Search PubMed⌕ Search

Biomedical subjects

P Furmanski

Publications and source records attributed to P Furmanski.

At least 73 records · Page 4Linked to original sources
PubMed1983

Effect of the extracellular matrix on plasminogen activator isozyme activities of human mammary epithelial cells in culture.

Multiple molecular forms of plasminogen activator were detected in normal human mammary epithelial cells in culture. Cells derived from (normal) breast mammoplasty specimens and grown on the surface of collagen gels exhibited three major classes of plasminogen activator isozymes (Mr = 100,000 [100K], 75,000 [75K], and 55,000 [55K]). The activity of the 100K and 75K isozymes was greatly reduced when the cells were grown on conventional tissue-culture-grade plastic surfaces. MCF-7, a human mammary carcinoma cell line, exhibited predominantly or exclusively the 55K isozyme, irrespective of the cell growth substratum. The activity of the 55K isozyme was more than twofold higher for MCF-7 cells grown on collagen gels than for cells grown on plastic. Progesterone, diethylstilbestrol, and estrogen stimulated the activity of the 55K isozyme of MCF-7 cells, but only when the cells were grown on a plastic surface. The plasminogen activator activities of the normal human mammary epithelial cells were not stimulated by these hormones, irrespective of the growth substratum. These results show that the expression of plasminogen activator isozymes by human mammary epithelial cells is subject to modulation by the extracellular matrix. Normal and malignant cells may differ in their responsiveness to these effects.

Breast↗
PubMed1982

Spontaneous regression of Friend virus-induced erythroleukemia IX. Role of complement in leukemia regression.

The role of complement was examined in the immunologically-mediated spontaneous regression of erythroleukemia induced by the RFV strain of the Friend virus complex. Hemolytic complement levels were not significantly altered during the leukemic, regressed and recurrent phases of the disease. No correlation was observed between leukemia regression and complement levels in normal, C5-deficient and hybrid mice. No correlation was observed between serum complement activity and leukemia recurrence or mortality due to leukemia. The data suggest that hemolytic complement, and thus those immune effector functions specifically dependent on full complement activity, are not involved in leukemia regression and do not influence the course of the disease.

Animals↗
PubMed1982

Effect of C-reactive protein on granulocyte-macrophage progenitor cells.

Pathophysiological concentrations of CRP inhibited the in vitro clonal proliferation of CFU-C's. CRP inhibition was specific for normal CFU-C's committed to the mononuclear phagocyte lineage. Macrophage progenitor cells stimulated by an inflammatory response were unaffected by CRP. CFU-C's which were committed to the granulocyte lineage, those which gave rise to both macrophages and granulocytes, and erythroid progenitor cells were also not affected by CRP. Only macrophage CFU-C's that possessed Fc receptors and were in S-phase at the time at CRP exposure were susceptible to inhibition of colony formation. The data suggest that CRP functions as a regulator of the cellular composition of an inflammatory response.

Animals↗
PubMed1982

Inhibition of normal erythropoiesis in mice with Friend virus induced erythroleukemia.

Mice in which erythroleukemia was induced by the Friend murine leukemia virus produced inhibitors of normal erythropoiesis. The inhibitors were released into media conditioned by bone marrow cells from leukemic, but not normal mice. The inhibitors were active at high dilution against normal erythroid progenitors (CFUE) in S-phase. Colony formation by CFUE from leukemic mice was stimulated by the same preparations of inhibitor. Fractionation of inhibitory media by gel filtration chromatography revealed 2 protease-sensitive, macromolecular components and a small molecular weight species. The cells responsible for production of the CFUE inhibitors were adherent, possessed macrophage but not T or B cell markers, and did not express viral antigens. The CFUE inhibitors were distinguishable from the previously described inhibitor of granulocyte-macrophage precursors, CFUC LIA, by antigenic specificity and cellular origin.

Animals↗
PubMed1981

Spontaneous regression of Friend-virus-induced erythroleukemia. VII. The genetic control of regression.

The genetic control of spontaneous regression of erythroleukemia was studied in parental and hybrid mice in which leukemia was induced by the regressing strain of Friend virus (RFV). Because in previous studies parental regressor mouse strains tested (N/PLCR, SIM, NIH Swiss) all had the FV-1n/n genotype and the progressor mouse strains (SIM.R, BALB/c) had the Fv-1b/b genotype, we detemined the influence of Fv-1 alleles on regression. Genes which influence regression were dominant and had partial penetrance in (progressor x regressor) F1 mice. Regression occurred in hybrid mice which inherited the Fv-1b/b genes of each of the progressor mouse strains. Regression and Fv-1 alleles also segregated independently in (N/PLCR x BALB/c) F2 mice, in random-bred Swiss mice heterozygous for the Fv-1 gene, in partially inbred Swiss recombinant progressor and regressor mouse lines, and in hybrid mice carrying the Fv-1b/b gene of SIM.R mice. Regressor SIM and progressor SIM.R mice, which were bred to be congeneic at the Fv-1 locus, also differ with respect to recovery from viremia, suggesting that their Rfv-3 genes differ and influence regression. Crosses of SIM and SIM.R mice with the A.BY (Rfv-3s/s) mouse strain confirmed that SIM and SIM.R carry Rfv-3r/r and Rfv-3s/s, respectively. We conclude that Fv-1b/b is not inhibitory to regression nor is the Fv-1 gene a genetic deteminant in the process. The data suggest that regression is influenced by several genes, including those (Rfv-1, Rfv-2, Rfv-3) shown to affect recovery from leukemia in other systems.

Alleles↗
PubMed1981

Prognostic value of concanavalin A reactivity of primary human breast cancer cells.

A prospective, double-blind study was carried out to determine whether activity with concanavalin A (Con A) of human breast cancer cells was related to early disease recurrence. Mammary epithelial cells were isolated from 138 primary human breast cancers. The cells were placed in culture, and their reactivity with Con A was determined with a hemadsorption assay in which human erythrocytes treated with various concentrations of Con A were incubated with the test (mammary epithelial) cells in situ. The Con A half-maximum value was determined as the concentration of Con A at which approximately 50% of the test cells adsorbed erythrocytes. Con A reactivity of the tumors was classified as high or low (half-maximum value less than or equal to 30 or greater than 30 microgram/ml, respectively). Patients were followed for 2 to 60 months after primary surgery (median, 22 months). Those patients having tumors that were highly reactive with Con A were at significantly greater risk of developing early recurrence of their cancers than were those patients with low-reactivity tumors. No correlation was found between Con A reactivity and the age of the patients, their menopausal status, the number of axillary lymph nodes infiltrated with tumor, the number of axillary lymph nodes infiltrated with tumor, the estrogen receptor content of the tumor, or the clinical stage of the disease. These data show that Con A reactivity is an independent discriminator for identifying those breast cancer patients who are at high risk of developing early recurrent disease.

Agglutination↗
PubMed1981

Growth of human mammary epithelial cells on collagen gel surfaces.

We have developed a method for sustained growth of human mammary epithelial cells in monolayer cultures. Epithelial organoids derived from solid breast tissues were grown on the surface of thin (approximately 1 mm) collagen gel layers in an enriched growth medium supplemented with hormones, growth factors, fetal calf serum, and horse serum. To transfer the cultures, the collagen layers were dislodged and digested with collagenase. The monolayers of cells released into suspension were then dissociated into single cells using trypsin-ethylene-diaminetetraacetate. Dissociated single cells were repleted with 75 to 95% efficiency onto collagen layers or tissue culture plastic surfaces. The dissociated cells could also be cryopreserved and reactivated with greater than 80% plating efficiency on collagen layers. Normal human mammary epithelial cells grown under these conditions progressed through 12 to 15 population doublings. The population-doubling times for normal and malignant mammary cells on collagen layers were 34 and 65 hr, respectively. After reaching confluence, cells in some cultures, derived from either normal or malignant tissues, penetrated the gel surface and grew into the collagen. Within the gels, the cells became organized into three-dimensional tubular structures. The use of collagen layers eliminates a major problem in growth of human mammary epithelial cells in culture, difficulty in efficient dissociation, and cell transfer from monolayers.

Breast↗
PubMed1980

The prognostic value of estrogen receptor determinations in patients with primary breast cancer: an update.

Patients with estrogen receptor (E2R)-positive breast cancers experience a longer disease-free interval and longer survival following primary surgery than do patients with E2R-negative tumors. The presence of E2R is correlated with patient age at diagnosis and tumor grade but not with the presence of metastatic foci in axillary lymph nodes. The difference in the rates of recurrence between E2R-positive and negative tumors is greater in pre- and perimenopausal patients than in postmenopausal patients.

Adult↗
PubMed1980

Absence of fibronectin and presence of plasminogen activator in both normal and malignant human mammary epithelial cells in culture.

Primary monolayer cultures of normal and malignant human mammary epithelial cells were tested for fibronectin by indirect immunofluorescence using antisera specific for fibronectin. This protein was not detectable on either the normal or malignant epithelial cells. Similar results were obtained for normal and malignant mouse mammary epithelial cell cultures. Control normal and transformed fibroblasts exhibited the expected result: the normal cells were positive and the transformed cells were negative. With the use of supernatant fluids from the same cultures or an agar-overlay assay on viable cells, high levels of plasminogen-dependent fibrinolytic activity were detectable in both the normal and malignant mammary cells. Thus, two characteristics that distinguish normal from transformed fibroblasts do not serve as markers of malignancy in mammary epithelial/carcinoma systems.

Animals↗
PubMed1980

Spontaneous regression of Friend virus-induced erythroleukemia. VI. Structural and antigenic differences between the regressing and conventional strains of virus.

The regressing and conventional strains of Friend virus were compared by neutralization assays, sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and tryptic peptide mapping of the individual viral components. Neutralization rates of the two viruses differed in the presence of monospecific anti-gp70 antiserum and sera from regressed or immunized mice. Neutralization of regressing Friend virus, but not conventional Friend virus, occurred when the viruses were incubated with anti-p15(E) and complement. Human serum inactivated conventional Friend virus more rapidly than regressing Friend virus, probably as a result of virolysis induced by the reaction of viral p15(E) with human complement component C1. Structural differences between the viruses were detected in their gp70 viral glycoproteins and p15(E) and p12 proteins. Analysis of different stocks and clonal isolates of the viruses showed that the differences between the gp70 and p15(E), but not the p12 proteins, were associated with the regressing phenotype of the regressing strain of Friend virus.

Animals↗
PubMed1980

A murine model system for the study of the human leukemia-associated inhibitory activity.

Mice inoculated with the RFV strain of Friend virus develop an erythroleukemia that spontaneously regresses. Bone marrow cells from leukemic mice produce a factor that inhibits colony formation in agar by normal CFU-Cs. CFU-Cs from leukemic animals are resistant to the factor. Bone marrow cells from some mice whose leukemia has regressed continue to produce the factor, and CFU-Cs from some regressed mice retain resistance to the factor. These observations dupllicate findings reported for patients with acute leukemias and those with leukemia in remission. The RFV system thus serves as an accurate experimental model for the study of hematopoietic cell interactions and the proliferative advantage of neoplastic cells in human leukemias.

Animals↗
PubMed1979

Spontaneous regression of Friend murine leukemia virus-induced erythroleukemia. IV. Effects of radiation and athymia on leukemia regression in mice.

The spontaneous regression of the erythroleukemia induced by the regressing Friend murine leukemia virus (F-MuLV) complex was inhibited by irradiation of the animals prior to F-MuLV inoculation. This inhibition was proportional to the dose of radiation used. Treatment of the mice with the bone-seeking isotope 89Sr also inhibited erythroleukemia regression, which implicates the same effector mechanisms involved in the resistance to F-MuLV or F-MuLV-induced immunosuprression. Erythroleukemias induced in athymic nude mice by the regressing F-MuLV complex exhibited higher rates of lethality than did the leukemias in heterozygous or homozygous thymus gland-containing controls. These data suggested the involvement of the immune system in erythroleukemia regression and the specific participation of thymus cells and an 89Sr-susceptible function, perhaps marrow-dependent cells, in the process of regression.

Animals↗
PubMed1979

Growth of normal and malignant human mammary epithelial cells in culture.

Normal and malignant human mammary epithelial cells were placed in culture. Normal cells were recovered from late-lactation milk and breast fluids, and malignant cells were isolated from primary breast tumors by collagenase digestion. The concentration of cells obtained from breast fluid samples was inversely proportional to the volume of fluid secreted. Most of these cells adhered rapidly to the substrate, did not replicate, displayed Fc receptor-dependent phagocytic activity, and were thus identified as macrophages. The remaining cells grew out into large islands comprised of one or two distinct morphologic types of mammary epithelial cells. Optimum growth of these cells was obtained in medium buffered to pH 6.8, and the epidermal growth factor markedly prolonged the exponential growth phase of the cells. Two morphologically distinct populations of epithelial cells were also observed in cultures established from individual breast tumors. Growth of the malignant cells was relatively unaffected by the pH of the culture medium, and the cells were unresponsive to exogenously added hormones. Overgrowth of malignant epithelial cells in primary cultures by stromal fibroblasts was retarded by replacement of standard growth medium with fresh medium containing a serum substitute; growth of the malignant epithelial cells was unaffected. A feeder layer of mitomycin C-treated human fibroblasts increased the plating efficiency of both normal and malignant cells in primary culture and also facilitated passage of these cells to secondary and tertiary cultures.

Breast↗