Whitlock-Witte cultures. The influence on myeloid progenitors might have been indirect, since the antibody did not prevent responsiveness to colony-stimulating factors in semisolid agar cultures. Furthermore, there was no inhibition, and some augmentation, of cell production when the antibody was added to established Dexter cultures. A cDNA clone that encoded the KMC8.8- recognized molecule was isolated by expression cloning and found to be identical in sequence to a previously published murine CD9 homologue. The antibody and cDNA clone were used to establish that CD9 is expressed by stromal cells, megakaryocytes, platelets, myeloid cells, and subpopulations of mature lymphocytes in mice. Treatment with the KMC8.8/CD9 antibody slightly augmented adhesion between myeloid cells and stromal cells, consistent with previous reports that this member of the tetraspan family of proteins can transmit proadhesive signals to human platelets and lymphoid cells. CD9 might participate in cell-cell interactions critical for correct orientation and movement of maturing myeloid cells in bone marrow.     

A staphylococcal slide test for detection of antineutrophil antibodies

We describe a simple test for direct or indrect detection of antineutrophil antibodies. Sensitized leukocytes adherent to glass slides and fixed with paraformaldehyde can be stored in buffer for at least 3 wk. Killed Cowan I staphylococci, containing protein A, bind to sensitized but not control cells, and binding is ascertainable by light microscopy. Indirect tests were positive for 39/41 patients suspected of having immune neutropenia and found to have antineutrophil antibodies by an indirect radiochemical opsonic method. Fifty-four control sera from healthy persons, patients with bone marrow failure, or with immune complex diseases without neutropenia, gave negative indirect tests. Direct tests for cell-bound antibody could be done even during severe neutropenia by reacting fixed autologous cells with staphylococci in the absence of added serum. In some patients only the direct test was positive.     

四种肝（癌）细胞系糖代谢的流量解析

 目的 分析人正常肝细胞（HL-7702）、不同转移潜能的肝细胞癌细胞系（SMMC-7721、HCCLM3）以及肝癌门静脉癌栓细胞系（CSQT2）的糖代谢流量及相关基因表达。方法 利用稳定同位素13C标记的葡萄糖与谷氨酰胺作为营养源,结合酶活实验,对四种细胞进行糖代谢流量解析。结果 MTT与Transwell实验证实了HL-7702、SMMC-7721、HCCLM3、CSQT2细胞的增殖与迁移能力依次增加。酶活实验与标记实验结果均显示,糖酵解与三羧酸循环的代谢活性在四种细胞中依次增加,具体表现为葡萄糖消耗与乳酸产生的增加,代谢流量比率在多种糖代谢产物中的上升,尤其是在CSQT2细胞中达到最高。结论 随着肝癌细胞的恶性程度及转移能力的增加,糖酵解与三羧酸循环的代谢活性增加。代谢流量分析可能用以判断肝癌的发生发展与转移。     

Alox5与髓系白血病关系的研究进展

白血病是一组造血细胞恶性增殖并伴有分化受阻的血液系统肿瘤,其病因及发病机制尚不完全清楚,目前尚不可治愈。已有研究表明,由花生四烯酸5-脂氧合酶(arachidonate 5-lipoxygenase,Alox 5)基因编码产生的花生四烯酸代谢通路中的5-脂氧合酶(5-lipoxygenase,5-LO)影响髓系白血病的发生和发展,是靶向白血病干细胞(leukemia stem cells,LSCs)恶性生物学特性的关键分子,是髓系白血病潜在的治疗靶点。本文就Alox 5基因与髓系白血病之间的关系进行综述。     

A maternal cafeteria diet during gestation and lactation promotes adiposity and impairs skeletal muscle development and metabolism in rat offspring at weaning

We examined the effects of a maternal cafeteria diet on skeletal muscle and adipose tissue development in the offspring at weaning. Rats born to mothers fed the cafeteria diet either during gestation alone or during both gestation and lactation exhibited a 25% reduction in muscle cross-sectional area with approximately 20% fewer fibres compared with pups fed a balanced chow diet. Maintaining the cafeteria diet during lactation increased intramuscular lipid content and fat pad weights characterized by adipocyte hypertrophy but not hyperplasia. These pups also had elevated muscle IGF-1, IGF-1 receptor, and PPARγ mRNA levels, which may indicate an attempt to maintain normal insulin sensitivity. The increased adiposity and elevated IGF-1, IGF-1 receptor and PPARγ mRNAs were not seen in the pups rehabilitated to the balanced diet during lactation. However, these pups exhibited reduced muscle cell proliferation (PCNA) with reduced insulin receptor and a trend towards reduced glucose transporter (GLUT)-4 mRNAs when compared with pups fed a balanced chow diet, indicating possible alterations in glucose uptake by muscle tissue. Therefore, rats born to mothers fed a cafeteria diet during gestation alone or during both gestation and lactation exhibited impaired skeletal muscle development and metabolic disorders normally associated with insulin resistance as early as the weaning stage.     

Estrogen receptor status in CHEK2-positive breast cancers: implications for chemoprevention

To investigate the relationship between CHEK2 mutation status and estrogen receptor (ER) status in unselected cases of early-onset breast cancer from Poland, we screened 4441 women diagnosed with breast cancer younger than 51 years and 7217 controls for three inherited mutations in CHEK2 (1100delC, IVS2+1G>A, del5395). ER status was compared between CHEK2 -positive and CHEK2 -negative breast cancer cases. A truncating mutation in CHEK2 was seen in 140 of 4441 cases and in 70 of 7217 controls [odds ratio (OR) = 3.3; 95% CI = 2.5–4.4; p < 0.0001]. ER status was available for 92 of 140 mutation carriers and for 3001 of 4301 non-carriers with breast cancer. The OR was higher for ER-positive cancers (OR = 3.9; 95% CI = 2.7–5.4; p < 0.0001) than for ER-negative cancers (OR = 2.1; 95% CI = 1.3–3.3; p = 0.002). Sixty-six of the 92 breast cancers in carriers of CHEK2 truncating mutations were ER positive compared with 1742 of the 3001 breast cancers in non-carriers (72% vs 58%; p = 0.01). Women with a CHEK2 mutation face a fourfold increase in the risk of ER-positive breast cancer and might be candidates for tamoxifen chemoprevention.