Glucocorticoids and androgens up-regulate the Zn-α2-glycoprotein messenger RNA in human breast cancer cells

Summary We have studied the hormonal regulation of the gene encoding Zn-₂-glycoprotein (Zn-₂-gp), a human protein with a high degree of amino acid sequence similarity to class I histocompatibility antigens that is produced by a specific subset of breast carcinomas. Northern blot analysis revealed that dexamethasone and 5-dihydrotestosterone strongly induced the accumulation of Zn-₂-gp mRNA in T-47D human breast cancer cells. Furthermore, the effect of these two hormones was shown to be additive, since the combination of both hormones produced a stimulation of Zn-₂-gp mRNA of at least 3-fold over that produced by either hormone alone. By contrast, the addition of 5-dihydrotestosterone, 17-estradiol, or progesterone failed to induce the expression of Zn-₂-gp. The stimulatory effect of glucocorticoids and androgens on Zn-₂-gp expression was produced in a time and dose dependent manner, without significantly affecting the cell proliferation rate. A time-course study demonstrated that the induction of Zn-₂-gp mRNA by androgens and glucocorticoids reached a level of 4 or 3.2-fold over the untreated control after seven days of incubation in the presence of a 10^–7 M concentration of 5-dihydrotestosterone or dexamethasone, respectively. A dose-response study showed that as little as 10^–11 M of 5-dihydrotestosterone or dexamethasone produced an accumulation of Zn-₂-gp mRNA of 2.4 or 2.1-fold over the control, respectively. On the basis of these results, we propose that Zn-₂-gp may be useful as a biochemical marker of breast carcinomas with a specific pattern of hormone responsiveness in whose development glucocorticoids and/or androgens may play a significant role.     

Recurrent breast cancer at 21 years after resection detected by serum tumor markers and manifested as dermatomyositis

A 52-year-old Japanese woman developed dermatomyositis. She had undergone a standard radical mastectomy for left breast cancer 21 years earlier. Though no physical sign of recurrent breast cancer appeared clinically, levels of tumor markers were abnormally elevated. Therefore, tamoxifen and CAF therapy were given. Further, the clinical course of dermatomyositis almost paralleled the level of serum tumor markers and the clinical course of her recurrent breast cancer. These markers were useful for detecting the recurrence, following the metastatic disease, and monitoring her response to therapy.     

Genetic variability in Gibberella fujikuroi and some related species of the genus Fusarium based on random amplification of polymorphic DNA (RAPD)

One of the most important rice pathogens is Fusarium moniliforme (perfect stage: Gibberella fujikuroi), the causal agent of the super-elongation (bakanae) disease. Thirty-seven strains of this species from different geographical regions were analyzed for their ability to produce gibberellins (GA) and for genetic relatedness by random amplified polymorphic DNA (RAPD). All GA-producing isolates showed nearly identical RAPD patterns using 51 oligonucleotide nona- and deca-mers as arbitrary primers. On the other hand, large differences between GA-nonproducing isolates were obtained. Comparison of the RAPD patterns with those of the tester strains of the six known mating populations (A,B,C,D,E,F) of G. fujikuroi showed that all producer strains belong to mating population C and all nonproducer isolates to other mating populations. Evidence for the usefulness of the RAPD technique to distinguish between mating populations was provided by sexual crossings. Consensus phylogenetic trees based on RAPDs were constructed by the Phylogenetic Analysis Using Parsimony (PAUP) system. In combination with morphological analysis, RAPD can distinguish between different species of the genus Fusarium. These investigations may find an application in the diagnosis of unknown Fusarium spp. and in distinguishing isolates of G. fujikuroi within the section Liseola.     

HBV不同血清学标志组合中HBV—DNA的分布特征

采用聚合酶链反应（PCR）技术对270例HBV不同血清学标志及不同组合进行了HBV-DNA的检测。揭示HBV-DNA在HBeAg标志中检出率最高,阳性率为100．00％;其次是HBsAg、抗-HBc和抗一HBe,阳性率分别为66．0％、65．9％和46．2％;在抗-HBS标志物中未能检出HBV-DNA。并示出了HBV-DNA在HBV血清学标志不同组合中的阳性率有着非常显著性差别,研究表明,在HBeAg阴性组合中,采用聚合酶链反应技术检测HBV-DNA的临床意义,同明还分析了HBV-DNA与性别、HBsAg滴度及ALT的关系。     

亲环素及其自身抗体与SLE活动性的相关性探讨

目的：探讨血浆与淋巴细胞内亲环素（ＣｙＰ）水平及抗亲环素自身抗体与全身性红斑狼疮（ＳＬＥ）活动性的关系。方法：用重组人亲环素（ｒｈＣｙＰ）制备单克隆和多克隆抗体,建立双抗体夹心ＥＬＩＳＡ法,测定血浆和细胞内ＣｙＰ水平,用ｒｈＣｙＰ包被反应板微孔,建立间接ＥＬＩＳＡ法检测抗ＣｙＰ自身抗体,对活动性和非活动性ＳＬＥ患者进行了观察。结果：ＳＬＥ患者含量分别为（３２３±４２０）μｇ／Ｌ和（２６４０±６５０）μｇ／ｇ蛋白,均显著高于正常对照组的（１６５±８０）μｇ／Ｌ和（２２９０±３８０）μｇ／ｇ蛋白;其中活动性ＳＬＥ患者又显著高于非活动性ＳＬＥ（Ｐ＜０．０５）。ＳＬＥ抗ＣｙＰ自身抗体阳性率（４８％）显著高于正常人（２．５％）,抗ＣｙＰ阳性与皮肤粘膜损害、关节痛、发热、白细胞减少、抗Ｓｍ抗体阳性密切相关。结论：血浆和淋巴细胞内ＣｙＰ升高和抗ＣｙＰ自身抗体阳性可反映ＳＬＥ活动性。     

化痰散结方含药血清诱导人肺癌细胞凋亡的机理研究

为探讨中药化痰散结方诱导人肺癌细胞 (SPC A1)凋亡的作用及其对正常人胚肺细胞的毒性作用 ,通过血清药理学方法 ,选择不同浓度的含药兔血清与人肺癌细胞共同孵育处理 ,并以正常人胚肺细胞 (HEL)作对照。结果 :人肺癌细胞经含中药兔血清作用 ,由贴壁生长而逐渐脱落 ,外形变圆 ,体积缩小 ,折光性增强 ;荧光镜下可见细胞核破碎 ,裂解为大小不等的凋亡小体 ;流式细胞仪检测显现典型的细胞凋亡峰 ,以 5%含药血清作用 4 8h凋亡峰最为明显 ,凋亡率为 4 2 .8% ;出现S期细胞阻滞 ;而该含药血清对人胚肺细胞无诱导凋亡作用。化痰散结方通过血清药理学方法诱导人肺癌细胞的凋亡 ,可能是其抗肿瘤的分子学机制之一。     

High Bilirubin Levels Interfere with Serum Tartrate-Resistant Acid Phosphatase Determination: Relevance as a Marker of Bone Resorption in Jaundiced Patients

Serum tartrate-resistant acid phosphatase (TRAcP) activity is considered to be a biochemical marker of bone resorption. Recently, a lack of specificity of collagen-related markers for assessing bone turnover has been observed in patients with chronic liver disease. Thus, it could be of great interest to determine serum TRAcP activity in such patients. However, nonspecificity of the analytical reaction could occur when hemolyzed, lipemic, or icteric specimens are analyzed. Therefore, we have studied the interference caused by bilirubin in the measurement of serum TRAcP activity using the Hillmann method. The interference was assessed in two pools of serum containing different bilirubin concentrations but with similar total AcP levels. Mixing proportional parts of the two pools, 10 samples were also obtained. Serum activities of total AcP and TRAcP, and the concentration of bilirubin were measured in the 10 samples. Both the actual and the expected values obtained by theoretical calculations were compared. Serum bilirubin values of 2.4 mg/dl showed a negative interference of 15% in the determination of serum TRAcP activity, whereas values of bilirubin higher than 10 mg/dl interfered totally with the measurement of serum TRAcP. Bilirubin did not interfere with the total AcP determination. This study clearly shows the interference of bilirubin in the determination of serum TRAcP. This finding should be considered when bone metabolism disorders are evaluated in jaundiced patients. Received: 6 April 1998 / Accepted: 1 October 1998     

Genetic markers in primary open-angle glaucoma

Purpose: To investigate possible associations between genetic markers and Primary Open-Angle Glaucoma (POAG). Methods: A number of genetic markers were typed in 84 unrelated patients with POAG and compared with a random sample of healthy individuals. The markers were Transferrin, Group Specific Component, G1m (1), G1m (2) and G3m (5) Allotypes, Adenylate Kinase, Adenosin Deaminase, Glyoxalase I and Acid Phosphatase and PCR-based markers HLA-DQA1 and D1S80. Results: No significant differences were found except the strong association between the group of POAG patients and Acid Phosphatase ACP^*C allele (² = 32.86; p < 0.0001). Conclusions: Since Acid Phosphatase gene is localized to chromosome 2p23, this result could be a first comprehensive step in the localization of POAG genes.     

Lack of prognostic significance of the monoclonal antibody Ki-S1, a novel marker of proliferative activity,in node-negative breast carcinoma

In a series of 205 node-negative breast cancers (NNBC), we determined staining by the novel antibody Ki-S1, a marker of tumor cell proliferation, in order to test its association with other prognostic variables and its prognostic significance. Ki-S1 was determined in routinely formalin-fixed paraffin-embedded tumor samples. Ki-S1 gave a nuclear staining in the majority of the carcinomas (188 of 205), with percentages of reacting nuclei ranging from 2% to 90% (median value of 7%). In 107 tumors frozen sections were available to also assess the Ki-67 antibody. Among these, 94 had a nuclear staining of cancer cells ranging from 5% to 80% (median value of 7%). In 46 tumors we also determined the MIB-1 antibody. The percentage of MIB-1 nuclear staining ranged from 1% to 50% (median value of 20%). There was no significant relationship between Ki-S1 and the other two cell kinetic markers. Ki-S1 labeling was significantly associated only with tumor size (p = 0.03).With a median follow-up of 6 years, Ki-S1 had no significant prognostic value for either relapse-free survival (RFS) or overall survival (OS)(Ki-S1 as continuous logarithmic variable; p = 0.86 and p = 0.23, respectively). For RFS the following variables had a significant prognostic value: Ki-67 ( 10% vs > 10%; p = 0.037); progesterone receptor (PgR) expression (– vs +/++; p = 0.041); tumor size (pT1 vs pT2–3; p = 0.042) and grading (GI vs GII–III; p = 0.047). For OS, tumor size (p = 0.0044), age (continuous variable; p = 0.0060), and Ki-67 (p = 0.043) were significantly prognostic.In multivariate analysis (final model), only tumor size retained a significant and independent prognostic value for RFS (p = 0.0042). For OS, both tumor size (p = 0.0029) and age ( 55 years vs > 55 years; p = 0.041) retained significance in the multivariate model.In conclusion, Ki-S1 does not seem to have prognostic relevance in this series of NNBC. Possible hypotheses to explain this observation are discussed.     

Reduced platelet MAO activity in healthy male students with blood group O

The association between the two genetic markers of affective disorders, ABO blood group system and platelet MAO (monoamine oxidase) activity was studied in 70 healthy young males. The platelet MAO activity of subjects with blood type O was significantly lower than that of subjects with blood type A and with blood types A + B AB + B together. This finding could constitute a "bridge" between the two genetic approaches to affective disorders.