bluuebunny/crossref_metadata_2025_split huggingface dataset:
Fetal myofibroblast‐like cells isolated from post‐radiation fibrosis in human breast cancer
Authors: Brouty‐Boyé D. , Raux H. , Azzarone B. , Tamboise A. , Tamboise E. , BéRanger S. , Magnien V. , Pihan I. , Zardi L. , Israël L. 
Published: February 2007

AbstractCells were isolated from post‐radiation fibrosis biopsies of patients with recurrent breast carcinoma. These cells were identified as fibroblasts and compared with fibroblasts from normal breast tissues for their proliferative activities, chromosome number and for the presence of various components of the extracellular matrix and cytoskeleton. The proliferative activity of the fibrosis‐derived fibroblasts did not significantly differ from that of normal breast fibroblasts. Both cell types required serum to grow and did not form colonies in soft agar. Cells from 2 of the 3 fibroses analyzed displayed aneuploid karyotypes with multiple structural abnormalities. All of the fibroblastic cells produced types I, III and V collagen, fibronectin and vimentin. However, in contrast to normal breast fibroblasts, fibrosis‐derived cells produced high amounts of oncofetal fibronectin. In addition, fibrosis fibroblasts also expressed the a‐actin isoform which is specific for smooth‐muscle cells. These results suggest that post‐radiation fibrosis in malignant breast contains atypical fibroblasts with fetal and myofibroblastic characteristics.
The association between alcohol and breast cancer risk: Evidence from the combined analysis of six dietary case‐control studies
Authors: Howe Geoffrey , Rohan Thomas , Decarli Adriano , Iscovich José , Kaldor John , Katsouyanni Klea , Marubini Ettore , Miller Anthony , Riboli Elio , Toniolo Paolo , Trichopoulos Dimitrios 
Published: February 2007

AbstractData from 1,575 cases and 1,974 controls enrolled in 6 previously conducted case‐control studies of diet and breast cancer have been analysed with respect to alcohol intake. There appears to be an absence of any association between consumption of up to 40 g of alcohol per day and risk of breast cancer, and a highly statistically significant and consistent elevated risk of breast cancer for drinkers of 40 g or more of alcohol per day, for whom the relative risk, as compared with that of non‐drinkers, is 1.69 (95% confidence interval 1.19 to 2.40). This association is not due to confounding by a number of diet‐related factors, including total calories, fat, fibre and vitamin C.
Loss of a tumor suppressor function during neoplastic progression of epithelial cells in vitro
Authors: Knowles Margaret A. , Eydmann Marian E. 
Published: February 2007

AbstractIn vitro transformation of rat urothelial cells is a multi‐step process. We have used cell fusion to analyse the role of recessive events during in vitro progression of an immortal urothelial cell line. Somatic cell hybrids were made between the transformed cell line RM2T and a series of immortal urothelial cell lines, including the progenitor line RM2AD, from which RM2T was isolated. The ability to produce colonies in soft agar (anchorage independence) was used as an in vitro marker of transformation, and a series of 10 hybrid clones and 4 mass populations of hybrids were assessed for suppression of this phenotype. Hybrids between early‐passage (< passage 35, anchorage‐dependent) RM2AD cells and late‐passage (>passage 35, anchorage‐independent) RM2T cells, showed suppression of anchorage independence when tested early after fusion (4/4 mass populations, 7/10 clones). This indicates that in vitro progression of this cell line is associated with loss of a function which can suppress growth in soft agar. Fusions between anchorage‐independent RM2T cells and a series of other anchorage‐dependent immortal urothelial cell lines generated hybrids which showed no suppression of anchorage independence, indicating that these anchorage‐dependent cells have lost the suppressor function identified in RM2AD. Our results indicate that loss of a suppressor function can contribute to urothelial transformation in vitro and that clonal populations of immortal cells, at apparently the same stage of transformation, differ in their ability to suppress anchorage independence of the cell line RM2T. These differences provide the basis for suppressor‐gene cloning experiments based on gene transfer.
Different drug sensitivity in two neuroblastoma cell lines established from the same patient before and after chemotherapy
Authors: Kuroda Hiroshi , Sugimoto Tohru , Ueda Kazumitsu , Tsuchida Shigeki , Horii Yoshihiro , Inazawa Johji , Sato Kiyomi , Sawada Tadashi 
Published: February 2007

AbstractDrug resistance is one of the major impediments to the treatment of advanced neuroblastoma. Two neuroblastoma cell lines established from the same patient before (KP‐N‐AY) and after (KP‐N‐AYR) chemotherapy are described. Both cell lines were established from bone‐marrow metastases of a 2½‐year‐old patient with stage IV neuroblastoma. Chromosomal analysis, catecholamine assessment and the surface membrane phenotype of these cell lines confirmed that the tumors were of neuroblastoma origin. Compared with the KP‐N‐AY cell line, the KP‐N‐AYR line had decreased N‐myc amplification but increased N‐myc expression. An in vitro sensitivity test using a clonogenic assay showed the KP‐N‐AYR cell line to be 3.0‐fold resistant to adriamycin and 2.7‐fold resistant to cis‐platinum as compared with the KP‐N‐AY cell line. The expression of the multi‐drug‐resistance gene (MDRI) was not observed in either cell line by the ribonuclease protection assay. The KP‐N‐AY cell line revealed only faint MDRI RNA by the polymerase chain reaction, whereas the KP‐N‐AYR cell line had no expression of the MDRI gene. The level of glutathione‐S‐transferase‐π was significantly higher in the KP‐N‐AYR cell line than in the KP‐N‐AY cell line. These findings suggest that the development of clinical drug resistance may be associated with the enhanced glutathione‐S‐transferase‐π activity but not with MDRI gene expression.
Changes in the ganglioside composition of human neuroblastoma cells under different growth conditions
Authors: Sasaki Hiroshi , Momoi Torn , Yamanaka Chutaro , Yorifuji Tohru , Kaji Masayuki , Mikawa Haruki 
Published: February 2007

AbstractThe ganglioside composition of human neuroblastoma cells (LA‐N‐1 and LA‐N‐5) was studied in samples obtained from (1) original cells in tissue cultures, (2) tumors grown in nude mice inoculated with original cells and (3) cells in tissue cultures re‐established from the mouse tumors. The amounts of „a”︁ pathway gangliosides (Gm2, G m1 and GD1a) and those of the „b”︁ pathway (GD3, GD2, GD1b and GT1b) differed according to the culture conditions. The „b”︁ pathway gangliosides were markedly increased in the tumors grown in nude mice. In contrast, the „a”︁ pathway gangliosides were abundant in cultures of both original and re‐established cells. We also measured the enzymatic activities of UDP‐N‐acetylgalac‐tosamine: GM3, N‐acetylgalactosaminyl transferase (EC 2.4.1.92) and of CMP‐N‐acetylneuraminic acid: GM3 sialyl transferase (EC 2.4.99.8) in neuroblastoma cells cultured under these conditions. These enzymes are thought to be the key enzymes involved in the synthesis of the „a”︁ and „b”︁ pathway gangliosides. Though there was no significant difference in the activity of N‐acetylgalactosaminyl transferase between original cells and tumors in nude mice, re‐established cells showed a definitely higher activity (3.5 times higher than in the original cells). On the other hand, tumors grown in nude mice had a markedly higher activity of sialyl transferase than that of original cells or re‐established cells. These findings suggest that the culture conditions and/or the type of cell growth play some role in the synthesis and expression of gangliosides in neuroblastoma cells.
A comparative study on the xenotransplantability of human solid tumors into mice with different genetic immune deficiencies
Authors: Zietman A. L. , Sugiyama E. , Ramsay J. R. , Silobrcic V. , Yeh E. T. H. , Sedlacek R. S. , Suit H. D. 
Published: February 2007

AbstractThese experiments set out to assess the role of NK and B cells in the resistance of nude mice to human tumor xenotransplantation. The transplantability of 9 fresh and 8 cultured human tumors was compared in 2 strains of mice with different genetic immune deficiencies: athymic NCr/Sed (nu/nu) nude mice, and nude‐beige‐xid (N:NIH‐nu‐bg‐xid/Sed mice). Flow cytometric studies showed both strains to be deficient in Thy. 1.2 (T) cells and unresponsive to stimulation by Concanavalin A (Con A) or direct T‐cell‐receptor triggering with anti‐CD3. The number of B cells was similar in the 2 strains, but the response to lipopolysaccharide (LPS) was markedly reduced in the nude‐beige‐xid animals. The number of asialoGM1,‐positive cells (predominantly NK) detected by flow cytometry was also reduced in the nude‐beige‐xid mice. The transplantability of the human tumors was found to be equivalent in the 2 strains. Quantitative cell‐transplantation assays performed for 2 of the tumor cell lines did not reveal any subtle transplantation advantage for the more broadly immune‐deficient animals. No evidence could, therefore, be found to suggest that NK or B cells were major determinants of human tumor xenotransplantability in these strains of mice.
Clonal selection within metastatic sp1 mouse mammary tumors is independent of metastatic potential
Authors: Samiei Mitra , Waghorne Carol G. 
Published: February 2007

AbstractOur previous studies using randomly integrated plasmid DNA as unique clonotypic markers of SP1 mouse mammary tumor cells transplanted into syngeneic CBA/J or nude mice demonstrated reproducible selection and eventual overgrowth of the primary transplant tumors by genotypically distinct metastatic subclones. Two independent metastatic SP1 clones, neo5 and ras1, were shown to exhibit „clonal dominance”︁ relative to the non‐metastatic SP1 tumor‐cell population. These results suggested that the capacity for preferential growth within the tumors may be related to cellular properties associated with metastatic ability. To investigate the clonal interactions of metastatic SPI clones present within the same tumor mass, we have analyzed tumors composed of paired mixtures of neo5 and ras1. The tumors were monitored for the relative proportion of each clone by Southern blot analysis. The ras1 clone was found to dominate over the neo5 clone in the majority of tumors examined, even when present as 1% of the mixed inoculum. This represents a 20‐ to 50‐fold enrichment of ras1, while the proportion of neo5 within the tumors was reduced at least 5‐fold. No evidence for selection of either clone was seen during co‐culture in vitro. Neo5 and ras1 are indistinguishable with respect to tumor igenic and metastatic potential when inoculated separately into different mice, suggesting that clonal dominance is independent of metastatic ability. Analysis of the metastases resulting from mixed inocula indicates that it is possible for a subpopulation representing less than 1% of the primary tumor mass to give rise to metastases. This also suggests that the process of metastasis within metastatic tumors is independent of clonal dominance.
Induction of tumor regression in experimental model of human head and neck cancer by human a‐lak cells and IL‐2
Authors: Sacchi Manuela , Vitolo Domenico , Sedlmayr Peter , Rabinowich Hanna , Johnson Jonas T. , Herberman Ronald B. , Whiteside Theresa L. 
Published: February 2007

AbstractIn a nude mouse model of human squamous‐cell carcinoma of the head and neck (SCCHN), locoregional therapy with interleukin 2 and human lymphokine‐activated killer (LAK) cells resulted in a significant inhibition of growth of 3‐day established tumors. The same model was used for therapy of 7‐day established tumors with highly enriched populations of human adherent (A)‐LAK (CD3− CD56+) cells and IL‐2. Peritumoral transfer of 10 × 106 A‐LAK cells, whose in vitro cytotoxicity against a SCCHN cell line (PCl‐1) was not significantly different from that of LAK cells, resulted in complete regression of all 3‐day or 7‐day human SCCHN in nude mice. An initial inflammatory‐type reaction, which appeared within hours of the first peritumoral cell transfer, was accompanied by infiltration initially by granulocytes and plasma cells, and later by mononuclear cells into the tumor stroma. A‐LAK cells labelled with a fluorescent dye prior to injection appeared in the tumor stroma within 24 hr and were localized around or in the basal epithelial tumor layer by 48 hr. Histologic sections revealed an increasing epithelial disorganization and progressively decreasing basal epithelial layer, which were proportional to the increasing number of A‐LAK cells transferred. Within 4 weeks, the tumors were reduced to amorphous keratinic remnants surrounded by the connective tissue containing abundant mononuclear cells. Local administration of human A‐LAK cells and IL‐2 to SCCHN tumors growing in nude mice led to accelerated tumor differentiation, keratinization and regression.
Biological response of multicellular emt6 spheroids to exogenous lactate
Authors: Bourrat‐Floeck B. , Groebe K. , Mueller‐Klieser W. 
Published: February 2007

AbstractThe influence of elevated lactate concentrations, as found in tumor microregions, on cellular growth, viability, and metabolic state was studied employing the multicellular spheroid model. Spheroids of EMT6/Ro cells were cultured at 37°C in 5% or 20% (v/v) oxygen, using stirred media with various concentrations of exogenous lactate ranging from 0.0 mM (standard conditions) to 20.0 mM. Elevated concentrations of exogenous lactate led to a considerable decrease of the maximum spheroid diameter at growth saturation, e.g., for 20% O2 from around 1700 μm to 700 μm in 0.0 and 20.0 mM lactate respectively. Histological investigations showed that the thickness of the viable cell rim was increased by elevated lactate concentrations in 20% O2, whereas this correlation was reversed in 5% O2. Cultivation of spheroids in increasing lactate concentrations was associated with a shift of metabolic pathways from net production to increased utilization of lactate in both 20% and 5% O2, as determined by standard enzymatic assays. Oxygen tension (PO2) values measured with micro‐electrodes were less in spheroids cultured in high lactate (9.0 and 20.0 mM) than under standard conditions, irrespective of the external oxygen concentration. This finding reflected a substantial increase in the cellular O2 consumption with elevated external lactate levels. At given lactate concentrations, respiration rates that were derived from measured PO2 distributions by theoretical considerations were significantly lower in 5% O2 than in 20% O2.
Characterization of a novel monoclonal antibody, 3H‐1, reactive with squamoproliferative lesions and squamous‐cell cancers
Authors: Parsons Peter G. , Leonard J. Helen , Kearsley John H. , Takahashi Hiroyuki , Lin‐Jian Xu , Moss Denis J. 
Published: February 2007

AbstractImmunization of mice with membranes from a virus‐transformed human keratinocyte cell line (KJD‐I/SV40) yielded an IgM monoclonal antibody (MAb 3H‐1) which reacted with the membrane and cytoplasm of KJD‐I/SV40 cells and in the perinuclear region of a squamous‐cell carcinoma line (Colo‐16). Immunohistochemistry of formalin‐fixed, paraffin‐embedded sections using MAb 3H‐1 gave intense staining of proliferating squamous epithelium in several characteristic patterns. Acanthotic squamous epithelium and well‐differentiated squamous‐cell carcinomas (SCC) demonstrated a membranous staining pattern whereas psoriatic skin and undifferentiated SCC of the head and neck exhibited diffuse cytoplasmic, focal cytoplasmic or, in some tumours, no staining. Simple squamous epithelium was unreactive. Western blotting revealed an antigen of 55 kDa. The epitope recognized by MAb 3H‐1 may be a marker for particular stages of squamous proliferation and differentiation.
B‐859‐35, a new drug with anti‐tumor activity reverses multi‐drug resistance
Authors: Hofmann Johann , Ueberall Florian , And Alexander Egle , Grunicke Hans 
Published: February 2007

AbstractIt has previously been shown that B‐859‐3S ((–)‐3‐meth‐yl‐5‐ 3‐(4,4‐diphenyl‐1‐piperidinyl)‐propyl‐1,4‐dihydro‐2,6‐dimethyl‐4‐(3‐nitrophenyl)‐pyridine‐3,5‐dicarbox‐ylate‐hydrochloride) exerts a selective carcinostatic effect on some tumors. In order to evaluate whether the anti‐cancer activity of B‐859‐35 can be modulated, we combined the new drug with several established anti‐tumor drugs. A combination of B‐859‐35 with VP‐16 (etoposide) in MDR(multi‐drug‐resistant‐gene)‐expressing Walker rat carcinoma cells shows synergism. A combination of B‐859‐35 with doxorubicin results in stronger synergism than verapamil/doxorubicin, especially at low concentrations of B‐859‐35. The resistance of mdrI (human multi‐drug‐resistance‐gene)‐expressing human HeLa KB‐8‐5 cells to doxorubicin can be reversed with nontoxic or weakly toxic concentrations of B‐859‐35 to the sensitivity of the parent KB‐3‐1 cells. The finding that an antitumor drug is able to reverse multi‐drug resistance makes B‐859‐35 an interesting drug for cancer treatment.
A lack of detectable modification of topoisomerase II activity in a series of human tumor cell lines expressing only low levels of etoposide resistance
Authors: Hill Bridget T. , Whelan Richard D. H. , Hosking Louise K. , Shellard Sharon A. , Hinds Michael D. , Mayes Janice , Zwelling Leonard A. 
Published: February 2007

AbstractEtoposide (VP‐16) resistance is expressed following in vitro exposure of HN‐1 and MCF‐7 human tumor cells to the drug itself or to fractionated × irradiation. VP‐16‐selected sublines prove cross‐resistant to Adriamycin, amsacrine and actinomycin D, whilst X‐ray‐pretreated sublines show cross‐resistance to only actinomycin D. These differential responses, in the HN‐1 series, are not associated with significant differences in amounts of immunoreactive topoisomerase (topo) II, altered topo‐II catalytic activity of nuclear extracts or changes in susceptibility of the topo II to VP‐16‐ or amsacrine‐induced DNA‐protein cross‐link formation. Therefore significant modifications in topo II appear not to be implicated in VP‐16 resistance in these HN‐1 sublines.
Down‐regulation of E‐cadherin expression in madin darby canine kidney (MDCK) cells inside tumors of nude mice
Authors: Mareel Marc M. , Behrens Jürgen , Birchmeier Walter , De Bruyne Georges K. , Vleminckx Kris , Hoogewijs Annemarie , Fiers Walter C. , Van Roy Frans M. 
Published: February 2007

AbstractThe 120‐kDa cell‐cell adhesion molecule E‐cadherin is localized at the epithelial junctional complex and participates in the organization and maintenance of epithelia. The Madin Darby canine kidney (MDCK) cell line expresses E‐cadherin in a stable way and forms polarized epitheloid structures in vitro. Harvey‐murine‐sarcoma‐virus‐transformed derivatives (MDCK‐ras) produce malignant (i.e., invasive and metastatic) tumors in nude mice. We obtained evidence that E‐cadherin is down‐regulated in nude mouse tumors and that this down‐regulation is reversible. MDCK‐ras‐e cell lines were cloned in vitro from MDCK‐ras cell cultures. They showed an epithelioid morphotype and expressed E‐cadherin at homogeneously high level. This characteristic has been conserved for at least 60 passages in vitro. MDCK‐ras‐e cells were not invasive in vitro. When injected into nude mice, however, they produced invasive and metastatic tumors. Primary tumors as well as large metastases were heterogeneous, showing E‐cadherin‐positive well differentiated epithelial structures and E‐cadherin‐negative undifferentiated areas. Metastasis‐derived cell cultures contained both E‐cadherin‐positive and E‐cadherin‐negative MDCK‐ras‐e cells during early passages in vitro. During further culture, however, they regained the homogeneous E‐cadherin‐positive characteristic of the original MDCK‐ras‐e cell line. The behavior of MDCK‐ras‐e cells in vitro, as compared with its in vivo behavior, points to the existence of host factors which are able to down‐regulate E‐cadherin expression. We hypothesize that this down‐regulation plays a basic role in invasion.
The effect of fetal calf serum on growth arrest caused by activators of protein kinase C
Authors: Bradshaw Tracey D. , Gescher Andreas , Pettit George R. 
Published: February 2007

AbstractThe growth of human‐derived A549 lung carcinoma cells is inhibited by activators of protein kinase C (PKC) such as 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA). In this study, the effect of serum deprivation on TPA‐induced growth retardation has been investigated. Cells cultured with 10% FCS and TPA (10−8 M) stopped growing for 6 days, whereas inhibition of DNA synthesis caused by TPA in cells which were grown in medium containing the serum substitute ultraser lasted for less than 48 hr. The ability of cells to respond to the growth‐inhibitory potential of TPA decreased with decreasing amounts of FCS in the cellular medium. Addition of fetuin or epidermal growth factor (EGF) to incubates with serum‐deprived cells increased the ability of TPA to affect growth, but addition of platelet‐derived growth factor (PDGF), transforming growth factor beta (TGF‐β) or retinoic acid (RA) was without effect. Growth arrest caused by bryostatin I, another PKC activator, was equally transitory in serum‐supplemented and serum‐deprived cells. Cytosol of serum‐deprived cells contained only 32% of specific phorbol ester binding sites compared to cells grown with FCS; PKC enzyme activity and immunodectable protein were similarly reduced in cells grown without FCS. There was no difference in rate of TPA‐induced down‐regulation of PKC activity and cytosolic phorbol ester receptor sites between cells grown with or without serum.
A case‐control study of oral cancer and pre‐diagnostic concentrations of selenium and zinc in nail tissue
Authors: Rogers Mary A. M. , Thomas David B. , Davis Scott , Weiss Noel S. , Vaughan Thomas L. , Nevissi Ahmad E. 
Published: February 2007

AbstractA case‐control study of oral cancer was conducted in western Washington state between 1983 and 1987. Cases (n = 379) were identified through a population‐based registry, and controls (n = 514) were selected by telephone using random digit dialing. Subjects participated in a personal interview, completed a food‐frequency questionnaire, and submitted clippings from the nails of each great toe for the determination of selenium and zinc concentrations. The odds ratio (OR) for low selenium levels in nail tissue (lowest 25% of the distribution compared to the upper 75%) was 1.4 (95% confidence interval (Cl) 1.0–2.2). Likewise, the odds ratio for low zinc levels in nails was 1.6 (95% Cl 1.0–2.3), but for low dietary zinc was 1.0 (95% Cl 0.7–1.7). Men with oral cancer had lower nail selenium levels than did the controls (OR = 1.9), but women with oral cancer did not (OR = 0.6). Individuals 20 to 39 years of age with oral cancer, in particular, were more likely to have lower selenium levels in nail tissue than controls (OR = 16.4). There was a significant interaction between selenium and ascorbic acid levels which could not be explained by cigarette use. Subjects at greatest risk had low levels of both nutrients (OR = 3.8 for smokers and OR = 5.7 for non‐smokers). However, since the elements were deposited in the nail matrix close to the date of diagnosis, the differences in the element concentrations between cases and controls may have been a result of the disease. Further etiologic studies of selenium, vitamin intake and oral carcinoma are warranted.