F R Miller

Wayne State University, Detroit, Michigan, United States

Are you F R Miller?

Claim your profile

Publications (52)258.05 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Utilizing the MCF10AT xenograft model for progression of human proliferative breast disease, we detected expression of the endogenous estrogen receptor (ER) gene only in MCF10AneoT and cells of the MCF10AT system, all of which stably express a transfected mutated T24 Ha-ras gene. ER transcripts were undetectable in the parental MCF10A cells and in MCF10A cells transfected with normal c-Ha-ras or vector. ER transcripts expressed in MCF10AT cells contain a normal full-length ER coding region and direct synthesis of a normally sized ER protein. The protein is functional based on its ability to mediate estradiol (E2)-induced increases of transcription from both endogenous and exogenous E2-regulated genes. Transcriptional activation of the endogenous ER gene does not appear to be related to a change in methylation status of the gene since a diagnostic CpG site in exon 1 that is methylated in ER-negative breast tumors and completely unmethylated in ER-positive breast tumors is hypomethylated to the same extent in ER-negative MCF10A cells and ER-positive MCF10AT cells. E2 increased both the number and size of soft-agar colonies formed by MCF10AT3c cells, a line from a third generation MCF10AT xenograft lesion. This suggests that xenograft passage has selected for growth regulatory pathways that are E2-responsive and that identification of these pathways and their role in progression will aid in determining how E2 acts to increase risk of breast cancer.
    No preview · Article · Dec 1998 · International Journal of Oncology
  • S Iravani · L Mora · F R Miller · P J Dawson
    [Show abstract] [Hide abstract]
    ABSTRACT: Human breast epithelial MCF10AT cells form simple ducts in nude/beige mice which eventually become hyperplastic and sporadically progress to carcinomas. Altered immunohistochemical detection of c-erbB-2, DF3, B72.3, p53 and Ki-67 was observed with progression and differentiation to two distinct histologic types of invasive carcinoma. c-erbB-2 and DF3 were detected in 50% and 18% of lesions at the stage of atypical hyperplasia and expression increased to 78% and 54% in invasive adenocarcinomas. In contrast, a group of six unusual undifferentiated tumors with squamoid features did not express c-erbB-2 or DF3, but both B72.3 (4/6) and p53 (6/6) were detected.
    No preview · Article · Mar 1998 · International Journal of Oncology
  • G H Heppner · F R Miller
    [Show abstract] [Hide abstract]
    ABSTRACT: Variability in disease presentation and course is a hallmark of cancer. Variability is seen among similarly diagnosed cancers in different patients or animal hosts and in the same cancer at different periods of time. This latter type of variability, termed "tumor progression," was defined by Foulds in a series of six rules that describe the independent behavior of individual cancers and the independent evolution of different cancer characteristics. Tumor progression is believed to result from variability among subpopulations of tumor cells within individual cancers and from selection of these subpopulations by conditions within the cancer environment, such that different subpopulations come to prominence over the course of cancer development and growth. Interactions among subpopulations, however, modulate tumor behavior as well as tumor evolution. The leading hypothesis for the origin of tumor subpopulations is the genetic instability of cancer cells. There are a number of possible mechanisms of genetic instability, some internal to cancer cells (mutation, amplification, mutator phenotypes, DNA repair deficiencies) and some present in the tumor microenvironment (endogenous mutagens). There are also potential epigenetic mechanisms of variability, including alterations in gene regulation, differentiation, adaptation, and cell fusion. Regardless of mechanism, the heterogeneity of tumor subpopulations poses a number of challenges to the practice of cancer research, including the design of reproducible and meaningful experiments. Tumor heterogeneity also has significant consequences for the clinical assessment of tumor prognosis and the development of effective treatment regimens.
    No preview · Article · Feb 1998 · International Review of Cytology

  • No preview · Article · Jan 1998
  • B Wang · H D Soule · F R Miller
    [Show abstract] [Hide abstract]
    ABSTRACT: The ability of activated c-Ha-ras (codon 12 valine) to transform human breast epithelial cells varied for three different immortalized normal human breast epithelial cell lines established from two different women. Although activated c-Ha-ras may transform and induce a preneoplastic phenotype in MCF10A cells, activated c-Ha-ras was not sufficient to transform MCF10-2A cells. Only two of three MCF10-2A clones which expressed mutant p21 protein acquired the ability to form colonies in soft agar. When xenografted into nude beige mice, two MCF10-2A clones formed squamous carcinomas and one formed no lesions at all. The ability to form tumors did not correlate with growth in soft agar. All three activated c-Ha-ras-transfected clones of MCF-12A formed colonies in soft agar but only two produced squamous carcinomas in nude beige mice. Unlike activated c-Ha-ras-transfected MCF10A cells, none of the activated c-Ha-ras-transfected MCF10-2A or MCF-12A clones formed ducts in xenografts. Rather, initial xenograft lesions consisted of nests of cells with squamous differentiation. These observations illustrate that additional events are involved in the transformation and progression of human breast epithelial cells with activated c-Ha-ras.
    No preview · Article · Nov 1997 · Anticancer research
  • L Tait · P. J. Dawson · S. R. Wolman · K Galea · F.R. Miller
    [Show abstract] [Hide abstract]
    ABSTRACT: Human breast epithelial MCF10AT cells injected with Matrigel into the subcutis of nude/beige mice form simple ducts which, with time, resemble human proliferative breast disease and sporadically progress to carcinoma. Basement membrane was visualized with a silver stain and myoepithelial cells detected by their reactivity with antibody against smooth muscle actin. The ducts formed in situ are bilayered, composed of both myoepithelial and luminal epithelial layers circumscribed by a distinct basement membrane. The human origins of both luminal and myoepithelial layers were confirmed with fluorescent in situ hybridization with a probe for human chromosome 9. Electron microscopic studies reveal actin bundles and the formation of hemidesmosomes bordering the basement membrane, consistent with myoepithelium, as well as the formation of desmosomes between luminal and myoepithelial cells.
    No preview · Article · Aug 1996 · International Journal of Oncology
  • F R Miller · R J Pauley · B Wang
    [Show abstract] [Hide abstract]
    ABSTRACT: MCF10AT cells are human breast epithelial cells which are able to establish preneoplastic lesions in immune deficient mice. Although, the preneoplastic phenotype was observed following transfection with a mutated c-Ha-ras (codon 12 valine), clones of MCF10AT are unable to form lesions in vivo. Restriction size fragment analysis was used to confirm that a clone unable to form the preneoplastic lesions retained the activated c-HA-ras and confirmed that the insertion site of the activated c-Ha-ras was the same for the clone as for MCF10AT1 which was selected for its ability to form lesions in vivo. Western blotting with antibody specific for the codon 12 valine c-Ha-ras demonstrated that p21 protein was comparable as well. Thus, the activated c-Ha-ras is not sufficient for the preneoplastic phenotype of human breast stem cell line MCF10AT.
    No preview · Article · Jul 1996 · Anticancer research
  • Source
    P J Dawson · S R Wolman · L Tait · G H Heppner · F R Miller
    [Show abstract] [Hide abstract]
    ABSTRACT: A human cell line (MCF10A) originated from spontaneous immortalization of breast epithelial cells obtained from a patient with fibrocystic disease. MCF10A cells do not survive in vivo in immunodeficient mice. However, T24 c-Ha-ras oncogene-transfected MCF10A cells (MCF10AT) form small nodules in nude/beige mice that persist for at least 1 year and sporadically progress to carcinomas. By reestablishing cells in tissue culture from one of the carcinomas, a cell line designated MCF10AT1 was derived that forms simple ducts when transplanted in Matrigel into immunodeficient mice. With time in vivo, the epithelium becomes proliferative and a cribriform pattern develops within the xenografts. A significant number progress to lesions resembling atypical hyperplasia and carcinoma in situ in women, and approximately 25% progress to invasive carcinomas with various types of differentiation including glandular, squamous, and undifferentiated. Cells have been established in culture from lesions representing successive transplant generations. With each generation, cells are somewhat more likely to progress to high risk lesions resembling human proliferative breast disease. Although the incidence of invasive carcinoma remained fairly constant at 20 to 25%, the frequency of nodules showing proliferative breast disease rose from 23% in the first transplant generation to 56% in the fourth transplant generation.
    Full-text · Article · Feb 1996 · American Journal Of Pathology
  • El. Iravani · P.J. Dawson · F.R. Miller
    [Show abstract] [Hide abstract]
    ABSTRACT: MCF10AT cells inoculated in Matrigel into nude/beige mice form preneoplastic lesions resembling proliferative breast disease and develop invasive carcinomas in approximately 25X of mice, of which 75% are adenocarcinomas, the remainder are squamous. We have compared gene expression in the two tumor types using standard immunocytochemical methods. Antibodies used detect DF3, c-erbB2, p53, and B72.3. Among fifteen adenocarcinomas DF3 was expressed in 10, c-erbB2 was expressed in 11, p53 was weakly expressed in 2, and B72.3 was not detected in any of them. In contrast, among seven squamous carcinomas DF3 was not detected in any, c-erbB2 was expressed by 1, p53 was detected in all 7, and B72.3 was detected in 4. Differences between the two tumor types were significant for all antibodies tested by the Fisher's Exact Test. In one tumor with both squamous and glandular areas the former reacted with p53 and B72.3, and the latter with DF3 and c - erbB2. The les ions are produced by a stem cell with a characteristic karyotype of (47xx,t(3;9),t(9;9;5), 6p+,t(3;17),9+). Our data demonstrate that different markers are typically expressed in histologically different tumors arising from a single cell line. The underlying genetic changes during progression are yet to be determined but MCF10AT appears to be a preneoplastic stem cell line which progresses to different cancer types depending upon alternative genetic pathways (CA28366).
    No preview · Article · Jan 1996
  • P V Shekhar · J Werdell · J K Christman · F R Miller
    [Show abstract] [Hide abstract]
    ABSTRACT: We have found that p53 expression is altered with progression to the metastatic phenotype of a series of neoplastic subpopulations of a single mouse mammary tumor. Single strand conformation polymorphism (SSCP) analysis of p53 transcripts indicate that the expressed p53 genes in each of the subpopulations contain one or more differences from wild type p53. Although the mutations in the coding sequence of p53 are different in each of the sublines, suggesting that independent mutational events have occurred, the mutations are clustered in exons 2-4 and in exon 6. In the metastatic subpopulations, there is either a complete loss of p53 transcriptional activity or accumulation of transcripts with an additional alteration in exons 4-5.
    No preview · Article · Jan 1995 · Anticancer research
  • P V Shekhar · F R Miller
    [Show abstract] [Hide abstract]
    ABSTRACT: The ras family of cellular oncogenes is one of the most frequently detected families of transformation-inducing genes in human solid tumors. The capacity of breast cancers to grow and metastasize have been related to enhanced expression of normal p21ras rather than the mutant form. Transformation in tumours that lack the mutant p21ras has been suggested to result from transcriptional deregulation of ras. cis-Acting sequence elements that participate in the regulation of gene expression in normal tissues and that could serve as potential targets for the deregulation of expression in tumors have been localized in several genes including c-myc and N-ras. Using a mouse mammary metastasis model system of closely related tumor subpopulations that vary in metastatic potential and with defined deficiencies, we show that c-Ha-ras plays a prominent role as a metastasis-modulating gene in this system. We have identified a highly conserved cis-acting sequence element in the first intron of the mouse and rat, and in the first exon of Ha- and Ki-ras genes of human, mouse and rat. This regulatory sequence confers strong transcription enhancer activity that is differentially modulated by steroid hormones in metastatic and nonmetastatic subpopulations. Our results indicate that perturbations in the regulatory activities of cis-acting sequences such as the one we have identified may play an important role in governing oncogenic potency of Ha-ras through transcriptional control mechanisms.
    No preview · Article · Jan 1994 · Invasion and Metastasis

  • No preview · Article · Dec 1993 · European Journal of Cancer Prevention
  • [Show abstract] [Hide abstract]
    ABSTRACT: Progression of proliferative breast disease has been associated with increased risk for development of invasive carcinoma. Cell lines have been developed to facilitate the study of this process. Human cell line MCF10A originated from spontaneous immortalization of breast epithelial cells obtained from a patient with fibrocystic disease, and cell lines MCF10AneoN and MCF10AneoT were created by stable transfection of these cells with the neomycin-resistance gene and either the HRAS gene or the mutated T-24 HRAS gene, respectively. Our goal was to develop an experimental model of progressive human proliferative breast disease. MCF10A, MCF10AneoN, and MCF10AneoT cells were injected subcutaneously into the dorsal flank of male nude/beige (C57/BALB/c nu/nu bg/bg) mice (12 mice for each cell type). These mice were examined periodically for formation and persistence or growth of palpable nodules. One mouse per group was killed 1 week after cell injection; thereafter, mice were observed as long as possible. Cells were recovered from palpable lesions by enzymatic dissociation of the excised lesions. Cells re-established in tissue culture from a week-14 tumor (MCF10AneoT.TG1) were injected into 12 male nude/beige mice. Southern blot hybridization analysis of the HRAS gene locus and cytogenetic analyses were performed. Transplanted MCF10A and MCF10AneoN cells formed transient, small palpable nodules that regressed and disappeared during the 4th and 5th weeks. In 10 of the 12 mice, T-24 HRAS gene-transfected MCF10A cells (MCF10AneoT) formed small, flat nodules that persisted for at least 1 year. Three of these xenografts became carcinomas. One (removed 7 weeks after transplantation) was an undifferentiated carcinoma composed of polygonal cells with large, vesicular nuclei and numerous mitoses. The second (removed after 14 weeks) was an invasive squamous cell carcinoma. The third (removed after 56 weeks) was a moderately differentiated adenocarcinoma. Initially, xenografts of MCF10AneoT.TG1 cells showed intraductal proliferative changes; after 23 weeks, the lesions showed histologic features resembling those seen in atypical hyperplasia of the human breast, and later lesions showed characteristics of carcinoma in situ. The MCF10 lineage of cells of three MCF10AneoT.TG1 xenografts was confirmed by DNA fingerprinting and karyotype analysis. MCF10AneoT and MCF10AneoT.TG1 comprise a transplantable xenograft model that produces a broad spectrum of human proliferative breast disease. The reproducible establishment of representative stages in early breast cancer progression from the MCF10 model offers a new opportunity to analyze critical events of carcinogenesis and progression in breast cancer.
    No preview · Article · Dec 1993 · JNCI Journal of the National Cancer Institute
  • Source
    B E Miller · F R Miller · T Machemer · G H Heppner
    [Show abstract] [Hide abstract]
    ABSTRACT: In order to examine in detail the sensitivity to chemotherapy of tumour cells at various organ sites and at various stages of metastasis, we have used a series of cell lines, all selected from sister subpopulations derived from a single mouse mammary tumour, which can be distinguished and quantitated from normal cells and from each other through growth in selective medium. For the studies described here, we used two lines, 4T07 and 66FAR, which will form colonies in vitro in medium containing 60 microM 6-thioguanine or 330 microM 2,6-diaminopurine, respectively. Both cell lines have similar sensitivity to the test chemotherapeutic agent, melphalan, in vitro. These two tumour cell lines were treated with melphalan in vivo, when growing either in lungs as experimental metastases at various times after cell injection or as palpable tumours growing subcutaneously. Responses to various doses of melphalan were measured by removing lungs or subcutaneous tumours and performing colony-forming assays in selective medium. The data indicate marked shifts in sensitivity as a function of metastatic stage. Analyses of dose-response curves show that both cell lines were similarly sensitive to melphalan at early times (45 min) after cell injection i.v. but became less sensitive at an intermediate time after injection (3 days). Differences between the two lines became apparent at later times after i.v. injection (by day 8 or 9) and in subcutaneous tumours, where a marked reduction in the shoulder of the dose response curve was seen in line 4T07, resulting in sensitivity equal to or greater than the of early times, whereas the dose response parameters of 66FAR remained at those of the intermediate time point. These results show that, in heterogeneous tumours, individual subpopulations of tumour cells may respond differently to chemotherapeutic agents at various disease stages. In vitro measures of tumour sensitivity do not predict these changes in in vivo sensitivity. Model systems similar to the one described here may yield information which will eventually be useful in maximising the efficacy of clinically relevant adjuvant chemotherapy regimens.
    Full-text · Article · Aug 1993 · British Journal of Cancer
  • P. V. M. Shekhar · C J Aslakson · F R Miller
    [Show abstract] [Hide abstract]
    ABSTRACT: A number of genes have been implicated in the metastatic process but relatively little is known regarding the specific event(s) in dissemination of malignant cells which are altered by specific genetic changes. In most cases, only a correlation between gene expression and a final outcome, e.g. patient survival or enumeration of metastatic nodules at necropsy for experimental animal models, exists. In other cases, gene expression has been correlated with one part of the metastatic cascade but possible alterations in additional steps were not determined. The ultimate effect of expression of any gene on specific steps in the metastatic cascade varies with the cell type. To minimize differences due to unspecified differences in background genetic mutations and expression, a model of closely related tumor subpopulations, which vary in metastatic potential and whose specific deficiencies are known, is described. This model may prove to be valuable in assessing the steps in the metastatic cascade affected by specific metastasis modulating genes.
    No preview · Article · Jul 1993 · Seminars in Cancer Biology
  • J Rak · F R Miller

    No preview · Article · Jun 1993 · International Journal of Cancer
  • Source
    J W Rak · D McEachern · F R Miller
    [Show abstract] [Hide abstract]
    ABSTRACT: A sequential, quantitative loss of Peanut agglutinin (PNA) binding with progression of mouse mammary cells from normal to preneoplastic to neoplastic phenotypes was observed. Normal mammary epithelium, preneoplastic mammary lesions designated D2HAN (D2-type hyperplastic alveolar nodules) and a series of nine spontaneous tumours (D2ST1, D2ST2, D2ST3, D2ST4, D2A1, D2F2, D2.0R, D2.1, EMT6R08) derived from mice bearing D2HAN were grown in culture and analysed by flow cytometry with respect to PNA binding intensity to the cell surface. Primary cultures of normal mammary epithelium strongly bound PNA. A stepwise decrease in PNA binding by preneoplastic D2HAN cells and subsequent tumours arising from those hyperplastic lesions was observed. Three cloned tumour subpopulations derived from such tumours exhibited dramatic differences in PNA binding ranging from high (D2.0R) to low (D2.1) to very low (D2A1 cells). Their growth rate in vitro was similar. However, an inverse correlation between PNA binding and malignant characteristics, such as the incidence and latency of subcutaneous tumours and the efficiency of the tumour cells to form lung colonies after i.v. injection, existed. Cells subsequently derived from tumours resulting from injection of the D2.0R clone (high PNA binding, low tumorigenicity) were found to have diminished PNA binding properties and to be more tumorigenic when reimplanted into syngeneic mice. The difference in PNA binding (up to 50-fold) between normal mammary cells and other mouse mammary tumour cells, i.e., unrelated to D2HAN lesions, was also seen. These include six sister subpopulations derived from a single BALB/cfC3H mouse mammary tumour (lines: 67, 66c14, 168FARN, 4TO7, 68H, 64pT) as well as SP1 spontaneous CBA/J mouse mammary carcinoma. The difference was greatly reduced by neuraminidase treatment suggesting a masking of PNA binding sites by sialic acid. Separation of cell lysates by SDS-PAGE revealed a high molecular weight PNA binding glycoprotein (greater than 250 kd) expressed by normal mammary epithelium and preneoplastic D2HAN cells, but not by tumour cells regardless of neuraminidase treatment. A PNA reactive glycoprotein of approximately 90 kd was uniquely expressed in normal mammary epithelial lysates, although neuraminidase treatment exposed a similar band in a few tumour lines. Normal mammary epithelium, preneoplastic D2HAN cells, and the poorly tumorigenic clone D2.0R expressed a PNA binding glycoprotein of approximately 150 kd. This band appeared to be specifically sialylated during transition from the high PNA binding, low tumorigenic phenotype of D2.0R cells to the low PNA binding, highly tumorigenic phenotype of cells isolated from tumours resulting from s.c. implantation of D2.0R cells.(ABSTRACT TRUNCATED AT 400 WORDS) Images Figure 8 Figure 9
    Full-text · Article · Jun 1992 · British Journal of Cancer
  • Source
    C J Aslakson · F R Miller
    [Show abstract] [Hide abstract]
    ABSTRACT: To identify selective steps in metastasis, those that eliminate nonmetastatic tumor cells more efficiently than metastatic cells, we have evaluated the sequential dissemination of tumor cells from a mammary fatpad, using both metastatic (4T1 and 66cl4) and nonmetastatic (67NR, 168FARN, and 4TO7) subpopulations of a single mouse mammary tumor. Each of these variant subpopulations is resistant to one or more selective drugs so they could be quantitatively identified by colony formation in selective media. We found that the 2 metastatic cell lines metastasized by different routes and that the nonmetastatic tumor cell lines failed at different points in dissemination. Line 67NR did not leave the primary site; clonogenic tumor cells were not detected in the nodes, blood, or lungs during the experiment (7 weeks). Tumor line 168FARN disseminated from the primary tumor because clonogenic cells were cultured from the draining lymph nodes throughout the experiment. However, dissemination essentially stopped in the node as cells were rarely isolated from blood, lungs, or lives. Whether 168FARN cells failed to reach these tissues or were killed very rapidly after traversing the lymph node is unknown. Line 4TO7 cells disseminated via the blood and were consistently recovered from lungs by day 19 but failed to proliferate. This panel of 5 subpopulations thus identifies different points of selective failure in tumor cell dissemination and should be valuable in the assessment of antimetastatic therapies.
    Preview · Article · Apr 1992 · Cancer Research
  • J W Rak · M Debiec-Rychter · F R Miller · C Y Wang
    [Show abstract] [Hide abstract]
    ABSTRACT: Bladder tumor cell lines derived from male F344 rats treated with N-buthyl N-(4-hydroxybuthyl) nitrosamine (BBN) or N-[4-(5-nitro-2-furyl)-2-thiazolyl] formamide (FANFT) have been established in vitro and characterized with respect to histology, karyotype, myc and c-Ha-ras oncogene expression or mutation, anchorage-independent growth and tumorigenicity in nude mice. This unique model system comprising 13 cell populations was employed to study common events during development of carcinogen-induced urothelial neoplasia. Differential expression of malignant phenotypes by these cell lines prompted us to examine their expression of carbohydrate structures binding peanut agglutinin (PNA), soy bean agglutinin (SBA) or leukoagglutinin (L-PHA), which are known indicators of tumor progression in rodents and humans. In the present study we analyzed the patterns of glycoproteins reactive with PNA and L-PHA by Western blotting. We also estimated quantitative differences in lectin binding to surfaces of normal rat urothelium and tumor cell lines by flow cytometry. The patterns of PNA or L-PHA reactive glycoproteins expressed by tumor cells were different from that of normal urothelium in culture. They were also different amongst the tumor cells. A unique non-sialylated, PNA binding glycoprotein (117 kD) was seen in the case of the highly tumorigenic F5 cell line and absent in normal urothelium as well as in other tumor cell lines. Normal cells did not express glycoprotein 60 kD binding PNA (only after desialylation), which was found in lysates of some but not all transformed cell lines. A very high molecular weight (much greater than 200), perhaps mucin-like sialoglycoprotein was found in normal urothelium but not in most of the tumor cell lines. Four major L-PHA reactive bands (greater than 200, 190, 100, 80 kD approximately) were found in normal urothelium. Some of those bands were overexpressed or missing in materials isolated from different tumor cell populations. Total cell surface binding of SBA and PNA by different tumor cell lines was very heterogenous (167-2% that of normal urothelium). No simple correlation between expression of the lectin binding glycoconjugates by urothelial carcinoma cells and other known functional, phenotypic or genetic alterations was found. We were also unable to demonstrate carcinogen-specific changes in expression of lectin binding to these tumor cell lines. Thus we conclude that lectin binding patterns are cell line specific. This may reflect distinct pathways of progression of individual cell lines. The potential sources of phenotypic variability between the cell lines were discussed.
    No preview · Article · Feb 1992 · Neoplasma
  • J.W. Rak · F Basolo · J.W. Elliott · J Russo · F.R. Miller
    [Show abstract] [Hide abstract]
    ABSTRACT: Fluorescent lectin binding to cell surfaces was quantitatively analysed by flow cytometry on mortal human breast epithelial cells MCF-10M, the immortalized cell line MCF-10A derived from MCF-10M and sublines of MCF-10A transfected with the neomycin resistance gene (MCF-10Aneo), the c-Ha-ras protooncogene (MCF-10AneoN), or transfected and transformed with the c-Ha-ras activated oncogene (MCF-10AneoT). Immortal MCF-10A cells bound 10-fold more peanut agglutinin (PNA) and soy bean agglutinin (SBA) than did MCF-10M cells. Transformed MCF-10AneoT cells bound approximately ten times more PNA than did non-transformed cells transfected with protooncogene (MCF-10AneoN). Treatment of the transfectants with neuraminidase abrogated the differences in PNA-binding and reduced the differences in SBA binding. SDS-PAGE separation of PNA binding glycoproteins revealed different patterns for all MCF-10A derived sublines.
    No preview · Article · May 1991 · Cancer Letters

Publication Stats

3k Citations
258.05 Total Impact Points


  • 1998
    • Wayne State University
      • Department of Pathology
      Detroit, Michigan, United States
  • 1996-1998
    • Karmanos Cancer Institute
      • Division of Hematology and Oncology
      Detroit, Michigan, United States
  • 1997
    • The Scripps Research Institute
      لا هویا, California, United States
  • 1983
    • University of Minnesota Duluth
      Duluth, Minnesota, United States
  • 1979
    • Baylor College of Medicine
      Houston, Texas, United States
  • 1978-1979
    • Brown University
      • Department of Medicine
      Providence, Rhode Island, United States