Consequences of angiogenesis for tumor progression, metastasis and cancer therapy.

The growth of solid tumors to a clinically relevant size is dependent upon an adequate blood supply. This is achieved by the process of tumor stroma generation where the formation of new capillaries is a central event. Progressive recruitment of blood vessels to the tumor site and reciprocal support of tumor expansion by the resulting neovasculature are thought to result in a self-perpetuating loop helping to drive the growth of solid tumors.

A comparison of the effects of human rIL-2 and autologous TCGF on Xenopus laevis splenocytes in vitro.

Prior studies have shown that intraperitoneal (ip) injection of 25 IU of human rIL-2 can effectively modulate in vivo immune reactivity to thymus-dependent and thymus-independent type 2 immunogens in Xenopus laevis, the South African clawed toad, but is less successful at affecting toad cells in vitro. Here we compare the capacities of human rIL-2 and autologous TCGF to modulate Xenopus splenocytes in vitro and find that autologous TCGF (1) is more effective at stimulating mitogenesis, (2) can serve as a ligand for inducible receptors that will also bind rIL-2 and an F1*-mouse anti-human p55 antibody, and (3) will regulate the expression these receptors.

Progressive loss of sensitivity to endothelium-derived growth inhibitors expressed by human melanoma cells during disease progression.

Tumor progression is frequently associated with changes in responsiveness of tumor cells to paracrine growth factors. A potential major source of such paracrine factors in solid tumors are endothelial cells since this type of cell can constitute a sizeable fraction of the cellular composition of solid tumors. As an initial step to examining the possible effects of endothelial cell-associated growth factors on tumor cell growth, a panel of human melanoma cell lines representative of different stages of tumor progression was employed for studies utilizing endothelial cell-derived growth modulators.

Growth advantage ("clonal dominance") of metastatically competent tumor cell variants expressed under selective two- or three-dimensional tissue culture conditions.

In previous experiments it was shown that injection into syngeneic CBA/J mice of cell mixtures containing an excess of non-metastatic SP1 mouse mammary carcinoma cells with a ras transfected metastatic variant of SP1 called C1, always resulted in the eventual dominance of the C1 subpopulation at the site of inoculation. This occurred despite the growth rates of the two cell populations being identical in vivo when grown separately. The means by which the C1 subpopulation achieved "clonal dominance" is thought to involve its responsiveness to stimulatory paracrine growth factors liberated by the non-metastatic SP1 population.

Increased resistance to oncostatin M-induced growth inhibition of human melanoma cell lines derived from advanced-stage lesions.

Human melanomas can become progressively resistant to the growth-inhibitory effects of a broad family of structurally diverse cytokines which includes interleukin 6 (IL-6). Uncovering this multicytokine resistance was made possible by the availability of cell lines established from early-stage radial growth phase or vertical growth phase primary melanomas as well as more advanced primary lesions and distant metastases. Because Oncostatin M (OSM) is also a member of the IL-6 family we evaluated the effects of this cytokine on the growth of human melanoma cell lines obtained from different stages of disease progression.

Sequential alteration of peanut agglutinin binding-glycoprotein expression during progression of murine mammary neoplasia.

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.

Cell line specific abnormalities in expression of PNA, SBA and L-PHA binding sites by carcinogen induced rat urothelial carcinomas.

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.

[The role of sclerotherapy in the treatment of esophageal varices in children].

The authors presented the actual views and their own results of using sclerotherapy in children with oesophageal varices. Oesophageal varices exist almost every time as a most dangerous complication in patients with portal hypertension. Acute haemorrhage caries a high mortality and the extremely important priority is control of bleeding as soon as possible.

[Investigations of the ototoxicity of dicortinef (ear drops)].

The authors investigated the ototoxic influence of Dicortinef in laboratory animals. Their examinations were performed on 15 guinea pigs (weighing 210-380 g.) after application of this medicine to the fenestra rotunda.

Cell surface glycosylation changes accompanying immortalization and transformation of normal human mammary epithelial cells.

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).

Absorption and luminescence spectroscopic analysis of tautomeric forms of protonatedN,N-dimethyl-N'-(1-nitro-9-acridinyl)-1,3-propanediamine (nitracrine) and its nitro isomers in poly(vinyl alcohol) films.

The electronic absorption, fluorescence, and phosphorescence excitation spectra, as well as the fluorescence and phosphorescence spectra, at either room or liquid nitrogen temperatures, were measured forN,N-dimethyl-N'-(1-nitro-9-acridinyl)-1,3-propanediamine and its three nitro isomers in acidified poly(vinyl alcohol) (PVA) film. The spectral characteristics obtained reveal the existence of the compounds studied in at least two structural forms. The results are interpreted in terms of the tautomeric phenomena which originate due to the migration of the hydrogen atom, which is bound to the nitrogen atom attached to the carbon atom (9), to the acridine ring nitrogen.

Differential influence of organ site on three subpopulations of a single mouse mammary tumor at two distinct steps in metastasis.

Tumor subpopulations 66c14, 168FARN, and 4T07 are drug-resistant variants selected from sister subpopulations derived from a single mouse mammary tumor. These subpopulations are heterogeneous in their capacities to form experimental metastatic growth in the lungs and liver. Initial survival kinetics of arrested cells, determined by the clearance of 125IUdR-labelled cells, and subsequent growth rates, determined by sequential recovery of clonogenic tumor cells from occult metastases, both correlated with organ-colonizing potential as determined by necropsy.

Lectin-resistant variants of mouse Lewis lung carcinoma cells. I. Selection and in vivo properties.

The availability of lectin-resistant cell lines with altered carbohydrate moieties in cell surface glycoproteins and glycolipids has greatly facilitated study of the involvement of cellular glycoconjugates in tumor growth and metastasis. We present here a new animal model for metastasis study based on mouse Lewis lung carcinoma LL2 in vitro cell line. From this line, five lectin-resistant variant sublines were selected with the following lectins: wheat germ agglutinin (WGAR), Ricinus communis agglutinin II (RCA IIR) and Aleuria aurantia agglutinin (AAAR).

[Histological and electron microscopic examinations of laryngeal papilloma in children and adults].

The authors present the results of histologic and electron microscopic investigations of larynx papillomas in 11 children and 8 adults. Comparative estimation showed the characteristic changes for clinical and morphological division of papilloma into adult-type and juvenile one. Detailed morphological analysis in adult-type papilloma either with dysplastic changes or with hyperkeratosis was performed.

Possible role of tumour stem-end cell cooperation in metastasis.

The explanation of some discrepancies in the current view on metastasis is proposed by the assumption that cooperation between clonogenic and differentiated cells is essential for the process.

Potentiation of cyclophosphamide-induced enhancement of experimental metastasis by splenectomy.

Role of spleen in CY-induced enhancement of experimental lung metastases of Lewis Lung Carcinoma LL2 cells was studied. Reconstitution with spleen cells abolished the enhancing effect of CY. Conversely, removal of spleen in CY treated mice caused about two-fold increase in the number of metastases.

Transplantable mouse mammary adenocarcinoma 16/c as a model in experimental cancer therapy. III. Sensitivity to antitumor drugs.

On the basis of biological characteristics of murine transplantable mammary adenocarcinoma 16/c, experimental conditions optimal for chemotherapeutic experiments were defined. Sensitivity of primary tumor and lung metastases to the treatment with drugs used in breast cancer therapy: cyclophosphamide, 5-fluorouracil and adriamycin was confirmed. These drugs were significantly more effective in combination than when administered as monotherapy.

Transplantable mouse 16/c mammary adenocarcinoma as a model in experimental cancer therapy. II. Modification of tumor-host interactions by therapeutic procedures.

The influence of therapeutic procedures on tumor--host interactions was analysed using 16/c mouse mammary adenocarcinoma model system. After partial removal of tumor burden the growth enhancement of remnant tumor mass was observed. Pretreatment of the host either with cyclophosphmide or X-rays resulted in enhancement of experimental metastasis formation.

[The problem of diagnosing tumors of the nose and paranasal sinuses].

A case of incorrect diagnosis of extensive nasal cavity, maxillary sinus and nasopharynx neoplasm was presented. The imitation of tumor symptoms was due by long lying in nasal cavity foreign body, inflammation of maxillary sinus and adenoiditis. The author underline that over hasty neoplasm diagnosis always exerts an unjustified and destructive psychologic influence on patient and his family.

Cytologic appearance of esthesioneuroblastoma in a fine needle aspirate.

Esthesioneuroblastoma (olfactory neuroblastoma) is a rare malignant neoplasm derived from the olfactory epithelium. It was diagnosed by cytologic study of fine needle aspiration biopsy smears of a tumor situated in the nasopharynx in a 57-year-old man.

Transplantable mouse 16/C mammary adenocarcinoma as a model in experimental cancer therapy. I. Kinetics of growth and spread.

Introduction of transplantable animal tumours has enabled the development of different model systems in which the site and type of tumour growth depends on the selection of suitable route for cells inoculation. Manipulation of the inoculation route of 16/C mammary adenocarcinoma results in local tumour growth either subcutaneous (s.c.