bluuebunny/crossref_metadata_2025_split huggingface dataset:
The MHC class‐II and CD44 molecules are involved in the induction of tumour necrosis factor (TNF) gene expression by human monocytes stimulated with tumour cells
Authors: Zembala Marek , Siedlar Maciej , Ruggiero Irena , Wieckiewicz Jerzy , Mytar Bozena , Mattei Maurizio , Colizzi Vittorio 
Published: February 2007

AbstractTumour necrosis factor alpha (TNF) mRNA is detected in the macrophage infiltrate surrounding the tumour, but the cellular/ molecular interactions leading to TNF gene expression in macrophages are unknown. The in vitro system in which human blood monocytes are stimulated with human cancer cells for TNF release was used to study such interactions. Monoclonal antibodies (MAbs) against various adhesion molecules (LFA‐I, LFA‐3, (CAM‐I, VNR, VLAβI chain) were unable to block TNF production in co‐culture of monocytes with a human pancreatic carcinoma (HPC) cell line. However, anti‐CD44 and anti‐HLA‐DR MAbs effectively blocked TNF release and TNF‐mRNA induction in monocytes. Pre‐incubation of monocytes with anti‐HLA‐DR and tumour cells with anti‐CD44 MAbs had a similar effect. It was concluded that CD44 molecules are involved in tumour‐monocyte interactions and that HLA‐DR determinants of monocytes are engaged in signal transduction for TNF gene activation. These findings may suggest that certain surface determinants of tumour cells act as ligands for MHC class‐II molecules and induce TNF production in monocytes.
Anti‐proliferative and anti‐estrogenic effects of ICI 164,384 and ICI 182,780 in 4‐OH‐tamoxifen‐resistant human breast‐cancer cells
Authors: Coopman Peter , Garcia Marcel , Brünner Nils , Derocq Danielle , Clarke Robert , Rochefort Henri 
Published: February 2007

AbstractThe effects of the anti‐estrogens 4‐hydroxytamoxifen (OHTam), ICI 164,384 and ICI 182,780 were tested on the MCF‐7/LCC2 breast‐carcinoma cell line, which grows significantly in the presence of OHTam and serves as a model for studying anti‐estrogen resistance of estrogen‐receptor‐positive breast cancer. Cell proliferation and cathepsin‐D secretion were strongly inhibited by either ICI 182,780 or ICI 164,384 alone or ICI 164,384 in combination with 17‐p‐estradiol (E2) or OHTam. ICI 164,384 alone did not affect the cathepsin‐D and pS2 mRNA levels, but antagonized the stimulatory effects of E2 or OHTam on these 2 mRNAs. OHTam was more effective than E2 in increasing cathepsin‐D mRNA levels, supporting the idea that anti‐estrogen‐resistant breast cancer continues to over‐express cathepsin‐D. These data show that the steroidal anti‐estrogens ICI 164,384 and ICI 182,780 retain their ability to inhibit cell proliferation and the estrogen‐responsiveness of cathepsin‐D and pS2 genes in the OHTam‐resistant MCF‐7/ LCC2 cell line. These pure anti‐estrogens may thus be efficient second‐line treatments of some Tamoxifen‐resistant tumors.
Analysis of HLA‐DR expression on keratinocytes in cervical neoplasia
Authors: Coleman Nicholas , Stanley Margaret A. 
Published: February 2007

AbstractWe have investigated the expression in vivo and in vitro of HLA‐DR in pre‐invasive squamous‐cell neoplasia of the uterine cervix. Immunohistochemistry of cervical biopsies demonstrated HLA‐DR expression by cervical keratinocytes in 50% of cases of high‐grade squamous intra‐epithelial neoplasia, although the molecule was rarely expressed in low‐grade squamous intra‐epithelial neoplasia and was absent from normal ectocervical cells. HLA‐DR‐positive high‐grade lesions were associated with significantly greater numbers of T lymphocytes in the immediately sub‐epithelial stroma than were the HLA‐DR‐negative high‐grade lesions. In vitro HLA‐DR expression was absent from normal ectocervical epithelium, and from the HPV type 16 containing cell lines W12 (representing low‐grade squamous intra‐epithelial neoplasia) and CaSki and SiHa (each representing high‐grade squamous intra‐epithelial neoplasia), both in monolayer and in organotypic raft culture. HLA‐DR expression was induced in all cell types following recombinant interferon gamma treatment. Our data suggest that the expression of HLA‐DR by keratinocytes in some high‐grade cervical lesions in vivo may be due to local induction of the molecule by pro‐inflammatory cytokines released by immunocompetent cells. The functional significance of HLA‐DR positivity in enabling an effective host immune response to neoplastic cervical keratinocytes remains unclear.
Parathyroid hormone‐related protein and human papillomavirus in gynecological tumors
Authors: Mackenzie Sharon L. , Gillespie Matthew T. , Scurry James P. , Planner Robert S. , Martin T. John , Danks Janine A. 
Published: February 2007

AbstractThe presence of parathyroid hormone‐related protein (PTHrP) and human papillomavirus (HPV) in a series of gynecological tumors from 131 unselected patients was examined. PTHrP was localized immunohistochemically using a highly specific rabbit polyclonal anti‐serum against PTHrP(1–16). The results confirmed that gynecological malignancies, although rarely associated with humoral hypercalcemia of malignancy (HHM), stained for PTHrP in a majority of the squamous‐cell carcinomas (SCC) at all sites, but only in a minority of adenocarcinomas, and then in areas of squamous metaplasia. This included a series of endometrial tumors. Detection of HPV types was achieved using a polymerase‐chain‐reaction (PCR) detection system enabling the detection of HPV types 6, 11, 16, 18,31,33 and 45. PTHrP production was not directly related to HPV infection, but correlated with the type of tumor.
Coordinate enhancement of gelatinase a mRNA and activity levels in human fibroblasts in response to breast‐adenocarcinoma cells
Authors: Noël Agnès C. , Polette Myriam , Lewalle Jean‐Marc , Munaut Carine , Emonard Hervé P. , Birembaut Philippe , Foidart Jean‐Michel 
Published: February 2007

AbstractGelatinases/type‐IV collagenases are metalloproteinases involved in some carcinoma invasion and metastatic processes. The exact cellular source of the 72‐kDa gelatinase A is controversial. We have analyzed the expression of mRNA coding for gelatinase A in vivo by in situ hybridization on breast‐cancer tissues. The mRNA for gelatinase A was present in fibroblasts. We have therefore evaluated the gelatinase‐A activity in vitro, in co‐cultures of different breast adenocarcinoma cell lines and human fibroblasts. In monoculture, none of the tumor cells tested produced detectable amounts of gelatinase A. The gelatinase‐A activity was enhanced in cultures of fibroblasts maintained in the presence of MDA‐MB 231 or SKBR3 cells, or their conditioned medium. This increased enzymatic activity was evidenced both in the culture medium and in the membrane fraction and was paralleled by enhancement of the steady‐state levels of mRNA. These results are an in vitro demonstration of a regulation of fibroblasts gelatinase‐A production by soluble factors secreted by breast‐tumor cells.
Chromosomal deletions in anaplastic meningiomas suggest multiple regions outside chromosome 22 as important in tumor progression
Authors: Lindblom Annika , Ruttledge Martin , Collins V. Peter , Nordenskjöld Magnus , Dumanski Jan P. 
Published: February 2007

AbstractMeningioma is a common, usually benign, sporadic and solitary tumor of the meninges covering the central nervous system. Meningiomas can become malignant, and such anaplastic tumors are associated with a high rate of recurrence and death from the disease. We analyzed 16 sporadic, anaplastic meningiomas for loss of alleles on the majority of chromosomal arms, in order to define regions in the genome which may be important for tumor progression. Loss of genetic material was observed on all but 2 chromosomes studied. While loss of heterozygozity (LOH) from chromosome 22 was the most frequent finding, LOH from the short arm of chromosome I was the second most common lesion occurring preferentially in tumors from men, and at a frequency almost as high as for LOH on chromosome 22. This suggests the existence of a tumor‐suppressor locus on Ip involved in meningioma carcinogenesis. Three tumor samples from one large, anaplastic tumor, each with distinct histopathological characteristics, were studied. All 3 samples showed deletions on 22q and Ip. However, only one tumor sample, with the most malignant histopathological phenotype, displayed, in addition to 22q and Ip, deletions on 9q and 17p. This case suggests that the latter 2 chromosomal regions may harbor genes which contribute to the progression of meningioma.
Sexually transmitted agents and cervical neoplasia in colombia and Spain
Authors: de Sanjosé S. , Muñoz N. , Bosch F. X. , Reimann K. , Pedersen N. S. , Orfila J. , Ascunce N. , González L. C. , Tafur L. , Gili M. , Lette I. , Viladiu P. , Tormo M. J. , Moreo P. , Shah K. , Wahren B. 
Published: February 2007

AbstractCase‐control studies of cervical intra‐epithelial neoplasia grade III (CIN III) and of invasive cervical cancer were carried out in Spain and Colombia to assess the relationship between cervical cancer and 6 common sexually transmitted agents (STAs). The CIN‐III studies included 525 cases and 512 controls matched for age and for the place of recruitment; the invasive‐cancer studies included 373 historically confirmed cases of squamous‐cell carcinoma and 357 age‐stratified controls selected randomly from the populations that generated the cases. Antibodies to Chlamydia trachomatis, Neisseria gonorrhoeas, Treponemo pallidum, herpes simplex virus type II (HSV‐2) and cytomegalovirus (CMV) were tested in 88% of the women. Cervical scrapes were examined for HPV DNA in 63% of the women using a polymerase‐chain‐reaction assay (PCR). Among controls, the highest antibody prevalence was to CMV (96.5%), followed by HSV‐2 (31.4%) and C. trachomatis (23.3%). For all STAs, the sera‐prevalence was markedly higher in Colombia than in Spain both for cases and for controls. After adjustment for the presence of HPV DNA, C. trachomatis was the only STA associated with CIN III in both countries; Spain and Colombia. In both countries, the risk of CIN III increased with increasing of C. trachomatis antibody titers. Among Spanish women, an increase in risk of invasive carcinoma was found for those with antibodies to N. gonorrhoeae; those with antibodies to HSV‐2 and those with antibodies to C. trachomatis. These associations were present only in HPV‐DNA‐negative women. Among HPV‐DNA‐positive women, none of the STAs considered were associated with cervical neoplasia. Our findings could be interpreted as indicating that past infections with HSV‐2, N. gonorrhoeae and C. trachomatis are surrogate markers of HPV, but because HPV DNA may have escaped detection, we cannot exclude that these STAs are also of separate etiologicaf significance.
Antigenic profile of mucosal melanoma lesions
Authors: Kageshita Toshiro , Kimura Toru , Yoshii Akira , Hirai Shunji , Ono Tomomichi , Ferrone Soldano 
Published: February 2007

AbstractTen primary and 6 metastatic mucosal melanoma lesions were tested, utilizing the immunoperoxidase reaction with a panel of 26 monoclonal antibodies (MAbs). The latter included MAbs recognizing membrane‐bound and cytoplasmic‐melanoma‐associated antigens, adhesion molecules and their receptors, and HLA Class‐I and Class‐II antigens. The melanoma lesions displayed differential reactivity with the panel of MAbs. Mucosal melanoma lesions differ from other types of melanoma in their antigenic profile, since they are the only type of melanoma to display a higher expression of p97 MAA, CEA‐MAA and NGF‐R in primary lesions than in metastatic ones. Furthermore, the pattern of HMW‐MAA expression in mucosal melanoma lesions is different from that in nodular and uveal melanoma lesions and only partly resembles that observed in acral lentiginous melanoma lesions. Like other types of melanoma, mucosal melanoma lesions display a heterogeneous expression of HLA antigens, a selective loss of reactivity with some of the anti‐HLA Class‐I MAbs and a higher frequency of abnormalities in HLA Class‐I antigen expression in metastatic than in primary lesions. Expression of HMW‐MAA, 110‐kDa MAA, p97 MAA, CEA‐MAA, NGF‐R and GD2 ganglioside in primary melanoma lesions was found to be associated with a poor prognosis. Although preliminary in nature, these results suggest that analysis of mucosal melanoma lesions with MAbs, in conjunction with information about the clinical course of the disease, will contribute to determine the biological and clinical significance of the distinct characteristics of the antigenic profile of mucosal melanoma lesions.
Three exceptional IgH/myc‐translocation‐carrying rat immunocytomas have breakpoints 50 to 80 kb 5′ of c‐myc
Authors: Axelson Håkan , Panda Chinmay Kumar , Klein George 
Published: February 2007

AbstractThe spontaneously arising immunocytoma of the Louvain rat (RIC) carries a consistent chromosomal translocation between chromosomes 6 and 7. This translocation juxtaposes immunoglobulin heavy chain and c‐myc sequences. In an earlier study on 14 RIC tumors, we found that the translocation breakpoint is located within 1.5 kb immediately upstream of c‐myc in 10 of the tumors. Here we describe 3 exceptional tumors that had no rearrangement within 20 kb 5′ of c‐myc. Using pulsed‐field gel electrophoresis we show that the translocation breakpoints in these tumors are located 50–80 kb 5′. of c‐myc and that c‐myc rearranges to the 3′ end of the IgH cluster.
Inhibition of gastrin‐induced proliferation of AR4–2j cells by calcium channel antagonists
Authors: Bertrand Viviane , Bastié Marie‐José , Vaysse Nicole , Pradayrol Lucien 
Published: February 2007

AbstractThe exact intracellular mechanisms by which gastrin enhances the proliferation of AR4–2J cells, a tumor pancreatic acinar cell line, are not precisely known. Calcium has long been considered as an intracellular signal involved in growth‐regulatory control of many cell types. Moreover, Ca++ channel blockers show growth‐suppressing effects in most proliferating cells. In the present study, we analyzed the role of nifedipine, a voltage‐dependent Ca++ channel antagonist, on AR4–2J cells which possess well‐defined voltage‐dependent Ca++ channels. The results showed that 10 nM gastrin induced a transient rise in intracellular calcium (Ca++), followed by a sustained phase which was dependent upon a Ca++ influx operating through nifedipine‐dependent and‐independent Ca++ channels. Both influxes are necessary for reloading the agonist‐sensitive Ca,++ pools. In parallel, we demonstrated that nifedipine at doses of I μM and 3 μM preferentially blocked the increase in cell number elicited by 10 nM gastrin and 0.1 μM Bay K 8644, a Ca++ channel agonist, suggesting that voltage‐sensitive Ca++ channel activity was required for gastrin‐stimulated mitogenesis. Moreover, nifedipine had no effect on the proliferation of AR4–2J cells growing in serum‐free medium, indicating that this drug did not simply exert a toxic effect. Therefore, Ca++ influx through voltage‐dependent Ca++ channels might be an important initial step representing a component of a synergistic cooperation between different signal transduction pathways involved in gastrin‐regulated growth.
Modulation of cytostatic drugs by nifedipine in two heterotransplanted human testicular‐cancer cell lines differing in their sensitivity to standard agents
Authors: Bokemeyer Carsen , Dunn Theresa , Harstrick Andreas , Lerch T. , Poliwoda Hubert , Schmoll Hans‐Joachim 
Published: February 2007

AbstractDrug resistance is an important clinical problem in testicular cancer patients with relapsed or refractory disease after first‐line chemotherapy. Here we report that the relative reduction in tumour volume in nude mice heterotransplanted with either H 12.1 or H 23.1 human testicular cancer cell lines was significantly increased by addition of the calcium antagonist nifedipine to the maximum tolerated dose (MTD) of cisplatin (DDP). The mean reduction in relative tumour volume at day 30 (rVR) reached statistical significance for both cell lines following combination therapy of DDP with nifedipine compared to DDP alone (55 ± 7% versus 12 ± 4% for H 23.1 and 60 ± 9% vs. 24 ± 4% for H 12.1). The synergistic anti‐tumour activity of DDP with nifedipine has also been confirmed in H 12.1 cells in vitro. However, in vivo, this combination was associated with a concordant increase in therapeutic toxicity. In contrast, no improvement in in vivo anti‐tumour activity was obtained by combining similar dose‐schedules of nifedipine with the MTD of epirubicin, or with MTDs of vinblastine or etoposide. These results are in agreement with our immunohistochemical finding that H 12.1 and H 23.1 do not over‐express the Pgp 170 grycoprotein which mediates the multiple drug resistance (MDR) phenotype and involves both anthracyclines and vinblastine, but not DDP. We conclude that another Pgp‐MDR modulator, nifedipine, is able to increase the anti‐tumour activity of DDP in vivo and in vitro via a specific but as yet unknown mechanism, which is most likely not MDR‐related. However, the increased anti‐tumour activity is, in vivo, associated with a considerable increase in overall toxicity. Further studies are necessary to decrease therapeutic toxicity, before clinically relevant models for modifiers of DDP‐resistance could possibly be applied to patients.
Karyotypic pattern of pancreatic adenocarcinomas correlates with survival and tumour grade
Authors: Johansson Bertil , Bardi Georgia , Pandis Nikos , Gorunova Ludmila , Bäckman Pia Lena , Mandahl Nils , Dawiskiba Sigmund , Andrén‐Sandberg åke , Heim Sverre , Mitelman Felix 
Published: February 2007

AbstractThe relationship between cytogenetic findings and clinico‐histopathological parameters was assessed in 29 patients with pancreatic adenocarcinoma. Karyotypic analysis revealed normal karyotypes (N) in 8 carcinomas and abnormal karyotypes (A) in 21. Within the A group, 8 cases had simple chromosome abnormalities (As), i.e., only one numerical or structural aberration, whereas 13 had complex changes with multiple numerical and structural abnormalities (Ac). No significant differences between the N and A groups were detected in terms of tumour grade, clinical stage, type of surgery performed, tumour site or size or the patient's age and survival. A correlation analysis between groups As and Ac revealed a significant difference with regard to grade, poorly differentiated carcinomas being more frequent in the Ac group. Patients in the Ac group had also a significantly shorter survival time than those in the As group. None of the other potentially prognostic parameters, i.e., grade, tumour site, stage and type of surgery performed, correlated significantly with clinical outcome. © 1994 Wiley‐Liss, Inc.
Increased production of immune activation marker neopterin by colony‐stimulating factors in gynecological cancer patients
Authors: Marth Christian , Weiss Günther , Koza Astrid , Reibnegger Gilbert , Daxenbichler Günter , Zeimet Alain G. , Fuchs Dietmar , Wachter Helmut , Dapunt Otto 
Published: February 2007

AbstractGranulocyte colony‐stimulating factor (G‐CSF) and granulo‐cyte‐macrophage colony‐stimulating factor (GM‐CSF) have recently been introduced in the treatment of chemotherapy‐induced neutropenia. Effects of these CSFs on the cellular immune system were evaluated in 38 neutropenic gynecological cancer patients during chemotherapy. In addition to restoring the leukocyte count, GM‐CSF‐to a greater extent than G‐CSF—also induced neopterin, a sensitive marker of macro‐phages activated by interferons. This effect was confirmed in vitro by investigating the effects of these CSFs on interferon‐γ‐mediated pathways in THP‐1 human myelomonocytic cells. The results suggest activation of immune effector cells by GM‐CSF. © 1994 Wiley‐Liss, Inc.
Regulation of ICAM‐1 (CD54) expression in human breast cancer cell lines by interleukin 6 and fibroblast‐derived factors
Authors: Hutchins David , Steel C. Michael 
Published: February 2007

AbstractFour human breast cancer cell lines (T47D, ZR‐75‐1, MCF7D and HS578T) were examined for the effects of cytokines on expression of cell surface antigens. Interferon (IFN)γ up‐regulated the expression of 1CAM‐1 (CD54) in all the cell lines and coordinately up‐regulated both CD54 and CD40 expression in T47D. Tumour necrosis factor (TNF)α, interieukin (IL)Iα ILIβ and IL6 also up‐regulated the expression of CD54 in all the cell lines but CD40 was unaffected. Levels of expression of CD IIa, CDI8, CD49b, CD58 and CD71 were unaltered by these cytokines. Conditioned medium (CM) generated from human fibroblasts, and Fn particular from foetal cells, was highly effective in up‐regulating expression of ICAM‐I but not of CD40 in the breast cancer cell lines. 1CAM‐1 induction correlated with IL6 bioactivity in these CMs. Combinations of IL6 with other cytokines, such as ILI, resulted in further increases in ICAM‐1 expression. Our observations suggest that IL6 is involved in intercellular signalling between mesenchyme and breast cancer epithelium. © 1994 Wiley‐Liss, Inc.
Glycolipids of germ cell tumors: Extended globo‐series glycolipids are a hallmark of human embryonal carcinoma cells
Authors: Wenk Jonathan , Andrews Peter W. , Casper Jochen , Hata Jun‐Ichi , Pera Martin F. , von Keitz Alexander , Damjanov Ivan , Fenderson Bruce A. 
Published: February 2007

AbstractGlycolipids of human germ cell tumor lines were analyzed co define the most common immunohistochemical profiles of embryonal carcinoma (EC), differentiated derivatives of EC, yolk sac carcinoma (YC) and choriocarcinoma (CC). Glycolipid composition was examined by high‐performance thin‐layer chromatography (HPTLC) combined with Immunostaining with a panel of anti‐carbohydrate monoclonal antibodies (MAbs). All EC cell lines were found to contain high levels of globo‐series glycolipids, including globotriosylceramide (Gb3), globoside (Gb4), Gb5 (Ga1β1 ± 1Gb4) and GL7 (sialyl Ga1β1 ± 3Gb4). Somatic differentiated derivatives (e.g., EC cells treated with retinoic acid) contained decreased levels of globo‐series glycolipids and increased levels of lacto‐ and ganglio‐series glycolipids, including GD3, GT3 and GD2. CC cell lines contained relatively large amounts of Gb3 but did not contain extended globo‐series glycolipids GbS and GL7. CC cell lines also contained a macroglycolipid reactive with the antibody to SSEA‐1 (Lex). Glycolipids were not detected in two YC cell lines, while other YC cell lines contained globo‐series core glycolipids (Gb3 and Gb4) and gangliosides. We conclude that EC, YC and CC have distinct patterns of membrane glycolipid expression that can be identified by HPTLC and immunostaining. Our results indicate that globo‐series glycolipids GbS and GL7, which carry stage‐specific embryonic antigens 3 and 4 (SSEA‐3 and SSEA‐4), are a hallmark of human EC cells. Cell lines derived from human germ cell tumors that do not express Gb5 and GL7 deserve to be re‐evaluated, since they may represent different stem cells, most likely equivalent to somatic cells and their developmentally committed precursors (e.g., neuroblasts). © 1994 Wiley‐Liss, Inc.