Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Mouse”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 163 records · Page 9Linked to original sources

Influenza virus: association of mouse-lung virulence with plaque formation in mouse kidney cells.

In genetic recombination experiments with the mouse-lung-adapted human influenza A/Engl/1/61 (H2N2) and an avian influenza strain A/Rostock/34 (FPV) (Hav1N1) which is avirulent for the mouse lung, recombinants in which hemagglutinin and neuraminidase were either segregated (Hav1N2; H2N1) or not segregated (Hav1N1) were selected. The recombinants were studied for mouse-lung virulence and their ability to propagate in mouse kidney cells, mouse embryo fibroblasts, chick embryo kidney cells and chick embryo fibroblasts. An association between plaque formation in mouse kidney cells and mouse-lung virulence was found.

Animals↗

Functional expression of mouse relaxin and mouse relaxin-3 in the lung from an Ebola virus glycoprotein-pseudotyped lentivirus via tracheal delivery.

The peptide hormone relaxin is a known modulator of connective tissue and the extracellular matrix by virtue of its ability to regulate matrix metalloproteinases (MMPs). Relaxin knockout mice exhibit age-related pulmonary fibrosis, and delivery of recombinant human H2 relaxin ameliorates fibrotic-like conditions in the mouse lung. We investigated whether lentiviral vectors (LVs) engineering the expression of murine relaxins could induce MMP activity in the mouse lung. Mouse relaxin and mouse relaxin-3 peptides engineered by recombinant LVs were biologically active as shown by stimulation of cAMP from both THP-1 and 293T cells stably expressing relaxin receptor LGR7 and by up-regulation of MMP-2 activity from primary C57BL/6 lung cell cultures. To provide the virions with enhanced tropism for the lung, LVs were pseudotyped with the Zaire strain of the Ebola virus glycoprotein (EboZ GP) and delivered by endotracheal intubation. LVs engineering luciferase pseudotyped with EboZ GP, but not with vesicular stomatitis virus glycoprotein resulted in successful LV transduction and transgene expression in C57BL/6 mouse lung by as early as d 4. Mice treated via tracheal delivery with EboZ GP pseudotyped LVs that engineered expression of mouse relaxins exhibited increased MMP-2 and MMP-9 activity in lung tissue up until the end of our study at d 21. Taken together, this study provides proof-of- principle that relaxin gene expression targeted to the mouse lungs can result in enhanced MMP activity offering potential for alleviating disease conditions characterized by dysregulation of extracellular matrix protein accumulation.

Administration, Inhalation↗

Purification and characterization of mouse decidual calcyclin: a novel stimulator of mouse placental lactogen-II secretion.

The effects of secretagogue(s) from mouse decidual tissue on the release of mouse placental lactogen-II (mPL-II) were studied. Decidual tissue was obtained from 10- and 11-day-pregnant mice. The tissue was homogenized, extracted, and the tissue extract was made 50% saturated with ammonium sulfate. Both the precipitate and supernatant were tested for their ability to stimulate mPL-II release from cultured trophoblasts. The supernatant contained an activity to stimulate the release of mPL-II. This activity was further purified using column chromatography. The purification resulted in isolation of a protein with a mol wt of 20 K as estimated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis under nonreducing conditions and 6 K under reducing conditions. Further characterization of this protein showed that it binds calcium and has an amino acid sequence that is highly homologous with calcyclin expressed in mouse embryonic fibroblast cells and with calcyclin from other species. This protein was designated mouse decidual calcyclin. Antiserum was raised against the purified decidual calcyclin for development of an RIA and for immunoblots. Western blots of various mouse tissue extracts and mouse serum from different physiological stages showed that the concentration of calcyclin was highest in decidual tissue. Detectable levels were found in extracts from trophoblast, lung, and stomach, but the concentrations in these tissues were about 100 times lower than in decidua. Decidual calcyclin was not detectable in mouse serum. Cultured decidual cells released calcyclin into the medium. On average, this release was about 7.8 ng/micrograms DNA.24 h. The rate of release did not change significantly during 4 days of culture. The ratio of calcyclin in cells per calcyclin released during 24 h averaged 2.3 and did not change significantly during the culture period. The purified decidual calcyclin stimulated the release of mPL-II from cultured trophoblasts in a dose-dependent manner at concentrations from 0.01 to 1 microgram/ml. The maximum stimulation averaged about 1.5 times above control. It is concluded that decidual calcyclin may be of physiological importance for the regulation of mPL-II secretion.

Amino Acid Sequence↗

A 3 kb sequence from the mouse cellular retinoic-acid-binding protein gene upstream region mediates spatial and temporal LacZ expression in transgenic mouse embryos.

A 3233 base pair (bp) sequence of the 5'-flanking region of the mouse cellular retinoic-acid-binding protein (CRABP) gene is determined. From this region, a 3 kb fragment located 150 bp upstream from the transcriptional initiation site is isolated and fused to a LacZ reporter sequence. Transgenic mouse embryos of this fusion gene show spatially and temporally specific expression of LacZ protein and the expression of this fusion gene at the RNA level is confirmed by RNAase protection assays, which detect specific fusion transcripts in RNA samples from tissues of transgenic mouse embryos. In contrast, transgenic mouse embryos of a shorter fusion gene containing only 583 bp from the same upstream region of the mouse CRABP gene fused to the same reporter sequence show no LacZ activities. Thus, it is concluded that the 3 kb sequence, but not the 583 bp sequence, of the mouse CRABP gene contains information for its temporally and spatially specific expression in mouse embryos.

Animals↗

Allelotype analysis in mouse hepatocellular carcinomas; frequent homozygous deletion of mouse homolog of p16/CDKN2 gene on chromosome 4 in culture.

Because allelotype analysis of many tumors has been important in the identification of new tumor suppressor genes, here we have analyzed hepatocellular carcinomas (HCCs) derived from F1 hybrid mice between C3H and MSM in detail. The analysis showed no allelic loss in primary HCCs, while the loss was detected in tumor cell lines established from HCCs. Recently, a candidate tumor suppressor gene termed p16/CDKN2, which was located near the interferon gene cluster on human chromosome 9p21, was identified by virtue of its frequent homozygous deletion in cell lines derived from many different tumor types. Since frequent allelic imbalances in the D4MIT9 locus and loss of heterozygosity in the alpha-interferon gene which was located near the mouse homolog of p16/CDKN2 (mouse p16) gene were detected in tumor cell lines, we investigated homozygous deletion of the mouse p16 gene by the comparative multiplex PCR method. The analysis revealed frequent homozygous deletion of the gene in thirteen of the tumor cell lines (13/25, 52%), but not in primary HCCs (0/25, 0%). These data indicate that gene deletions including the mouse p16 gene on chromosome 4 in tumor cell lines occur during the culture and that allelic imbalances are uncommon in mouse primary HCCs. Our results suggest that mouse p16 plays an important role in mouse hepatocarcinogenesis in vivo in progression or immortalization in vitro.

Alleles↗

[Serological examinations on natural infections with mouse pathogens in inbred mouse strains: difference in antibody detection among the strains (author's transl)].

Serological surveys on several infections were performed on the inbred mouse strains maintained at the Central Institute for Experimental Animals. In the first survey, 11 strains of mouse, which were 8 weeks of age or older and were kept in separate cages in the same animal room, were tested for antibodies to Salmonella enteritidis, Corynebacterium kutscheri, Tyzzer's organisms, Mycoplasma pulmonis, mouse hepatitis virus (MHV), Sendai virus (HVJ), pneumonia virus of mice (PVM) and minute virus of mice (MVM). Positive results were obtained in MHV, HVJ, PVM and MVM. Positive rates for these viruses except for MVM were different among mouse strains. In the second survey, 5 strains of mouse kept together in the same cage for 4 weeks after weaning were examined for MHV and HVJ antibodies. Positive rates to MHV were different among mouse strains as observed in the first survey. For HVJ antibody, no difference was demonstrated in positive rates unlike in the first survey, but the titers varied between the strains. These results suggest the difference in antibody response to natural infections dependent on mouse strains.

Animals↗

Abnormalities in the SJL mouse provide evidence for different mechanisms for the induction and transfer of tolerance to mouse thyroglobulin.

Experimental autoimmune thyroiditis (EAT) induced by immunization of susceptible (H-2k) mice can be significantly suppressed by pretreatment with soluble mouse thyroglobulin administered intravenously. Lightly irradiated recipients of spleen cells from donors pretreated in this way show a reduced response when subsequently challenged with mouse thyroglobulin and adjuvant (Kong et al., 1982; Parish et al., 1988). Previous studies on the SJL mouse revealed, among other abnormalities, a lack of suppressor cells (Cooke & Hutchings, 1984; Hutchings, Varey & Cooke, 1986; Amagai & Cinader, 1981) and therefore tolerance induction to mouse thyroglobulin and subsequent transfer was examined in these animals. The SJL mouse could be tolerized by i.v. administration of mouse thyroglobulin, but transfer of spleen cells from these animals failed to mediate suppression in syngeneic recipients. Several congenic strains of B10 mice showed similar 'in situ' tolerance without subsequent successful transfer and we conclude that the tolerance system described may be mediated by two distinct pathways and that the SJL appears to be defective only in the second pathway. Studies on other mouse strains suggest that the ability to be tolerized or to transfer tolerance is not dependent on a particular H-2 or I-E.

Animals↗

[Cloning of cDNA of SRG4, a mouse spermatogenesis related gene and expression in mouse different developing stages].

Spermatogenesis required lots of genes taking part in this process. In prevision studies, Odf1, Odf2, Sak57, Spag4, Spag5 were identified in mouse and rat sperm tail developing. Two ESTs, BG101130 and BG100990, which coded amino acid sequences with high homology to rat Spag4, were found from mouse spermatocytes. By electrical hybridization, a 1 155 bp sequence was obtained and named as SRG4 (Spermatogenesis Related Gene 4) (GenBank accession number: AY307077), which included the full-length sequence of mouse testis hypothetical gene AK006225. The opening reading frame of SRG4 was 87 approximately 1 133 bp, and was proved by RT-PCR in mouse testis. The information analysis showed SRG4 gene was located in 2H1-H2, and the putative protein was 348-amino acid with a coiled-coil region, suggesting SRG4 might function as a transmembrane protein. The homologies of amino acid sequences were 74% between TSARG4 and SRG4 gene and 45% between SRG4 and rat Spag4 gene, respectively. RT-PCR and Northern blot results showed SRG4 gene expressed specifically in mouse testis. Changes of SRG4 expression in mouse different developing stages were observed. The results showed SRG4 gene expressed slightly in two weeks postpartum, and expressed abundantly from three weeks, and reached the top at 4 -5 weeks. This indicted SRG4 gene may play an important role in mouse spermatogenesis.

Amino Acid Sequence↗

Cloning of the cDNA and gene for mouse mast cell protease 4. Demonstration of its late transcription in mast cell subclasses and analysis of its homology to subclass-specific neutral proteases of the mouse and rat.

Based on the amino-terminal amino acid sequence of the mature form of mouse mast cell protease 4 (MMCP-4), previously identified in peritoneal connective tissue mast cells (CTMC) and Kirsten sarcoma virus-immortalized mast cells (KiSV-MC), a 26-mer oligonucleotide probe was constructed and used to clone cDNAs for MMCP-4 from a KiSV-MC1 cDNA library. MMCP-4 is the first secretory granule serine protease of CTMC to be molecularly cloned. Using a cDNA probe derived from the 3'-untranslated portion of the MMCP-4 cDNA, the gene for MMCP-4 and a second highly related gene (mouse mast cell protease-like, MMCP-L) were cloned from a BALB/c mouse genomic DNA library and sequenced entirely, including approximately 2 kilobases of the 5'-flanking region. MMCP-4 and MMCP-L have five exons of identical length, four introns of nearly identical length, and approximately 900 base pairs of 5'-flanking DNA with sequence similarity by dot matrix analysis. By RNA blot analysis with gene-specific probes for MMCP-4 (bases 497-633 of the cDNA) and MMCP-L (bases 502-638 of the cDNA), mRNA for MMCP-4 was present in KiSV-MC5, CTMC, and the intestine of a mouse infected with the parasite Nippostrongylus brasiliensis markedly enriched for mucosal mast cells (MMC); MMCP-L mRNA was detected only in the intestine of the N. brasiliensis-infected mouse. MMCP-4 mRNA was not expressed in normal mouse intestine or in interleukin 3-dependent bone marrow-derived mast cells, which can serve as precursors to both MMC and CTMC. This finding suggests that MMCP-4 is transcribed relatively late in the development of both the CTMC and MMC subclasses and underscores the fact that mouse bone-marrow-derived mast cells are immature mast cells, rather than tissue culture equivalents of the MMC subclass.

Amino Acid Sequence↗

Encephalitogenic activity of the small form of mouse myelin basic protein in the SJL/J mouse.

Mouse myelin basic proteins (MBP) were prepared by ion-exchange chromatography of an acid extract of homogenized, delipidated mouse brain. The use of a linear salt gradient during ion-exchange chromatography gave three peaks, 1, 2, and 3, of MBP. Sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) analysis of these peaks showed that peaks 2 and 3 were a mixture of the large and small forms of mouse MBP, whereas peak 1 was solely the small form. Tryptic peptides of mouse and rat small form MBP were compared by high-performance liquid chromatography. The elution times and absorbances at 210 nm were identical for 16 of 21 peaks derived from small form MBP of the two species. Amino acid analysis showed that 10 corresponding peaks from the small form of mouse and rat MBP had identical amino acid composition. When tested for encephalitogenicity in SJL/J mice, both the mixture of large and small forms of mouse MBP and the small form mouse MBP were highly encephalitogenic.

Amino Acid Sequence↗

Effects of experimental infection of the deer mouse (Peromyscus maniculatus) with mouse hepatitis virus.

Three deer mice (Peromyscus maniculatus) given 10(4) TCID50 of mouse hepatitis virus -S intranasally all had significant serum neutralization titers to mouse hepatitis virus -S 3 weeks later. Ten other deer mice were given 10(3) TCID50 of mouse hepatitis virus -3 intranasally and placed with sentinel laboratory mice (CF1, C3H/Rv, and nu/nu) and uninoculated deer mice. One inoculated deer mouse died, but mouse hepatitis virus was not isolated. No other inoculated or uninoculated animals exhibited signs of disease. No sentinel animals exhibited serum neutralization titers for mouse hepatitis virus -3. Three of the remaining nine inoculated deer mice had positive antibody titers. It was concluded that deer mice do not develop clinical manifestations of mouse hepatitis virus or transmit the virus to potentially susceptible laboratory mice.

Animals↗

Suppression of tumorigenicity in hybrids of tumorigenic Chinese hamster cells and diploid mouse fibroblasts: dependence on the presence of at least three different mouse chromosomes and independence of hamster genome dosage.

Somatic cell hybrids were generated between Chinese hamster cell lines (Cl-4 and TK 17-O) with a near-diploid number of partially abnormal chromosomes and embryonic mouse fibroblasts (BALB/c). Hybrids harboring a near-diploid, near-triploid, and near-tetraploid set of hamster chromosomes plus 22 to 30 mouse chromosomes were analyzed for the expression of the transformed or tumorigenic phenotype, respectively, indicated by their capacity to form colonies in soft agar and by tumor formation after s.c. injection into nude mice. The hybrids showed (partial) suppression of tumorigenicity and of anchorage independence. The minimum number of hybrid cells required to initiate tumor growth in nude mice was 100- to 50,000-fold higher, and the latency period was 3- to 6-fold longer in comparison with the highly tumorigenic parental hamster cells. Suppression of tumorigenicity was also found in intraspecific Chinese hamster hybrids involving tumorigenic cells (E 36-O and TK 17-O) and embryonic hamster fibroblasts. To identify those mouse chromosomes associated with suppression of tumorigenicity, we investigated the expression of mouse isozyme genes and the presence of mouse chromosomes in interspecific suppressed hybrids and their tumorigenic hybrids described previously. No single mouse chromosome, even if present in two copies, and no combination of two different mouse chromosomes was sufficient to suppress tumorigenicity in these hybrids. This conclusion is based on either the presence of these chromosomes in hybrids isolated from tumors or their absence in suppressed hybrids.

Agar↗

Characterization of [3H]naltrindole binding to delta opioid receptors in mouse brain and mouse vas deferens: evidence for delta opioid receptor heterogeneity.

Naltrindole (NTI) is a potent and selective nonpeptide delta opioid receptor antagonist. This study reports on the binding characteristics of [3H]NTI (specific activity = 30.5 Ci/mmole) for mouse brain and vas deferens (MVD) tissues. In brain, [3H]NTI had unusually high specific binding to delta receptors (80% at its Kd concentration) relative to other selective delta receptor radioligands. Saturation Kd values with 95% confidence intervals for mouse brain and MVD tissue preparations were 56.2 (41.8-75.7) and 104 (25.8-420) pM, respectively. These Kd values were significantly different (P = .028) and [3H]NTI binding to both tissues was best fit by a one-site model. Receptor densities were 83.9 (66.8-106) fmol/mg of protein for mouse brain and 14.8 (7.03-31.2) fmol/mg of protein for the MVD. Binding inhibition studies showed that NTI and the delta opioid receptor agonists [4'-Cl-Phe4]DPDPE and [D-Ala2, Glu4]deltorphin had high affinity for the sites labeled by [3H]NTI in both tissue preparations whereas mu [Tyr-Pro-psi-MePhe-D-Pro-NH2 (PL-17)] and kappa (U-69593) agonists had micromolar affinity. Both agonists recognized multiple sites in mouse brain under control (with 5 mM Mg++) and treatment (with 50 microM guanylyl-5'-imido-diphosphate and 100 mM NaCl) conditions but only single-site binding was observed for MVD (only control condition tested). [D-Ala2, Glu4]deltorphin showed about 6.5-fold selectivity for a portion (approximately 33%) of mouse brain sites (Ki = 130 pM) compared to sites labeled by [3H]NTI in MVD (Ki = 1200 pM) under control conditions. No significant difference was observed for [4'-Cl-Phe4]DPDPE binding affinity to both tissues (Ki = 450-680 pM) under control conditions. The affinity of opioid agonists, but not antagonists at [3H]NTI binding sites in mouse brain, was substantially reduced by the presence of guanylyl-5'-imidodiphosphate and sodium ions consistent with guanine nucleotide-binding protein regulation of the delta receptors. The portions of high- and low-affinity sites recognized by [4'-Cl-Phe4]DPDPE and [D-Ala2, Glu4]deltorphin in mouse brain labeled by [3H]NTI under treatment conditions were not significantly different (each subtype represented approximately 50% of the total population) suggesting delta receptor heterogeneity in this tissue. It is concluded that [3H]NTI binds to delta opioid receptor affinity states and subtypes with equal affinity and can be used for their characterization in conjunction with different treatment conditions and ligands.

Animals↗

Mixed xenogeneic chimerism (mouse+rat-->mouse) to induce donor-specific tolerance to sequential or simultaneous islet xenografts.

We previously reported that donor-specific rat islet xenografts were accepted by fully xenogeneic (rat-->mouse) chimeras when the islets were transplanted at least six weeks following reconstitution. The purpose of the present study was to examine whether a similar outcome would occur for mixed xenogeneic (mouse+rat-->mouse) chimeras if the islets were placed coincident with the time of bone marrow infusion. As with fully xenogeneic chimeras (rat-->mouse), synchronous donor-specific F344 rat (Rt1A1) islet xenografts were significantly prolonged (MST > 139 days) in mixed xenogeneic (mouse+rat-->mouse) chimeras, while MHC-disparate third-party WF rat (Rt1Au) grafts were rejected (MST = 21.2 days). The transplanted donor-specific islets were functional to maintain euglycemia and they were regulated in function to respond to a glucose challenge. For potential clinical application, it would be of obvious benefit if the islet xenografts could be placed at the time of bone marrow transplantation. We therefore performed similar studies using donor islets administered simultaneously with bone marrow. Donor-specific islet xenografts were permanently accepted by all mouse recipients (n = 5). When MHC-disparate third-party rat islets were transplanted, only 3 of 8 islet xenografts were rejected; the other 5 remained functional from 77 to 90 days posttransplantation. Although prolonged and functional, the MHC-disparate islets that were accepted exhibited histologic evidence of fibrosis and rejection, while those matched to the donor did not. These data therefore suggest that donor-specific islet xenografts are permanently accepted if placed simultaneously or sequentially following mixed xenogeneic bone marrow reconstitution.

Animals↗

The expression of mouse biliary glycoprotein, a carcinoembryonic antigen-related gene, is down-regulated in malignant mouse tissues.

Mouse biliary glycoprotein (Bgp) is a member of the carcinoembryonic antigen gene family and is highly expressed in the epithelial cells of normal hepatic biliary ducts and intestine. Nine mouse Bgp isoforms have been identified through molecular cloning and shown to be splice and allelic variants of one Bgp gene. These glycoproteins function in vitro as intercellular adhesion molecules and serve as the mouse hepatitis virus receptors. Since human carcinoembryonic antigen is overexpressed in gastrointestinal tumors, we have investigated the expression of mouse Bgp in primary tumors and carcinoma cell lines. Our results demonstrate that the expression of the major mouse Bgp isoforms is down-regulated in tumors at the transcriptional and the posttranscriptional levels. This decrease in expression is corroborated by immunostaining of primary colonic tumors with anti-mouse Bgp antibodies. In addition, Bgp expression is influenced by transcriptional control mechanisms involving DNA methylation of the Bgp gene upstream regulatory region. Our results demonstrate that mouse Bgp protein expression is decreased upon malignant transformation and further suggest that Bgp proteins may be involved in the maintenance of the differentiated cellular phenotype.

3T3 Cells↗

A rare common integration site of proviruses of the mouse mammary tumor virus in P-type mammary tumors of mouse strain GR.

The mouse mammary tumor virus (MMTV) can induce mammary tumors in mice by proviral activation of the cellular oncogenes int-1 or int-2. Activation of these genes, however, is observed in only a few hormone- and pregnancy-dependent mammary tumors of the mouse strain GR. To study the possible involvement of other oncogenes we cloned three MMTV proviral-host fragments (MT 40, 42, and 53) from different mammary tumors of GR with a single acquired MMTV provirus. From a genomic library of normal mouse DNA we isolated phages with insert DNAs that covered 20-30 kb of the uninterrupted regions. Suitable probes devoid of repetitive DNA sequences were isolated in order to screen other mammary tumors for MMTV proviral integrations in these regions. Only two mammary tumors, MT 40 and 42, showed integration of extra MMTV proviruses within the same region. The integrations occurred only 60 bp apart. The other mammary tumors, however, did not contain MMTV proviral integrations in this region, nor in the MT 53 region. Using mouse-hamster somatic cell hybrid DNA, the MT 40/42 integration region was assigned to mouse chromosome 7, and the second region, MT 53, to chromosome 16. The two regions bear no homology to known cellular oncogenes. We did not observe any mRNA being expressed from these cloned segments either in tumors or in normal mammary glands. These findings indicate that plaque(P)-type mammary tumors in mouse strain GR do not originate from MMTV provirus insertions in a particularly favored integration region, but that there may be a variety of integration sites in these tumors.

Animals↗

The Mouse Genome Database (MGD): the model organism database for the laboratory mouse.

The Mouse Genome Database (MGD) is the community database resource for the laboratory mouse, a key model organism for interpreting the human genome and for understanding human biology and disease (http://www.informatics.jax.org). MGD strives to provide a highly curated, highly integrated information resource that not only includes the consensus view of current knowledge about the mouse, but also provides comparative genomic information particularly for human and rat genomes. MGD includes extensive information about mouse genes, supporting all gene attribute assertions with experimental data, statements of evidence and citation. Detailed information about alleles and mouse mutants includes genotype, molecular variant and phenotype descriptions. Extensive collaboration with other data providers such as NCBI, RIKEN and SWISS-PROT provides standardization of gene:sequence associations and robust interconnections between large information systems based on shared sequence curation. Recent integration of large datasets of mouse full-length cDNAs and radiation-hybrid mapped ESTs, the continued development and use of extensive structured vocabularies and the expansion of the representation of phenotypes highlight this year's developments.

Alleles↗

Transforming growth factor-beta represses transcription of the mouse mammary tumour virus DNA in cultured mouse mammary cells.

Increased expression of mouse mammary tumour virus (MMTV) is associated with hyperplastic alveolar growth and subsequent development of mammary cancers in the mouse. The expression of this virus is repressed when mammary tumour cells undergo sarcomatous transformation. We have demonstrated that a spontaneous progression of mouse mammary adenocarcinoma cells into highly malignant cells with the transformed phenotype is accompanied by an increased expression of transforming growth factors alpha and beta (TGF alpha and TGF beta), as well as a decreased expression of MMTV. Mouse mammary adenocarcinoma cells transformed with activated ras oncogene also expressed high levels of the transforming growth factors and a low level of MMTV. Thus a reverse correlation exists between the increased expression of the transforming growth factors and a low level of expression of MMTV. Mouse mammary cells that express high levels of MMTV when treated with exogenous TGF alpha and TGF beta 1 showed a down regulation of MMTV expression in response to TGF beta 1 but not to TGF alpha. These results demonstrate that the repression of MMTV expression in mouse mammary tumour progression may be due in part to an increased expression of TGF beta.

Animals↗