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PubMed1981

Prt-4 and Prt-5: new constituents of a gene cluster on chromosome 7 coding for esterproteases in the submandibular gland of the house mouse (Mus musculus).

The heredity and linkage of gene loci were established for two different enzymes with esterproteolytic activity from mouse submandibular gland: protease A and protease E. Based upon strain distribution and biochemical properties of the two esterproteases, the existence of two corresponding structural loci is proposed: Prt-4 (protease A) and Prt-5 (protease E). Prt-4 and Prt-5 proved to be different from Tam-1. From a four-point-cross, the gene order Gpi-1-(Tam-1, Prt-4, Prt-5)-c is suggested. Thus a gene cluster was shown to exist on chromosome 7 coding for esterproteases, all of which are controlled by testosterone.

Alleles↗
PubMed1991

Quercetin inhibits the growth of a multidrug-resistant estrogen-receptor-negative MCF-7 human breast-cancer cell line expressing type II estrogen-binding sites.

It has been demonstrated that the flavonoid quercetin (3,3',4',5,7-pentahydroxyflavone; Q) inhibits the growth of several cancer cell lines. There is evidence suggesting that the antiproliferative activity of this substance is mediated by the so-called type II estrogen-binding site (type II EBS). We looked for the presence of type II EBS and the effect of Q on the proliferation of an Adriamycin-resistant estrogen-receptor-negative human breast-cancer cell line (MCF-7 ADRr). By whole-cell assay using estradiol labelled with 6,7-tritium [( 3H]-E2) as a tracer, we demonstrated that MCF-7 ADRr cells contain type II EBSs. Competition analysis revealed that diethylstilbestrol (DES) and Q competed with similar potency for [3H]-Es binding to type II EBSs. The antiestrogen tamoxifen (TAM) competed for type II EBSs, albeit to a lesser extent than either DES or Q. Growth experiments demonstrated that Q and DES exerted a dose-dependent inhibition of cell proliferation in the range of concentrations between 10 nM and 10 microM, whereas TAM was less effective. Q could also inhibit colony formation in a clonogenic assay. Our results indicate that multidrug-resistant estrogen-receptor-negative MCF-7 cells express type II EBSs and are sensitive to the inhibitory effect of Q. This substance could be the parent compound of a novel class of anticancer agents.

Binding Sites↗
PubMed1983

Prednimustine in combination with methotrexate and 5-fluorouracil in advanced breast cancer: a phase I-II study.

Forty-seven patients with advanced breast cancer were treated with a combination of prednimustine (P), methotrexate (M), 5-fluorouracil (F), and tamoxifen (TAM). Twenty-six patients received P, 80 mg/m2 day 1-5 (series I) and 21 patients received P, 100 mg/m2 day 1-5 (series II). Both series of patients received M, 40 mg/m2 day 1 and 8 and F, 600 mg/m2 day 1 and 8 with a cycle duration of 4 weeks. All patients received TAM 20 mg twice daily. As concerns the haematologic toxicity, WBC were depressed significantly more often than platelet counts, and during the first 3 cycles 70% of the patients had a WBC nadir corresponding to toxicity grade II or more. No signs of cumulative haematologic toxicity were observed. Nausea and vomiting were registered in 40 out of 47 patients but in 35 of these only of grade I-II. Only one patient developed alopecia requiring a wig. The response to treatment could be evaluated in 28 patients, 21 of whom experienced response (CR or PR) of a median duration of 13 months. In conclusion, it seems that prednimustine can be safely used in combination with methotrexate and 5-fluorouracil. The frequency of alopecia is definitely lower than with CMF. Whether this relates also to subjective side effects will require a randomized study, as will a final conclusion concerning the efficacy compared to that of CMF.

Aged↗
PubMed1996

The effects of cyclosporin A, tamoxifen, and medroxyprogesterone acetate on the enhancement of adriamycin cytotoxicity in primary cultures of human breast epithelial cells.

Adriamycin (Adr), the single most active agent used in the treatment of breast cancer, may become ineffective as treatment progresses due to the development of multidrug resistant (MDR) tumors. A major mechanism associated with MDR is increased P-glycoprotein (Pgp) expression. This study examined the abilities of the anti-estrogen tamoxifen (TAM) and the progestin medroxyprogesterone acetate (MPA) as well as cyclosporin A (CsA), a known resistance modifier, to enhance the cytotoxic effects of Adr on human breast epithelial cells (HBEC) in primary culture. Pgp and estrogen receptor (ER) expression were determined in each of the cultures by immunocytochemical assays using the monoclonal antibodies C219 and H222 Sp gamma, respectively. The Adr-sensitive, Pgp-, ER+ MCF-7 cell line and the Adr-resistant, Pgp+, ER- MCF7-AdrR cell line were used as controls. Primary cultures were categorized as HBEC from tissues with or without previous chemotherapy. Pgp was detected in 1 of the 15 cell cultures from tissues without previous chemotherapy and in 5 of the 6 cell cultures from tissues previously exposed to chemotherapy. Incubation with either CsA or MPA plus Adr enhanced Adr toxicity in Pgp+ but not Pgp- cell cultures, whereas TAM had no effect on the sensitivity of any of the cultures. Of the 21 primary cultures of HBEC, 3 were ER+. There was no correlation between the enhancement of Adr cytotoxicity and ER status. The data suggest that MPA as well as CsA may be useful as modifying agents in overcoming Pgp-associated multidrug resistance.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1990

In vitro sensitivity testing of human breast cancer cells to hormones and chemotherapeutic agents.

The sensitivities of human breast cancer cells to hormones and chemotherapeutic agents were measured using a new in vitro assay. Tumor cells from individual patients were cultured on collagen-coated dishes in medium containing the patient's serum. The rationale for use of the patient's serum is that the components of this serum interact with the cells and therapeutic agents in vivo. Cells were incubated for the length of the assay in the presence or absence of estrogen (E2) with or without tamoxifen (TAM) or in the presence or absence of cortisol (F). At 1 day after cell seeding, cells were exposed to a chemotherapeutic agent, Adriamycin, melphalan, or 5-fluorouracil, for 24 h. After a 48-h recovery period, [3H]-thymidine ([3H]-TdR) was added to the cultures for 24 h. Depending on the concentration, E2 generally stimulated or inhibited incorporation of [3H]-TdR into the DNA of cells from estrogen-receptor (ER)-positive tumors. TAM eliminated the effects of E2. F generally stimulated or inhibited incorporation in cells with no correlation to ER status. Stimulation of [3H]-TdR incorporation by hormones increased cell sensitivity to Adriamycin. In contrast, hormone inhibition of [3H]-TdR incorporation decreased cell responsiveness to this drug. This rapid assay, which can measure the sensitivities of breast carcinoma cells to hormones and drugs and identify effective combinations of therapeutic agents, should lead to a rational selection of treatment for the individual patient.

Adult↗
PubMed1997

Meta-Analysis of the Second Collaborative Study of Adjuvant Chemoendocrine Therapy for Breast Cancer (ACETBC) in Patients with Stage II, Estrogen-Receptor-Positive Breast Cancer.

The second 5-year study of postoperative adjuvant therapy in patients with breast cancer between 1985 and 1988 was performed by the Study Group for Adjuvant Chemoendocrine Therapy for Breast Canecr (ACETBC). This report describes the results of a meta-analysis of the outcome. A total of 3012 patients with stage II, estrogen-receptor-positive primary breast cancer who underwent radical surgery (total mastectomy with at least axillary dissection) were eligible for the analyses. On the day of surgery, all patients received 13 mg/m(2) of mitomycin C (MMC) intravenously. Patients were then given one of two adjuvant chemoendocrine therapies for 2 years:regimen A, consisting of tamoxifen citrate (TAM) 30 mg/day, or regimen B, consisting of TAM 30 mg/day plus tegafur (Futraful, FT)600 mg/day. The results from all eligible patients were included in a meta-analysis according to the method of Peto et al. The odds reduction rate was 12 +/-13% (log-rank test, P= 0.35)for the 5-year survival rate and 16 +/- 10% (log-rank test, P=0.093)for the 5-year non-recurrence rate. In terms of the 5-year non-recurrence rate. regimen B(with FT)yielded slightly, but not significantly, better results than regimen A. In addition, stratified analyses were carried out with respect to the 5-year non-recurrence rate. Regimen B(with FT)yielded significantly better results than regimen A in patients with four or more positive axillary nodes (log-rank test, P= 0.039) and yielded slightly, but not significantly, better results than regimen A in premenopausal patients (log-rank test, P= 0.079).

Journal Article↗
PubMed1994

The Role of Chemoendocrine Agents in Postoperative Adjuvant Therapy for Breast Cancer: Meta-analysis of the First Collaborative Studies of Postoperative Adjuvant Chemoendocrine Therapy for Breast Cancer (ACETBC).

The first collaborative studies of postoperative adjuvant chemoendocrine therapy for breast cancer (ACETBA) were carried out in 6 regions of Japan from 1982 to 1985, and the results were subjected to meta-analysis. Subjects consisted of stage II and IIIa cases who underwent radical mastectomy with Brt + Ax or more extensive resection for primary breast cancer. Regimen A consisted of tegafur (Futraful:FT) alone at 600 mg/day, and regimen B of FT at 600 mg/day with tamoxifen (TAM) at 20 mg/day. The duration of the treatment was one year in the Tohoku and Kinki regions, and 2 years in the other 4 regions. Meta-alalysis by Peto's method showed an odds reduction of 20+/- 7% (logrank test: P = 0.0069) for the 5-year overall survival rate in 4740 eligible patients, and 25 +/- 6%(logrank test: P <0.0001)for the 5-year disease-free survival rate. The odds reductions were both statistically significant, indicating that the adjuvantchemoendocrine therapy was effective. Subset analysis of data on 5-year disease-free survival showed that FT plus TAM therapy was better in ER-positive and post-menopausal patients, whether axillary lymph nodes were positive or negative.

Journal Article↗
PubMed1994

Conventional Dose CAF Therapy versus Low Dose Adriamycin Therapy in the Treatment of Advanced Breast Cancer.

A controlled randomized trial was conducted to compare the effectiveness of a conventional dose of CAF therapy with that of a low dose of adriamycin (ADR) therapy for the treatment of advanced Breast Cancer. The doses of medication for the conventional CAF therapy were 100 mg/body of cyclophosphamide (CPA) p.o. daily fort wo weeks, 30 mg/m(2) of ADR and 500 mg/m(2) of 5-fluorouracil (5-FU) i.v. on days 1 and 8 for induction, and 200 mg/body of 5-FU and 20 mg/body of tamoxifen (TAM) p.o. daily for maintenance. Those for the low dose ADR therapy were 15mg/m(2) of ADR i.v. at two-week intervals for one year and 200 mg/body of 5-FU and 20 mg/body of TAM p.o. daily. Eighty patients were entered in this trial. All patients were randomly divided into two groups with stratification for estrogen receptor status. Of 78 patients among them, 38 undergoing the CAF therapy and 40 undergoing the low dose ADR therapy, were evaluated for efficacy assesment. The background factors analyzed were well balanced in both groups. The response rate was 47%(6CR, 12PR out of 38) in the CAF group and 43% (3CR, 14PR out of 40) in the low dose ADR group. There was no significant difference in response rates and survival rates as determined by the Kaplan Meier method between the two groups. The CAF therapy had significantly more toxicity than the low dose ADR therapy. Therefore, it was concluded that this low dose ADR therapy can be regarded as a treatment of choice for advanced breast cancer.

Journal Article↗
PubMed2003

[Urological complications of endometriosis].

Endometriosis (E) of the urinary tract is often not diagnosed at the beginning of the disease, particularly in cases with bladder wall involvement resulting in persistent dysuria and pelvic pain. Therefore, cystitis-like symptoms in younger women without evidence of urinary tract infections should be considered to be caused by E. Characteristic endoscopic findings may be missed and deep transurethral resection may be necessary for harvesting endometriotic tissue. This situation and improvement of diagnosis by ultrasound are demonstrated by a case report. The development of endometrial polyps in the uterus after tamoxifen (TAM) management is a well-known side effect of this antiestrogenic therapy. We observed a woman with endometrial polyps in the bladder after TAM. Endometriotic ureter stenosis in the absence of colics or other symptoms may results in irreversible loss of kidney function. Verification of the diagnosis is a common task of urology and gynecology. In three of six cases treated in our institution within 5 years, E of the ureter was first ascertained by the presence of ureter damage following surgical treatment of E. In two cases bowel E was present at the same time. Conservative treatment by suppression of ovarian function in most cases of stenosis of the ureter does not avoid the need for subsequent resection and reimplantation because of persistent fibrosis of the ureter wall.

Adult↗
PubMed2004

Microsatellite markers associated with two Aegilops tauschii-derived greenbug resistance loci in wheat.

A new source of greenbug (Schizaphis graminum Rondani) resistance derived from Aegilops tauschii (Coss.) Schmal was identified in W7984, a synthetic hexaploid wheat line and one parent of the International Triticeae Mapping Initiative (ITMI) mapping population. Segregation analysis of responses to greenbug feeding in a set of recombinant inbred lines (RILs) identified a single, dominant gene governing the greenbug resistance in W7984, which was placed in chromosome arm 7DL by linkage analysis with molecular markers in the ITMI population. Allelism tests based on the segregation of responses to greenbug feeding in F2 and testcross plants revealed that the greenbug resistance in W7984 and Largo, another synthetic line carrying the greenbug resistance gene Gb3, was controlled by different but linked loci. Using the ITMI reference map and a target mapping strategy, we have constructed a microsatellite map of Gb3 in a mapping population of 130 F7 RILs from Largo x TAM 107 and identified one marker (Xwmc634) co-segregating with Gb3 and four markers (Xbarc76, Xgwm037, Xgwm428 and Xwmc824) closely linked with Gb3. Deletion mapping of selected microsatellite markers flanking the Gb3 locus placed this resistance gene into the distal 18% region of 7DL. Comparative mapping in the ITMI and Largo x TAM 107 populations using the same set of microsatellite markers provided further evidence that greenbug resistance in W7984 and Largo is conditioned by two different loci. We suggest that the greenbug resistance gene in W7984 be designated Gb7. The microsatellite map of Gb3 constructed from this study should be a valuable tool for marker-assisted selection of Gb3-conferred greenbug resistance in wheat breeding.

Animals↗
PubMed2006

Activation of complement C3, C5, and C9 genes in tumors treated by photodynamic therapy.

Cancer therapies, which deliver a rapidly induced massive tumor tissue injury, such as photodynamic therapy (PDT), provoke a strong host response raised for dealing with the inflicted local trauma. Activated complement system was identified as an important element of host response elicited by tumor PDT. The expression of genes encoding complement proteins C3, C5, and C9 was studied following tumor PDT mediated by photosensitizer Photofrin using mouse Lewis lung carcinoma (LLC) model. Treated tumors and the livers of host mice were collected at different times after PDT and the expression of the investigated genes was analyzed by RT-PCR. The results show a significant up-regulation of C3, C5, and C9 genes in PDT-treated tumors at 24 h after therapy, while no significant increase in the expression of these genes was found in the liver tissues. The expression of C3, C5, and C9 genes also became up-regulated in untreated tumor-associated macrophages (TAMs) co-incubated in vitro with PDT-treated LLC cells. This effect was abolished or drastically reduced in the presence of antibodies blocking heat shock protein 70 (HSP70), Toll-like receptor (TLR) 2 and TLR4, and specific peptide inhibitors of TIRAP adapter protein and transcription factor NF-kappaB. The presented study reveals that complement genes C3, C5, and C9 become up-regulated in tumors treated by PDT, but not in the host's liver. Tumor-localized up-regulation of these genes can be largely attributed to monocytes/macrophages invading the treated lesion after PDT. This effect appears to be induced by the recognition of danger signals from PDT-treated tumor cells such as HSP70 by TAMs that involve the TLR2- and TLR4-triggered signal transduction pathways leading to the activation of NF-kappaB.

Animals↗
PubMed1999

Low dose T-cell lymphocyte infusion combined with marrow T-cell depletion as prophylaxis of acute graft vs host disease for HLA identical sibling bone marrow transplantation.

T-cell depletion (TCD) of the bone marrow graft remains the most effective method to prevent severe graft versus host disease after allogeneic bone marrow transplantation. Early studies of HLA-identical sibling transplants showed that although T-cell depletion decreased GVHD, T-cell depleted transplants had higher risks of graft failure and leukemia relapse, leukemia free survival (LFS) was not improved compared to non-T-cell depleted transplants. In order to avoid graft failure and increased risk of relapse associated with this approach, we initiated a pilot study of T-cell depletion of the marrow graft combined with reinfusion of a fixed quantity of CD2+ peripheral blood T-cells. Depletion technique consisted in negative purging using CD2 and CD7 monoclonal antibodies (MoAbs) followed by rabbit complement cytolysis. This approach was associated with an intensified conditioning regimen using total body irradiation, high-dose cytosine arabinoside and melphalan (TAM) for all but one patient. Twenty-one patients were included with a mean age of 40 years. Only one acute severe Graft Versus Host Disease (GVHD) was observed and all patients engrafted. At 63 months, probability of survival is 42.86% with a relapse risk of 19.89%, two patients died from B-cell lymphoproliferative disease, seven other died from the procedure partially because of the use of the TAM as pretransplant regimen. This approach is being pursued by a gene therapy trial using herpes-simplex - 1 thymidine kinase gene expressing peripheral donor T-cells.

Adult↗
PubMed2003

Construction of a BAC library and generation of BAC end sequence-tagged connectors for genome sequencing of the African malaria mosquito Anopheles gambiae.

A Bacterial Artificial Chromosome (BAC) genomic DNA library of Anopheles gambiae, the major human malaria vector in sub-Saharan Africa, was constructed and characterized. This library (ND-TAM) is composed of 30,720 BAC clones in eighty 384-well plates. The estimated average insert size of the library is 133 kb, with an overall genome coverage of approximately 14-fold. The ends of approximately two-thirds of the clones in the library were sequenced, yielding 32,340 pair-mate ends. A statistical analysis (G-test) of the results of PCR screening of the library indicated a random distribution of BACs in the genome, although one gap encompassing the white locus on the X-chromosome was identified. Furthermore, combined with another previously constructed BAC library (ND-1), ~2,000 BACs have been physically mapped by polytene chromosomal in situ hybridization. These BAC end pair mates and physically mapped BACs have been useful for both the assembly of a fully sequenced A. gambiae genome and for linking the assembled sequence to the three polytene chromosomes. This ND-TAM library is now publicly available at both http://www.malaria.mr4.org/mr4pages/index.html/ and http://hbz.tamu.edu/, providing a valuable resource to the mosquito research community.

Animals↗
PubMed1988

Effect of estradiol and tamoxifen on the anchorage-independent growth of the subpopulations derived from MCF-7 breast carcinoma cells: cytogenetic analysis of the stem cell subpopulation.

The MCF-7 breast carcinoma cell line can be separated by Percoll density gradient centrifugation into several subpopulations, A to F, one of which (E) has been previously suggested to be highly enriched in stem cells. The anchorage-independent growth of the different fractions and its sensitivity to estradiol (E2) and tamoxifen (TAM) was assayed. The anchorage-independent growth capacity of the different fractions was E greater than A greater than B greater than D greater than C,F. The E fraction had the highest clonogenic index (6.62 +/- 1.18) and was unaffected by E2 or TAM. The karyotypic analysis of the E fraction revealed features similar to those of the unfractionated cell line. It is suggested that the high growth rate of fraction E is due to an enrichment in stem cells and not to the existence of a different clone.

Breast Neoplasms↗
PubMed1986

Hormonal effects of PGF2 alpha output by cultures of epithelial and stromal cells in human endometrium.

Estradiol stimulation and progesterone inhibition of human uterine PGF2 alpha production were studied using in vitro preparations of endometrial tissue and cells. Measurement of PGF2 alpha levels in media from primary cultures of glandular epithelia and stoma revealed that basal outputs were similar in both cell types but could be increased by estradiol only in epithelial cells. Tamoxifen (Tam) and trans-4-hydroxy tamoxifen (OHTam) did not affect basal PGF2 alpha outputs by secretory endometrium in organ culture and by monolayer cultures of epithelial cells, but counteracted the stimulatory effects of estradiol in both systems. The almost pure antiestrogenic activity exhibited by OHTam was at least 10 times greater than that of Tam, suggesting that the estrogen-stimulated increases in uterine PGF2 alpha output are mediated by specific estrogen receptors. Fragments of endometrium also released lipocortin, a phospholipase A2-inhibiting protein believed to mediate inhibitory effects of glucocorticoids on prostaglandin production in several types of cells. Although dexamethasone increased lipocortin and decreased PGF2 alpha output in secretory endometria in vitro, progesterone inhibited both lipocortin and PGF2 alpha output. The mechanisms by which P inhibits PGF2 alpha production remain to be elucidated.

Annexins↗
PubMed1986

Tamoxifen and progesterone effects in target tissues during the perinatal period.

The biological effects of tamoxifen (TAM), progesterone (P), or a combination of TAM + P were investigated in the uterus and vagina of newborn guinea pigs after short (2 days) and long (12 days) treatments. In both tissues, tamoxifen provoked a significant trophic effect which is indicated by the increase in weight, protein and DNA content. In the uterus, progesterone also provoked an increase in weight, protein and DNA content, but much less than that provoked by tamoxifen. In contrast, in the vagina progesterone had no effect on the weight, protein and DNA content, but progesterone did not block the agonistic effect provoked by tamoxifen. The situation was different when progesterone receptor was concerned. Tamoxifen in both tissues (particularly in the vagina) stimulated the progesterone receptor very significantly. Progesterone blocked the number of specific binding sites of progesterone and the stimulatory effect provoked by tamoxifen.

Animals↗
PubMed1990

Cyclic AMP content and invasive capacity of metastatic variants of the BW-5147 murine T-cell lymphoma.

The invasive behaviour of 8 lymphoma cell lines were tested by an in vitro monolayer invasion assay. The metastatic cell lines (TAM 4D1.2, DCH10Sp, TAM 4D6.2, E4 and BWLi) were more invasive than their non-metastatic counterparts (TAS 5C4, BWO and DCH 10). There was a positive correlation between their invasiveness and the PGE1- and forskolin stimulated cellular cAMP levels. Invasiveness and basal cAMP levels could not be correlated. Pretreatment with pertussis toxin (50 ng/ml) for 24 hours provoked did not significantly affect the basal and PGE1-stimulated cAMP levels in all cells. Yet, the toxin catalysed the ADP-ribosylation of 40 kDa components in all cells and provoked a significant increase in the invasiveness of non-metastatic cell lines and a decrease in the invasiveness of metastatic cell lines. These data suggest that the invasiveness of T-lymphoma cell lines might be controlled by a complex interplay between different signal transducing pathways in the membrane, rather than by the intracellular level of cAMP.

Alprostadil↗
PubMed1988

Medroxyprogesterone acetate and tamoxifen do not decrease aggressive behavior in CF-1 male mice.

Intact CF-1 male mice were given daily injections of either medroxyprogesterone acetate (MPA, an antiandrogen), tamoxifen (TAM, an antiestrogen), or the two drugs in combination and tested for aggressive behavior toward bulbectomized stimulus males. None of the treatments decreased fighting behavior over a 20-day test period and the presence of TAM led to increased aggression even in the presence of MPA. Testis weight was reduced by MPA while both compounds decreased seminal vesicle weight. The mechanisms involved in the observed effects are considered as well as the implications of the results for the clinical use of these compounds as modulators of testosterone-facilitated behaviors.

Aggression↗