bluuebunny/crossref_metadata_2025_split huggingface dataset:
Tumor‐cell killing by MAbs against fucosyl GM1, a ganglioside antigen associated with small‐cell lung carcinoma
Authors: Brezicka Fred‐Thomas , Holmgren Jan , Kalies Inge , Lindholm Leif 
Published: February 2007

AbstractMonoclonal antibodies (MAbs) reactive with the ganglioside fucosyl GM1 (Fuc‐GM1), an antigen associated with small‐cell carcinoma of the lung (SCLC), were tested for their ability to mediate tumor‐cell killing in vitro in conjunction with humoral and cellular effectors and to inhibit tumor engraftment in nude mice in vivo. MAbs F12 and F15, both IgG3k, induced human complement‐mediated cytolysis of 3 Fuc‐GM1‐expressing tumor cell lines: one rat hepatoma cell line, H4‐II‐E, and 2 human SCLC cell lines, NCI H69 and NCI H128. F12 and F15 also induced ADCC of these cell lines in the presence of either murine or human effector cells. Addition of sub‐cytolytic amounts of fresh human serum as complement source resulted in enhanced ADCC induced by MAb F12 (IgG3). Also a Fuc‐GM1‐reactive MAb of IgM isotype, F9, was able to induce such complement‐aided ADCC (CADCC). F12 and F15 both proved to effectively inhibit engraftment of H4‐II‐E tumors in nude mice. A single dose of a modest amount (40 μg) of MAb conferred 65 to 100% protection against development of tumors. Our results demonstrate that Fuc‐GMI can act as a target antigen on tumor cells for specific immunotherapy in vitro and in a mouse model in vivo. Complement and murine and human mononuclear effector cells were effective mediators of tumor cytolysis in vitro in the presence of murine Fuc‐GM1‐reactive MAbs. Our results also suggest that humoral and cellular effectors may co‐operate in specific tumoricidal reactions and that these may be induced by antibodies of both IgG and IgM isotypes.
Association between restriction fragment length polymorphism of the L‐myc gene and lung metastasis in human breast cancer
Authors: Champeme Marie‐Hélène , Bieciie Ivan , Latil Alain , Hacene Kamel , Lidereau Rosette 
Published: February 2007

AbstractEcoRI restriction fragment length polymorphism (RFLP) of the L‐myc gene was examined in leukocyte DNAs isolated from 381 breast cancer patients. No differences in the patterns of L‐myc RFLP were found between breast cancer patients and healthy individuals. However, among 97 patients who relapsed, a statistical correlation was found between L‐myc RFLP and lung metastases (p < 0.05). These results are in close agreement with previous findings in patients with cancer of the lung, bone or kidney, and suggest that L‐myc RFLP may be a useful marker for predicting lung metastasis in some human cancers.
Genital papillomavirus infection and cervical dysplasia—opportunistic complications of hiv infection
Authors: Laga Marie , Icenogle Joseph P. , Marsella Richard , Manoka Abib Thiam , Nzila Nzilambi , Ryder Robert W. , Vermund Sten H. , Heyward William L. , Nelson Ann , Reeves William C. 
Published: February 2007

AbstractCertain human genital papillomaviruses (HPV) are strongly associated with cervical dysplasia and cancer. Evidence is accumulating that HPV infection and ano‐genital cancers are more common in patients with the acquired immunodeficiency syndrome. The objective of our study was to evaluate the extent to which HPV infection and associated cervical disease constitute opportunistic complications of human immunodeficiency virus (HIV) infection in a population of sexually promiscuous, HIV‐infected women in Kinshasa, Zaire. In 1989 we obtained Pap smears and cervicovaginal lavage specimens for HPV DNA testing from 47 HIV‐seropositive and 48 HIV‐seronegative prostitutes who were part of a cohort under observation since 1988. Thirty‐eight percent of the HIV‐seropositive and 8% of the seronegative women (odds ratio = 6.8; p = 0.001) had HPV DNA detected by either Vira Type, a dot‐blot assay which detects specific genital HPV types, or low‐stringency Southern blot, which detects all HPV types. Eighty‐two women (86%) had an interpretable Pap smear; 11 of 41 (27%) HIV‐seropositive women and one of 41 (3%) seronegative women had cervical intra‐epithelial neoplasia (CIN) (odds ratio = 14.7; p = 0.002). HIV seropositivity, HPV infection and CIN were highly associated. Eight (73%) of 11 seropositive women with CIN had HPV detected. Both HPV infection and cervical cancer may emerge as opportunistic complications of HIV infection in populations in which HIV, HPV and cervical cancer are common.
Quantitative dot blot analyses of blood‐group‐related antigens in paired normal and malignant human breast tissues
Authors: Ura Yasuaki , Dion Arnold S. , Williams Charlene J. , Olsen Brian D. , Redfield Ernest S. , Ishida Masao , Herlyn Meenhard , Major Pierre P. 
Published: February 2007

AbstractMembranes were prepared from 31 breast‐cancer specimens and adjacent mammary tissues, dot‐blotted to nitrocellulose paper, and reacted with monoclonal antibodies (MAbs) (A, B, Lewis a, Lewis b, sialylated Lewis a, Lewis x, and Lewis y) and lectins (Ulex europaeus, peanut agglutinin) having various blood‐group specificities. The expression of epithelial membrane antigen was assayed with MAb MA5. The ratio of breast‐cancer to normal mammary membrane preparations (C/N ratios) of these reagents was measured by densitometric scanning. We observed a decrease in the levels of A, B, Lewis a, Lewis b, sialylated Lewis a, and Lewis y antigens and an increase of Lewis x, T, and MAS‐reactive determinants in breast cancers. The incidence of incompatible A, as well as A and B, antigens was demonstrated for 2 patients of blood group B and O respectively. When the receptor content was plotted against the C/N ratio of these various reagents, a significant inverse relationship between the C/N ratio of Lewis x antigen and estrogen (ER) and progesterone receptor (PR) content was observed in breast cancers. The mean C/N ratio of Lewis x antigen was significantly higher in the ER‐negative/PR‐negative (ER−/PR−; 2.33 ± 1.17), as compared with the ER‐positive/PR‐positive (ER+/PR+; 0.97 ± 0.80). According to these observations, Lewis x antigen expression may be influenced by hormonal stimuli such as estrogen and progesterone.
Immunologic aspects of fibrosis in mouse mammary carcinomas
Authors: Vaage Jan 
Published: February 2007

AbstractThe nature of the fibrosis associated with mammary carcinomas MC2 and MC3 was investigated in syngeneic C3H mice. Accelerated and enhanced peri‐tumor cellular and fibrotic responses and retarded tumor growth were observed in actively immunized and in adoptively immunized mice, and in mice treated with IL‐2. T lymphocytes and, particularly, macrophages were closely associated with collagen deposition at the tumors. The collagen deposition frequently resulted in the encapsulation and regression of the less invasive tumor MC2. A cellular fibrous response was not observed at tumors implanted into athymic C3Hnu/nu mice. The results suggest that tumor fibrosis may in some circumstances be promoted by an immune response.
Altered prolactin response of the lymphocytes of tumor‐bearing mice
Authors: Biswas Ratna , Chattopadhyay Utpala 
Published: February 2007

AbstractInteraction of prolactin and glucocorticoid on thymocytes and splenocytes of normal and tumor‐bearing mice with reference to their mitogen‐responsive blastogenesis has been studied. Prolactin alone had little or no mitogenic effect on thymocytes and splenocytes of normal mice but it was co‐stimulatory, with ConA, in inducing blastogenesis in normal splenocytes. Thymocytes and splenocytes of tumor‐bearing mice responded differently to prolactin. Hormone alone inhibited growth of thymocytes but at certain concentrations stimulated splenocytes. When cultured with prolactin and ConA, the thymocytes of tumor hosts responded with increased proliferation compared to that induced by ConA alone. Glucocorticoid suppressed ConA‐induced lymphocyte proliferation in both normal and tumor‐bearing mice. Prolactin reversed the inhibitory effect of glucocorticoid in normal mice but failed to abrogate inhibition in tumor hosts. Altered responsiveness of lymphocytes of tumor hosts to prolactin was not a function of circulating prolactin, as the serum prolactin level was similar in normal and tumor‐bearing mice. Prolactin, however, could not reverse estradiol‐induced suppression of lymphocyte proliferation. The lactogenic hormone, but not somatogenic hormones, altered the glucocorticoid inhibition of lymphocyte growth.
Lethal deformation of cancer cells in the microcirculation: A potential rate regulator of hematogenous metastasis
Authors: Weiss L. , Nannmark U. , Johansson B. R. , Bagge U. 
Published: February 2007

AbstractThe hypothesis has been advanced that deformation‐induced lethal mechanical trauma, resulting in surface‐membrane rupture, is inflicted on circulating cancer cells trapped in the microcirculation, and that this rapid cell‐killing mechanism is a potentially important rate regulator for hematogenous metastasis. We describe and discuss an in vivo test of this hypothesis. Vital fluorescence microscopy was performed on the microcirculation of cremaster muscle preparations in mice, following retrograde injections into the femoral artery of acridine orange‐stained sarcoma cells. Cancer cells having mean diameters of 16.5 μm in suspension, were deformed from spheres into cylinders having a mean length of 53 μm, in 7‐μm diameter capillaries. Most of these cells were dead several minutes after injection. It was estimated that sphere‐to‐cylinder shape‐transitions of this magnitude required an average increase of 52% in apparent cell surface area. Evidence is presented that most of this apparent increase was achieved by non‐lethal surface “unfolding”, utilizing membrane “excess”. That cancer‐cell deformation of the magnitude observed in vivo is the direct cause of lethal, surface‐membrane rupture was indicated by the observed loss of membrane integrity in cells deformed from spherical to cylindrical shape in vitro, by aspiration into micropipettes of capillary dimensions. The experimental observations are therefore consistent with the hypothesis.
Splicing of the vase exon of neural cell adhesion molecule (NCAM) in human small‐cell lung carcinoma (SCLC)
Authors: van Duijnhoven H. L. P. , Helfrich W. , de Leij L. , Roebroek A. J. M. , van de Ven W. J. M. , Healey K. , Culverwell A. , Rossell R. J. , Kemshead J. T. , Patel K. 
Published: February 2007

AbstractExpression of the neural cell adhesion molecule (NCAM) on small‐cell lung carcinoma (SCLC) cell lines and tumour tissue has been investigated. Cell lines were found to express highly sialylated NCAM. Neuraminidase treatment revealed the presence of the 140‐ and 120‐kDa isoforms with differential expression of a 95‐kDa protein. Similar data were obtained with SCLC tumour tissues. These results were corroborated by Northern blotting where mRNA of 6.7 and 5.5 kb coding for the 140‐ and 120‐kDa isoforms, respectively, were identified. In a few tumours, a weaker band of 7.4‐kb mRNA coding for the 180‐kDa NCAM was also identified. This result could not be confirmed biochemically due to shortage of material. Finally, a 5‐kb transcript was identified in all SCLC samples examined. The NCAM isoform coded by this mRNA remains unknown. Using the polymerase chain reaction (PCR), we have demonstrated the presence of the VASE mini‐exon in some isoforms of SCLC NCAM. The VASE mini‐exon sequence in human SCLC differs from the published murine sequence by only one base change. This substitution does not result in altered amino‐acid sequence.
Occurrence of tumours in the descendants of CBA male mice prenatally treated with diethylstilbestrol
Authors: Turusov V. S. , Trukhanova L. S. , Parfenov Yu. D. , Tomatis L. 
Published: February 2007

AbstractThere is well documented evidence both in humans and in experimental animals that exposure to diethylstilbestrol (DES) during pregnancy results in an increased incidence of tumours in the progeny. The increased cancer risk has been reported to persist in the second generation descendants of DES‐exposed pregnant mice. In the present experiment, female mice of the CBA strain were treated at day 17 of pregnancy with I μg/g body weight of DES. The descendants of DES‐treated mothers, described as F1DES, were mated among each other or with untreated animals. The F1DES females were found to be sterile when mated with either F1DES or untreated males. F1DES males were successfully mated with untreated females. In the female offspring so obtained, but not in the male, a statistically significant increased incidence of tumours was observed, in particular of uterine sarcomas, and also of benign ovarian tumours and of lymphomas.
Mucin synthesis and secretion in relation to spontaneous differentiation of colon cancer cells in vitro
Authors: Niv Yaron , Byrd James C. , Ho Samuel B. , Dahiya Rajvir , Kim Young S. 
Published: February 2007

AbstractThe synthesis and secretion of mucin‐like high‐molecular glycoprotein was studied in 2 human colon cancer cell lines that spontaneously differentiate in culture (Caco‐2 and T84) and in 2 cell lines that do not spontaneously differentiate (LS174T and HT29). Mucin, quantitated by 3H‐glucosamine labelling and chromatography on Sepharose CL‐4B was found to be produced by all 4 cell lines. The mucinous nature of the labelled high‐molecular glycoprotein was verified by enzymatic degradation treatments (heparinase, hyaluronidase, chondroitinase ABC, and N‐glycanase), alkaline‐borohydride treatment, inhibition of labelling by the glycosylation inhibitor benzyl‐α‐GaINAc, and by CsCl‐density‐gradient centrifugation. In all 4 cell lines, an inverse correlation of mucin synthesis with cell density was demonstrated. In Caco‐2 cells, the spontaneous post‐confluent enterocytic differentiation with increased brush‐border enzyme expression was associated with a decrease in mucin synthesis and in the activities of polypeptidyl GaINAc transferase and β 1,3‐galactosyltransferase activity. Using cDNA probes for 2 distinct human intestinal mucins (MUC2 and MUC3), we found that all 4 colon cancer cell lines expressed mucin message, but the types of mucin mRNA expressed differed. These data indicate that mucin‐like glycoproteins can be synthesized by cell lines derived from non‐mucinous colon cancer, whether or not they undergo spontaneous differentiation in culture. These cell lines may serve as in vitro models for studying apomucin heterogeneity and control of mucin gene expression.
Characterization of A U‐937 subline which can be induced to differentiate in serum‐free medium
Authors: Öberg Fredrik , Hult Nina , Bjare Ulf , Ivhed Irene , Kivi Sirje , Bergh Jonas , Larsson Lars‐Gunnar , Sundström Christer , Nilsson Kenneth 
Published: February 2007

AbstractWe report the selection and characterization of a U‐937 subline which is capable of long‐term growth in serum‐free medium and can be induced to differentiate. The subline (U‐937‐ISF) can be maintained in standard RPMI‐1640 medium supplemented by antibiotics only. As compared to the serum‐dependent U‐937 parental cell line, U‐937‐ISF produced lower amounts of lysozyme and elastase and had a decreased surface expression of complement receptor I (CD35) and myeloid antigens CDw17 and CD38. Apart from these alterations, the U‐937‐ISF cells appear to be morphologically, cytogenetically and phenotypically similar to the parental U‐937 clone‐1 cells. The capacity of U‐937 clone‐1 cells to undergo phorbol myristic acid (PMA)‐, vitamin D3 (VitD3)‐ and retinoic‐acid (RA)‐induced differentiation was retained in the U‐937‐ISF cells as evidenced by the induced growth arrest, development of a monocyte/macrophage morphology and increased expression of differentiation‐associated antigens, e.g. CD11b, CD11c, CD14 and CD18. The growth‐inhibitory response to cytokines involved in the activation and differentiation of monocytes, IFN‐γ, TNF‐α, IL‐1β, IL‐6 and GM‐CSF, was normal. Our results suggest that the U‐937‐ISF subline can be used as a serum‐free model system for studies on various aspects of monocyte differentiation.
HTLV‐I‐positive and HTLV‐I‐negative peripheral T‐cell lymphomas in Taiwan Chinese
Authors: Shih Lee‐Yung , Kuo Tseng‐Long , Dunn Po , Liaw Shiumn‐Jen 
Published: February 2007

AbstractThe clinico‐pathologic features of 107 adult Chinese patients with peripheral T‐cell lymphoma (excluding primary cutaneous lymphoma) are described and a comparison between HTLV‐I+ and HTLV‐I−patients is made. There were 27 HTLV‐I+ and 80 HTLV‐I−patients. The virus‐positive and‐negative groups both had a male predominance and an identical median age of 48. Most patients in both groups presented with stage‐IV disease, B symptoms, lymphadenopathy and hepatosplenomegaly. The HTLV‐I+ group had a significantly higher incidence of skin and pulmonary lesions, bone marrow and peripheral blood involvement, hypercalcemia, and elevated LDH level compared to the HTLV‐I−group. Sinonasal lesions (10), mediastinal mass (5), and GI tract involvement (6) were only seen in the HTLV‐I−group. Leukocytosis with the presence of circulating pleomorphic lymphoid cells was characteristic of HTLV‐I+ cases, while cytopenia was more frequently present in HTLV‐I−cases. All of the 24 HTLV‐I+ patients tested were CD4+CD8−; of the 67 HTLV‐I−patients tested, 46 were CD4+CD8−, 9 were CD4−CD8+, 5 were CD4−CD8−and 7 were CD4+CD8+. Phenotypic studies revealed significant differences in the expression of CD7 and CD25 between virus‐positive and‐negative groups. Both groups responded poorly to therapy. The median survival of HTLV‐I+ and HTLV‐I−patients was 4 months and 13.5 months, respectively. Apart from the presence of more than 3 extranodal lesions, none of the other clinical features or histologic subtypes had prognostic significance in the entire group or either of the subgroups. This series of peripheral T‐cell lymphomas in Taiwan indicate that HTLV‐I+ and HTLV‐I−patients had many features in common, but presented several distinct differences.
Analysis of regulation of T‐cell responses by soluble inhibitory factors from the sera of patients with Hodgkin's disease
Authors: Damle R. N. , Advani S. H. , Gangal S. G. 
Published: February 2007

AbstractSoluble inhibitory factors (SIF) have been demonstrated in the sera of cancer patients, which interfere with the T‐cell activation process. We have shown that the major contributory factor to the inhibitory effect of sera from patients with Hodgkin's disease (HD) could be the soluble form of Interleu‐kin‐2 receptors (slL‐2R). The parameters studied to show the presence of SIF include (i) inhibition of mitogen‐induced proliferation; (ii) status of high‐and low‐affinity IL‐2R; and (iii) internalization of IL‐2‐IL‐2R complex, by lymphocytes from healthy donors activated with mitogen in presence of HD sera. Parameters studied to show the inhibitory role of slL‐2R include (i) quantitation of sIL‐2R in HD sera; (ii) effect of high‐sIL‐2R‐containing sera on mitogen‐induced proliferation and detection of IL‐2 in activated lymphocyte culture supernatants; (iii) effect of exogenous IL‐2 supplementation; and (iv) abrogation of inhibitory activity of sIL‐2R‐containing sera after passing them through IL‐2 affinity columns. Our results show that 6/23 HD sera tested had high inhibitory activity (>50% inhibition of mitogen‐induced proliferation). The SIF did not affect expression of high‐and low‐affinity IL‐2 receptors, or internalization of the complex by activated lymphocytes. Ten of the 15 sera tested showed significantly high levels of sIL‐2R. Pooled sera with high sIL‐2R content inhibited mitogen‐induced proliferation of normal lymphocytes with a concomitant reduction in IL‐2 activity in the lymphocyte culture supernatants. When supplemented with exogenous IL‐2, there was a partial recovery of the inhibitory effect. When sIL‐2R containing serum pool was passed on IL‐2 affinity columns, the inhibitory effect was reduced. The eluted “sIL‐2R” adsorbed on the IL‐2 column showed anti‐proliferative effect.
A novel O‐acetylated ganglioside detected by anti‐GD2 monoclonal antibodies
Authors: Ye Jian Nan , Cheung Nai‐Kong V. 
Published: February 2007

AbstractMurine monoclonal antibody (MAb) 3F8 was previously shown to react with disialoganglioside GD2, but not with GD3, GTIb, GDIb, GDIA,' GMI, GM3 and GM4. However, when the base‐treatment step was omitted from the standard neuroblastoma ganglioside extraction procedure, immuno‐thin‐layer‐chromatography (ITLC) using 3F8 and other anti‐GD2 MAbs revealed a new ganglioside band, abbreviated as NG (Rf 0.342) besides GD2 (Rf 0.183). It migrated below GD3 (Rf 0.358) on high‐performance (HP) TLC plate and its binding to 3F8 on ITLC could be inhibited by rat anti‐3F8 idiotypic antibody Idio‐2, while the binding of GD2 to MAb 3F8 was not affected. Immunochemical analysis showed that this new neuroblastoma ganglioside contained alkali‐sensitive O‐acetylated sialic‐acid residues recognized by MAb DI.I. After base treatment, its subsequent identity on ITLC was confirmed to be GD2. Lactonization of GD2 yielded 2 major bands, with Rf values (0.401, 0.583) distinct from that of the new ganglioside band. In addition, MAb DI. I did not bind to any of these GD2 lactones. Of 15 anti‐GD2 MAbs studied, 13 reacted strongly with the novel ganglioside NG. By ITLC, this NG was found in ganglioside extracts of fresh surgical tumor specimens (4/4 neuroblastomas, I/I schwannoma and I/I anaplastic astrocytoma), and nude mice/rat xenografts (2/2 neuroblastomas, 2/2 osteogenic sarcomas). These data provided the first evidence that O‐acetylated GD2 is a naturally occurring ganglioside derivative in human tumors and that it could cross‐react with most anti‐GD2 antibodies.
Expression of insulin‐like growth factors I and II and their receptor mRNAs in primary human astrocytomas and meningiomas; in vivo studies using in situ hybridization and immunocytochemistry
Authors: Antoniades Harry N. , Galanopoulos Theofanis , Neville‐Golden Janine , Maxwell Marius 
Published: February 2007

AbstractThese studies demonstrate the expression of IGF‐I, IGF‐II, and their respective receptor mRNAs in primary human astrocytomas and meningiomas. In situ hybridization and immunocy‐tochemistry have localized a strong expression of both IGF‐I and IGF‐II mRNAs and of their protein products in the tumor cells of astrocytomas and meningiomas. The expression of IGF‐I and IGF‐II mRNAs in the tumor cells was accompanied by the co‐expression of their respective type‐I and type‐II IGF receptor mRNAs. Control, non‐malignant human brain expressed IGF‐I mRNA and IGF‐I and IGF‐II receptor mRNAs. There was no significant expression of IGF‐II mRNA in the control brain specimens. Control pachymeninges (dura mater) expressed low levels of IGF‐I mRNA and IGF‐I receptor mRNA. There was no significant expression of IGF‐II and IGF‐II receptor mRNAs in pachymeninges. The co‐expression of IGFs and their receptors in brain tumors may contribute in their development and maintenance. The strong inappropriate expression of IGF‐II mRNA and its protein product in the tumor cells of astrocytomas and meningiomas, but not in normal brain specimens, may serve as molecular markers for the early detection of these tumors.