Expression of peanut agglutinin receptors on virus-induced preleukemic cells in mice.

Reisner, Yaīr; Sharon, Nathan; Haran-Ghera, Nechama

doi:10.1073/pnas.77.4.2244

Cited by 18 publications

(4 citation statements)

References 16 publications

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“…The failure of PNA to bind to mucin in the normal colon after neuraminidase treatment makes this explanation unlikely, although sialic acid residues could be present in mucin which are resistant to hydrolysis by the bacterial neuraminidase. Glycoconjugates that are bound by PNA are present on the surface membranes of several types of transformed cells and are absent from their nontransformed counterparts in certain animal models (18) as well as in human breast (14,(19)(20)(21), lymphoproliferative (22,23), and urinary tract malignancies (24). This suggests that the appearance of glycoconjugates bound by PNA may be common in malignant transformation.…”

Section: Discussionmentioning

confidence: 97%

Alterations in human colonic mucin occurring with cellular differentiation and malignant transformation.

Boland¹,

Montgomery²,

Kim³

1982

Proc. Natl. Acad. Sci. U.S.A.

279

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The binding of fluorescein isothiocyanate (FITC)-conjugated lectins to mucin in the human colon was studied by using fluorescence microscopy. In normal mucosa, lectins that preferentially bind to exposed N-acetyl-galactosamine residues (Dolichos biflorus agglutinin and soybean agglutinin) bound selectively to the goblet cell mucin of well-differentiated cells in the upper colonic crypt. By contrast, lectins that require exposed nonreducing galactose residues for binding (Ricinus communis agglutinin, and Bauhinia purpurea agglutinin) preferentially labeled the mucin of less-differentiated goblet cells located in the lower portion of the colonic crypt. The lectin derived from Arachis hypogaea (peanut agglutinin) has a high affinity for a carbohydrate structure not normally exposed in human tissues. This lectin did not label the goblet cell mucin in the normal colon. However, the mucin was labeled in all 21 colon cancer specimens examined. Additionally, the nonmalignant epithelium immediately adjacent to colon cancer (termed "transitional mucosa") also contained goblet cell mucin that was labeled by FITC-peanut agglutinin. Three conclusions may be drawn from the selective binding characteristics of FITC-lectins to colonic mucins. First, an alteration in the exposed, nonreducing carbohydrate residues occurs in human colonic mucin during the process of goblet cell differentiation. Second, an exposed carbohydrate structure that is not normally present in human tissues is expressed in the mucin produced by malignant colonic epithelium. Third, the presence of the cancerassociated carbohydrate structure in the mucin of transitional mucosa suggests that this tissue may be in the process of early malignant transformation.

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Section: Discussionmentioning

confidence: 97%

Alterations in human colonic mucin occurring with cellular differentiation and malignant transformation.

Boland¹,

Montgomery²,

Kim³

1982

Proc. Natl. Acad. Sci. U.S.A.

279

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“…These systems include the slime mold (6,14,40), the intestine (10) and colon (9, 12,). prenatal cerebral tissue (30), developing pancreas (21), leukemic cells (32)(33)(34), and the epidermis (4, 16,19,26,28,38). These modifications in cell surface glycoconjugates may be physiologically significant, because the carbohydrate moiety has been implicated in cell differentiation (17,36), proteolytic stability (8,29), secretion (18), membrane insertion (20), and enzymatic activity (11).…”

mentioning

confidence: 99%

Modification of cell surface glycoprotein: addition of fucosyl residues during epidermal differentiation.

Zieske¹,

Bernstein²

1982

The Journal of Cell Biology

103

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When cutaneous sections from the newborn rat were treated with a-fucosidase, Ulex europeus agglutinin I (UEA) binding to the cell surface of the differentiated cells in the epidermis was diminished and there was an appearance in these cell layers of binding by Bandeiraea simplicifolia I-B4 lectin (BS I-B4), which normally is specific for the basal cells. A similar treatment with a-galactosidase resulted in a loss of BS I-B4 binding, but had no effect on UEA binding. Glycoproteins isolated from the membranes of epidermal cells showed a threefold increase in the ratio of binding to UEA versus BS I-B4 affinity columns as the proteins were derived from the more differentiated cell populations. These data suggest that a-fucosyl residues are added to the glycoproteins on the cell surfaces of differentiated cells, thus blocking a-galactosyl residues and changing the lectin binding specificity as epidermal cells move out of the basal cell layer.

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“…Potentially neoplastic cells have been shown in systemically irradiated (2,3) (5). Furthermore, few properties of potentially neoplastic cells are known (6,7) because they have neither been grown nor otherwise isolated from the putative organs of their in vivo residence.…”

Section: Introductionmentioning

confidence: 99%

Mechanism of T-cell lymphomagenesis: transformation of growth-factor-dependent T-lymphoblastoma cells to growth-factor-independent T-lymphoma cells.

Haas¹,

Rothenberg²,

Bogart³

et al. 1984

Proc. Natl. Acad. Sci. U.S.A.

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In a previous paper we described the induction by x-irradiation or radiation-induced leukemia virus-inoculation of two classes of lymphoid T-cell neoplasms: The first class, designated T-cell lymphoblastoma (TCLB), consists of growth-factor-dependent eudiploid cells that home to the spleen and give rise to splenic tumors on injection into syngeneic mice; the second class, designated T-cell lymphoma (TCL), consists of growth-factor-independent aneuploid or pseudodiploid cells that give rise to local tumors at the site of subcutaneous injection. This paper describes the generation of a family of growth-factor-independent aneuploid or pseudodiploid TCL cells after the injection into the thymus of growthfactor-dependent diploid TCLI cells. In contrast to the donor TCLB cells, the resulting TCL cells could be cloned in semisolid medium, produced local tumors at the site of subcutaneous injection, and proliferated in a growth-factor-independent fashion in vitro. The induced growth-factor-independent TCL cells were chromosomally and phenotypically unstable and continued to evolve both in vivo and in vitro. After propagation in the thymus, the cells often showed stable translocations in addition to the evolving aneuploidy. We propose that the chromosome abnormalities induced during the proliferation of growth-factor-dependent TCLB cells in the thymus constitute a general mechanism by which neoplastic cells progress from growth-factor dependency to independency.The mechanism of evolution of T-cell lymphomas (TCL) within the thymus of systemically irradiated or radiation-induced leukemia virus (RadLV)-inoculated C57BL/6 (B6) mice is as yet unknown. Some models suggest that in the preneoplastic thymus there exists a continuing regenerative hyperplasia of cells leading to neoplasia, with the subsequent crowding out of the normal lymphocytes by neoplastic lymphoblasts (1). This We have propagated and cloned in culture a class of T lymphoblasts from the spleens and lymph nodes of irradiated or RadLV-inoculated mice long before these had developed a thymic lymphoma (8). These neoplastic cells (T-cell lymphoblastoma; TCLB) precede the appearance of thymic lymphomas by 6-10 weeks. The isolation of these TCLB cells (8) suggests that they, or cells possessing similar properties, may be precursors to a class of autonomous neoplastic TCL cells. TCLB cells are distinct from thymic TCL cells in the following ways: (i) They are growth-factor dependent, autostimulating [producing their own growth factor(s)], and eudiploid; and (ii) they do not form colonies in soft agar unless the cultures are supplemented with exogenous conditioned medium. When injected in vivo, TCLB cells give rise to splenic tumors. Their tumorigenicity depends on the fact that they home to the spleen; they do not induce tumors at the site of subcutaneous inoculation. These characteristics of TCLB cells have been stable through prolonged propagation in vitro in mass culture, through cycles of single-cell cloning, and through repeated in vivo (splenic) passa...

show abstract

Expression of peanut agglutinin receptors on virus-induced preleukemic cells in mice.

Cited by 18 publications

References 16 publications

Alterations in human colonic mucin occurring with cellular differentiation and malignant transformation.

Alterations in human colonic mucin occurring with cellular differentiation and malignant transformation.

Modification of cell surface glycoprotein: addition of fucosyl residues during epidermal differentiation.

Mechanism of T-cell lymphomagenesis: transformation of growth-factor-dependent T-lymphoblastoma cells to growth-factor-independent T-lymphoma cells.

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