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PubMed2004

Genome annotation of a 1.5 Mb region of human chromosome 6q23 encompassing a quantitative trait locus for fetal hemoglobin expression in adults.

BACKGROUND: Heterocellular hereditary persistence of fetal hemoglobin (HPFH) is a common multifactorial trait characterized by a modest increase of fetal hemoglobin levels in adults. We previously localized a Quantitative Trait Locus for HPFH in an extensive Asian-Indian kindred to chromosome 6q23. As part of the strategy of positional cloning and a means towards identification of the specific genetic alteration in this family, a thorough annotation of the candidate interval based on a strategy of in silico / wet biology approach with comparative genomics was conducted. RESULTS: The ~1.5 Mb candidate region was shown to contain five protein-coding genes. We discovered a very large uncharacterized gene containing WD40 and SH3 domains (AHI1), and extended the annotation of four previously characterized genes (MYB, ALDH8A1, HBS1L and PDE7B). We also identified several genes that do not appear to be protein coding, and generated 17 kb of novel transcript sequence data from re-sequencing 97 EST clones. CONCLUSION: Detailed and thorough annotation of this 1.5 Mb interval in 6q confirms a high level of aberrant transcripts in testicular tissue. The candidate interval was shown to exhibit an extraordinary level of alternate splicing - 19 transcripts were identified for the 5 protein coding genes, but it appears that a significant portion (14/19) of these alternate transcripts did not have an open reading frame, hence their functional role is questionable. These transcripts may result from aberrant rather than regulated splicing.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed2002

Expression and targeting of the tight junction protein CLDN1 in CLDN1-negative human breast tumor cells.

Claudins and occludin constitute the major transmembrane proteins of tight junctions (TJs). We have previously identified the human homologue of the murine Cldn1, CLDN1 (SEMP1) that is expressed in normal, mammary gland-derived epithelial cells but is absent in most human breast cancer cell lines. To investigate the potential functions of CLDN1 protein in tumor and normal epithelial cells, we developed an I-NGFR retroviral vector and monoclonal anti-CLDN1 antibody. In subconfluent and confluent breast cancer cells, MDA-MB-435 and MDA-MB-361, endogenous CLDN1 expression was not detected by an anti-CLDN1 monoclonal antibody by Western blot analysis or quantitative RT-PCR. When CLDN1-negative breast cancer cell lines were transduced with a CLDN1 retrovirus the cells express CLDN1 mRNA constitutively as shown by quantitative RT-PCR. Immunofluorescence analyses of the CLDN1 retroviral transduced breast tumor cells using monoclonal antibodies against CLDN1 reveals a subcellular distribution at cell-cell contact sites similar to the CLDN1 homing pattern in T47-D cells, which express endogenous CLDN1. This cell-cell contact co-localization of CLDN1 was evident in CLDN1-transduced breast tumor cells which fail to express occludin protein (MDA-MB-361 and MDA-MB-435) and express relatively little ZO-1 protein (MDA-MB-435), suggesting that other proteins may be responsible for targeting of CLDN1 to cell-cell contact sites. The re-expression of CLDN1 decreases the paracellular flux of 3 and 40 kDa dextran despite the absence of occludin in the MDA-MB-361 tumor cells. Our findings indicate that in CLDN1-negative breast tumor cells, the basal protein partner requirements for physiological homing of the CLDN1 protein are intact, and that CLDN1 gene transfer and protein expression itself might be sufficient to exert a TJ-mediate gate function in metastatic tumor cells even in the absence of other TJ-associated proteins, such as occludin.

Animals↗
PubMed2000

Analysis of mechanisms underlying BRMS1 suppression of metastasis.

Introduction of normal, neomycin-tagged human chromosome 11 (neo11) reduces the metastatic capacity of MDA-MB-435 human breast carcinoma cells by 70-90% without affecting tumorigenicity. Differential display comparing MDA-MB-435 and neo11/435 led to the discovery of a human breast carcinoma metastasis suppressor gene, BRMS1, which maps to chromosome 11q13.1-q13.2. Stable transfectants of MDA-MB-435 and MDA-MB-231 breast carcinoma cells with BRMS1 cDNA still form progressively growing, locally invasive tumors when injected in mammary fat pads of athymic mice but exhibit significantly lower metastatic potential (50-90% inhibition) to lungs and regional lymph nodes. To begin elucidating the mechanism(s) of action, we measured the ability of BRMS1 to perturb individual steps of the metastatic cascade modeled in vitro. Consistent differences were not observed for adhesion to extracellular matrix components (laminin, fibronectin, type IV collagen, type I collagen, Matrigel); growth rates in vitro or in vivo; expression of matrix metalloproteinases, heparanase, or invasion. Likewise. BRMS1 expression did not up regulate expression of other metastasis suppressors, such as NM23, Kai1, KiSS1 or E-cadherin. Motility of BRMS1 transfectants was modestly inhibited (30-60%) compared to parental and vector-only transfectants. Ability to grow in soft agar was also decreased in MDA-MB-435 cells by 80-89%, but the decrease for MDA-MB-231 was less (13-15% reduction). Also, transfection and re-expression of BRMS1 restored the ability of human breast carcinoma cells to form functional homotypic gap junctions. Collectively, these data suggest that BRMS1 suppresses metastasis of human breast carcinoma by complex, atypical mechanisms.

Animals↗
PubMed2002

Variable promoter region CpG island methylation of the putative tumor suppressor gene Connexin 26 in breast cancer.

Intercellular communication via gap junctions is a mechanism for tumor suppression. Connexin 26 (Cx26) is a structural component of gap junctions expressed by breast epithelial cells. Expression levels of Cx26 are reduced in many breast tumors. Methylation-sensitive single-stranded conformation analysis showed variable methylation in the promoter region CpG island in 11 out of 20 (55%) breast cancer patients. Heterogeneity in methylation patterns was observed both between and within tumors. The degree of methylation ranged from a few CpG dinucleotides to almost all the CpG dinucleotides in the analyzed region. The most frequently methylated CpG was in an Sp1 site known to be important for Cx26 gene expression. One of eight breast cancer cell lines (MD-MBA-453) was methylated in the promoter region and did not express Cx26. Treatment of MDA-MB-453 with 5-aza-2'-deoxycytidine resulted in the re-expression of Cx26 mRNA. Methylation of the promoter region is likely to be an important mechanism in modulating the expression of Cx26 in breast cancer.

Antimetabolites, Antineoplastic↗
PubMed1994

Rapid acquisition of multicellular drug resistance after a single exposure of mammary tumor cells to antitumor alkylating agents.

BACKGROUND: Clinical drug resistance is either intrinsic (de novo) or often acquired rapidly in conjunction with chemotherapy. By contrast, the selection of drug-resistant mutant cell lines in monolayer culture systems is usually a more protracted process. Sublines of mouse EMT-6 mammary tumor cells selected for resistance to various alkylating agents in vivo after serial passage into syngeneic mice manifest their resistance in vitro only when cultured as three-dimensional multicellular aggregates or spheroids. PURPOSE: We examined whether a single exposure of mouse EMT-6 or human MDA-MB-231 breast cancer cells to alkylating agents in vitro is sufficient for the induction of a resistance phenotype, which may be detected by re-applying the drugs to cells grown as three-dimensional aggregates. METHODS: Mouse EMT-6 and human MDA-MB-231 breast cancer cells cultured as three-dimensional aggregates were exposed to a single dose of alkylating agent for 1-5 days. Aggregates were dispersed, and cells were plated as monolayer cultures for up to 8 weeks to allow for recovery. Colony-forming ability was assessed after a subsequent alkylating-agent exposure of cells cultured as monolayers or three-dimensional aggregates. RESULTS: A single in vitro exposure to 12.5-microM cisplatin (CDDP) for 5 days or 25 microM 4-hydroperoxycyclophosphamide (4-O2H CTX) for 1 or 3 days without changing the medium was sufficient to induce transient but substantial resistance in EMT-6 cells as determined by clonogenic assays. Such resistance was not detected when monolayer cell cultures were used. The concentration of 4-O2H-CTX and the length of time the cells remained in three-dimensional culture after initial exposure to this drug was associated with the degree of subsequent drug resistance of cells grown as three-dimensional cultures. Furthermore, this acquired resistance after a single drug exposure was accompanied by changes in the three-dimensional architecture of the cell aggregates, which now formed much more compact multicellular spheroids. Similarly, a single exposure to 4-O2H-CTX was enough to bring about resistance in MDA-MB-231 cells detectable only in three-dimensional cultures, as well as the change in three-dimensional architecture. CONCLUSIONS: Rapid acquisition of resistance likely represents a physiologic mechanism of adaptation operative at the multicellular level rather than a stable genetic change and may be one of the reasons for the rapid development of drug resistance acquired by tumors in vivo. IMPLICATIONS: In vivo drug exposure may result in transient and low levels of drug resistance that may nevertheless be clinically relevant.

Animals↗
PubMed1998

[Early exclusion of ischemic myocardial damage made possible by new biochemical cardiac markers].

New immunochemical assay methods for the cardiac markers creatine kinase (CK) MB mass, myoglobin, troponin T (TnT), troponin I (TnI), fatty acid binding protein (FABP) necessitate re-evaluation of their usefulness in the early diagnosis of myocardial damage. Cardiac markers play an important part in the exclusion of myocardial damage in patients with chest pain and an inconclusive ECG at admission. A serial CK-MB mass determination is particularly suitable for this exclusion of myocardial damage. The sensitivity of TnT shortly after an infarction is comparable with that of CK-MB mass; a single determination on admission is insufficient. The marker myoglobin is of limited value owing to the brief duration of myoglobin rise and insufficient heart specificity. An increased TnT or TnI value in patients with unstable angina pectoris is a prognostically negative sign. It is still not clear how this prognosis can be improved. A negative troponin finding appears not to exclude early complications. The department of Emergency Cardiac Care of the Academic Medical Centre, Amsterdam, the Netherlands, currently prefers the serial measurement of the CK-MB mass, in the future possibly to be supplemented by a troponin determination.

Angina Pectoris↗
PubMed2002

Early dysfunction and long-term improvement in endothelium-dependent vasodilation in the infarct-related artery after thrombolysis.

OBJECTIVES: This study assessed the degree of endothelial dysfunction in post-acute myocardial infarction (AMI) and its subsequent status in the infarct-related artery (IRA) in patients treated with thrombolysis. BACKGROUND: Coronary flow reserve alterations in the IRA after thrombolysis have been described, but the endothelium-dependent vasomotion has not been investigated, to date. METHODS: Endothelial function in patients after thrombolysis was assessed by infusion of acetylcholine (ACh) at increasing doses in the IRA. Diameter changes in the distal segments were evaluated using quantitative coronary angiography. Patients with coronary atherosclerosis constituted the control group. Clinical variables, electrocardiography and biochemical markers were used to determine the timing of reperfusion and the extent of the infarct. Patients in the AMI group were re-evaluated one year later. RESULTS: In the initial assessment, 16 patients showed a vasoconstriction response to ACh in the IRA compared to the control group (-20 +/- 21% vs. 4 +/- 4%; p < 0.01). Significant correlations between the degree of vasoconstriction and maximum value of the creatine kinase-MB fraction and number of new Q waves were observed. Of the 12 patients re-evaluated, 4 had complete occlusion of the IRA. In the remaining eight patients with patent artery, an improvement in response to ACh was observed relative to the initial study (+3 +/- 11%, vs. -19 +/- 15%, p < 0.05). CONCLUSIONS: In patients with AMI treated with thrombolysis, severe endothelial dysfunction in the IRA is observed early. In patients who retain patency of the IRA, the endothelial dysfunction improves during the follow-up and suggests a component of stunned endothelium in the first few days post-AMI.

Aged↗
PubMed1997

Human mini-chromosomes in mouse embryonal stem cells.

We have introduced human mini-chromosomes of 4 Mb and approximately 15 Mb in size into mouse embryonal stem cells. Although these human mini-chromosomes are stable in hamster and chicken cells, they re-arrange or segregate aberrantly in the embryonal stem cells and are rapidly lost in the absence of selection. However, one of the mini-chromosomes re-arranged, acquired mouse centromeric sequences and was then stably maintained for at least 60 population doublings in culture. This mini-chromosome, which is 4 Mb in size, is a candidate for a mouse germ line chromosome vector.

Animals↗
PubMed2005

Application of a new type of moving bio-film in aerobic sequencing batch reactor (aerobic-SBR).

A moving bio-film (MB), made from the inner tube of used tyres was applied in a conventional-aerobic-SBR for increasing the system efficiency and quality of bio-sludge due to good sedimentation (the density of 1.925+/-0.21 g/cm(3)), non-biodegradability and re-usability of the media without any regeneration. The total bio-sludge mass of the MB-aerobic-SBR was about 30% higher than that of the conventional-aerobic-SBR resulting in a reduction of the F/M value of the system and amount of suspended bio-sludge waste. The amount of suspended bio-sludge waste, SVI and SRT of the MB-aerobic-SBR under a low organic loading of 80+/-9.3g BOD(5)/m(3)-d were 1,485+/-146 mg/d, 51+/-3.7 ml/g and 10.1+/-5.1 days, respectively while they were 1,800+/-152 mg/d, 69+/-4.0 ml/g and 8.3+/-5.3 days, respectively in the conventional-aerobic-SBR. The BOD(5), TKN and TP removal efficiencies of the MB-aerobic-SBR were about 1-2, 2-3 and 10-12% higher, respectively, than that of the conventional-aerobic-SBR. Also, the BOD(5) and COD removal efficiencies of the MB-aerobic-SBR were higher than 95% even when the system was operated with synthetic wastewater containing 800 mg/l BOD(5) under a very low HRT of 1.5 days (organic loading of 528+/-50.8 g BOD(5)/m(3)-d). The effluent BOD(5), COD, total kjeldahl nitrogen, total phosphorus and suspended solids of the MB-aerobic-SBR under a high organic loading of 528+/-50.8 g BOD(5)/m(3)-d were 45+/-5.1, 37+/-3.6, 4.1+/-1.0, 1.5+/-0.80 and 41+/-2mg/l, respectively.

Aerobiosis↗
PubMed2006

ST7-mediated suppression of tumorigenicity of prostate cancer cells is characterized by remodeling of the extracellular matrix.

Multiple lines of evidence have provided compelling evidence for the existence of a tumor suppressor gene (TSG) on chromosome 7q31.1. ST7 may be the target of this genetic instability but its designation as a TSG is controversial. In this study, we show that, functionally, ST7 behaves as a tumor suppressor in human cancer. ST7 suppressed growth of PC-3 prostate cancer cells inoculated subcutaneously into severe combined immunodeficient mice, and increased the latency of tumor detection from 13 days in control tumors to 23 days. Re-expression of ST7 was also associated with suppression of colony formation under anchorage-independent conditions in MDA-MB-231 breast cancer cells and ST7 mRNA expression was downregulated in 44% of primary breast cancers. Expression profiling of PC-3 cells revealed that ST7 predominantly induces changes in genes involved in re-modeling the extracellular matrix such as SPARC, IGFBP5 and several matrix metalloproteinases. These data indicate that ST7 may mediate tumor suppression through modification of the tumor microenvironment.

Base Sequence↗
PubMed1986

Pathogenesis of haemagglutinating encephalomyelitis virus (HEV) in mice experimentally infected by different routes.

Three-day-old suckling mice inoculated intracerebrally (i.c.) with the 67N strain of haemagglutinating encephalomyelitis virus (HEV) showed nervous signs and died. The virus was passaged 10 times in suckling mice and was designated the MB-67N strain. The pathogenesis of MB-67N was studied with various ages of mice and inoculation routes. All mice inoculated i.c. with a large dose of virus died regardless of age, although a smaller dose caused fatal infection only in suckling mice. By intranasal, intraperitoneal and subcutaneous inoculation, the virus also killed suckling mice under 16 days old, but not older mice, even with a large dose. The susceptibility of mice for the MB-67N strain was influenced by age and inoculation routes. High titres of virus were re-isolated from the brain of diseased mice after inoculation by any route, but not from other organs. Histologically, numerous areas of severe focal necrosis were produced in the cerebral cortex. Specific immuno-fluorescence and numerous viral particles were found in the cytoplasm of nerve cells by immuno-fluorescence staining and electron microscopy. These findings indicate that the MB-67N propagates mainly in the central nervous system and nerve cells serve as a main target of virus replication.

Animals↗
PubMed2004

Evaluation of antineoplastic action of 5-aza-2'-deoxycytidine (Dacogen) and docetaxel (Taxotere) on human breast, lung and prostate carcinoma cell lines.

The antineoplastic activity of 5-aza-2'-deoxycytidine (5-AZA-CdR) and docetaxel (Taxotere, Taxo) alone or in combination against human MDA-MB-231 breast, Calu-6 lung and DU-145 prostate carcinoma cell lines was evaluated by clonogenic assay. We also investigated by RT-PCR the capacity of these agents to re-activate the expression of E-cadherin and maspin, two tumor suppressor genes that were silenced by DNA methylation. 5-AZA-CdR and Taxo in combination produced a greater loss of clonogenicity than either agent alone. In MDA-MB-231 breast carcinoma cells, Taxo did not interfere with the re-activation of E-cadherin and maspin genes by 5-AZA-CdR. These results provide a rationale for clinical trials on the combination of 5-AZA-CdR and Taxo in patients with advanced cancer.

Antineoplastic Agents↗
PubMed1999

Fate of unstable Bacillus subtilis subgenome: re-integration and amplification in the main genome.

The plastic Bacillus subtilis genome was dissected into two physically separate genomes, the 3.9 Mb main genome and the 0.3 Mb subgenome. DNA replication of the main genome was initiated from the normal replication origin (oriC) and that of the subgenome was from a 7.2 kb oriN-containing fragment artificially inserted. When the 7.2 kb fragment was shortened to a 1.5 kb fragment that contains oriN but lacks the segregational function, the subgenome became unstable and was rapidly lost from the cell, producing inviable cells due to the loss of essential genes carried by the subgenome. Stable survivors were isolated in which the subgenome had re-integrated and multiplied in the main genome. These results suggest that a reduced genetic stability of the subgenome induces size variation of the B. subtilis genome.

Bacillus subtilis↗
PubMed1984

Clinical effectiveness of the Du Pont aca measurement of creatine kinase MB in serum from patients in a coronary-care unit.

We evaluated the clinical effectiveness of measuring creatine kinase (CK; EC 2.7.3.2) isoenzyme MB and lactate dehydrogenase (LD; EC 1.1.1.27) isoenzymes in diagnosis of acute myocardial infarction. We used an agarose electrophoresis method to measure CK and LD isoenzymes and the Du Pont aca column method to measure CK-MB. Serial blood specimens were drawn from 100 patients consecutively admitted to our Coronary Care Unit. Because of the low diagnostic specificity for CK-MB measurements by both agarose electrophoresis and the discrete-analysis method, as compared with reported values, we re-evaluated our isoenzyme data by using Receiver Operating Characteristic curves. Such analysis of the data established optimal decision levels of greater than or equal to 25 U/L and greater than or equal to 18 U/L plus greater than or equal to 6% of total CK for serum CK-MB measured by the agarose electrophoresis and the aca methods, respectively, and an optimal decision level of greater than or equal to 0.92 for the ratio of LD 1/2 measured after agarose electrophoresis. At these decision levels we obtained a sensitivity of 100%, 100%, and 95% and a specificity of 94%, 92%, and 90% for CK-MB (agarose electrophoresis), CK-MB (aca), and the LD 1/2 ratio, respectively.

Autoanalysis↗
PubMed1991

Nucleotide sequence and expression of the glucoamylase-encoding gene (glaA) from Aspergillus oryzae.

The glucoamylase-encoding gene (glaA) from Aspergillus oryzae was cloned using its cDNA as a probe, which had been isolated previously. From comparison of nucleotide (nt) sequences of genomic clones with its cDNA, the glaA gene was found to contain four short putative introns, 45-56 nt in length. The A. oryzae glaA gene shared 62% homology at the nt level with the A. niger glaA gene with the four introns located at the same position. The 5'-flanking region contained a TATA box at nt-72 from the start codon, and two putative CAAT sequences at nt-87 and -331. Genomic Southern analysis and physical mapping showed that the glaA gene is located on the smallest chromosome (3.4 Mb) of six separated bands of chromosomes. Clones containing the glaA gene, when re-introduced intro A. oryzae, resulted in a three- to eightfold increase in glucoamylase activity.

Amino Acid Sequence↗
PubMed1992

Growth regulation of estrogen receptor-negative breast cancer cells transfected with complementary DNAs for estrogen receptor.

BACKGROUND: The growth of estrogen receptor (ER)-positive breast cancer cells is hormonally regulated, but the majority of breast cancers are ER negative and unresponsive to hormonal therapy. PURPOSE AND METHODS: To test whether hormonal control over replication can be re-established in ER-negative cells, we transfected ER-negative MDA-MB-231 (clone 10A) cells with sense and antisense constitutive ER expression vectors containing the gene for either wild-type or mutant ER linked to the gene for neomycin resistance aminoglycoside phosphotransferase (neo). A Northern blot analysis was done on total RNA from eight of the 10 transfectant clones produced to detect messenger RNA coding for ER and neo, and a Western blot analysis was done on protein extracted from the cells of one mutant and two wild-type ER sense transfectant clones to determine the molecular weight of the ER in transfectants. Levels of ER in transfectants were measured both by enzyme immunoassay and by ligand-binding methods. To ascertain whether the ER in wild-type and mutant sense transfectants was functional, we tested the effects of 17 beta-estradiol (E2) and/or an antiestrogen, ICI 164,384, on 1) ER-activated gene regulation (by transient transfection of these cells a second time with a reporter plasmid containing an estrogen response element linked to the chloramphenicol acetyl transferase [CAT] gene), 2) induction of progesterone receptor, 3) DNA replication, and 4) cell cycle kinetics. RESULTS: Messenger RNA coding for ER and for neo was detectable in both sense and antisense transfectant clones. Sense transfectants (both mutant and wild-type) expressed ER protein with a molecular weight similar to that found in ER-positive control cells. By the ligand-binding method high levels of ER were detected in both wild-type and mutant transfectants, although by the enzyme immunoassay method lower levels were detected in mutant transfectants. ER from both wild-type and mutant sense transfectants appeared functional, since E2 stimulated the expression of reporter-linked CAT and of progesterone receptor in these transfectants. E2 inhibited DNA replication in wild-type sense transfectants at a concentration of 10(-10) M and mutant sense transfectants at a concentration of 10(-8) M, and ICI 164,384 blocked this effect. CONCLUSION: ER-negative breast cancer cells stably transfected with either a mutant or wild-type ER gene regain hormonal responsiveness; however, E2 inhibits rather than stimulates cell growth. IMPLICATION: Reactivation of quiescent ER may provide a novel therapeutic approach for controlling ER-negative breast cancers.

Base Sequence↗
PubMed2004

[Study on the clinical value of serum cardiac troponin T in early diagnosing of acute non-Q-wave myocardial infarction and prognostic evaluation].

OBJECTIVE: To investigate the value of serum cardiac troponin T (cTnT) in diagnosing earlier acute non-Q-wave myocardial infarction (NQMI) and judging the prognosis. METHODS: Seventy-four NQMI patients and 118 Q-wave myocardial infarction (QMI) patients were studied. Serum cTnT and MB isoenzyme of creatine kinase (CK-MB) levels were monitored on fixed time. On the 15th day of hospitalization, 99 mTc-MIBI myocardial single photon emission computed tomography (SPECT) was performed to assess the infarct size index. Clinical informations of the two groups such as cardiac dysfunction, re-infarction, fatal cadiac arrhythmia, sudden death were collected. RESULTS: The time for serum cTnT beginning to rise was earlier than CK-MB. Its peak time value was paralled to that of CK-MB, and cTnT elevation lasted longer than CK-MB. Serum cTnT and CK-MB peak value showed positive correlation with the infarct size index (both P<0.01). The peak values of cTnT and CK-MB in NQMI group were lower than those in QMI group, and the infarct size was smaller than QMI group (all P<0.05). The frequencies of cardiac events were significantly raised in both groups when there was a high level of serum cTnT. But the proportion in NQMI group was less than those in QMI group (P<0.05). The cardiac events in NQMI group were less than that in QMI group (P<0.05). CONCLUSION: Serum cTnT is an effective marker for diagnosing earlier NQMI, detecting myocardial damage, estimating infarct size and prognosis in the nearly future.

Aged↗