bluuebunny/crossref_metadata_2025_split huggingface dataset:
Characterization of a highly invasive and spontaneously metastatic human malignant melanoma cell line
Authors: Welch Danny R. , Bisi J. E. , Miller B. E. , Conaway D. , Seftor E. A. , Yohem K. H. , Gilmore L. B. , Seftor R. E. B. , Nakajima M. , Hendrix Mary J. C. 
Published: February 2007

AbstractAlthough the incidence of, and deaths due to, malignant melanoma are rising at a rapid rate, few experimental models mimic the highly metastatic properties associated with the pathogenesis of the human disease, making study of the disease difficult. Thus, new human models are required to understand melanoma biology, especially its metastatic properties. Here we describe C8161, a highly invasive and spontaneously metastatic human melanoma cell line, which grows progressively in the subcutis of athymic nude mice with an average doubling time of approximately 6 days. By the time the tumor reaches a diameter of I cm, amelanotic metastases in lymph nodes, skin, peritoneal wall, spleen and lungs have formed. By comparing C8161 to variants from other well‐characterized human malignant melanomas (A375 and MeWo) with differing metastatic traits, properties presumed to be involved in metastatic propensity were examined. C8161 showed a 2‐ to 14‐fold higher ability to invade reconstituted basement membrane barriers in the MICS and correspondingly high type‐IV collagenase mRNA levels and collagenolytic activity, as compared with other melanoma cell lines. Likewise, differential adhesion to immobilized RBM or HUVEC monolayers was observed, but did not correlate to rank orders of malignant properties. Recently, a correlation between surface expression of ICAM‐I and secondary tumor formation by human melanomas has been described in several laboratories. Basal levels of ICAM‐1 on C8161, A375 and MeWo human melanomas were compared, but no correlation with metastatic potential was noted. Proto‐oncogene expression in C8161 cells was compared with A375P and A375M variants using Northern blot analysis, c‐mycexpression was 6‐fold greater than both A375 variants; c‐fosexpression was 3.4‐fold less than A375P and 1.7‐fold less than A375M; c‐junin C8161 cells was 2.5‐fold and 2.1‐fold greater than expression in A375P and A375M, respectively. Because C8161 is so highly malignant, amenable to experimental manipulation, and its behavior in nude mice mimics the clinical course of malignant melanoma, this cell line will prove valuable for studying properties associated with human melanoma tumor progression.
Skin fibroblast cell lines derived from non‐hodgkin's‐lymphoma (NHL) patients show increased sensitivity to chronic gamma irradiation
Authors: Hannan Mohammed A. , Greer William , Smith Blake P. , Sigut David , Ali Mohammed A. , Amer Mageed H. 
Published: February 2007

AbstractCultured fibroblast cells from 19 patients with non‐Hodgkin's lymphoma (NHL), 3 patients with ataxia telangiectasia (AT), 3 AT heterozygotes and 11 (presumed) normal subjects were studied for impaired colony‐forming ability after chronic gamma irradiation. Five cell lines from the NHL patients were also examined for the sensitivity to acute gamma irradiation, as compared with those of normal subjects. To ascertain the degree of radiosensitivity of different cell lines, a comparison was made of the Dl0 values (radiation dose resulting in 10% survival) for each cell line, estimated “by eye” from the actual survival curves, and also from the calculated curves fitted to a log‐linear model. It was observed that the acute gamma irradiation failed to show any appreciable difference in the radiation response of the cell lines from NHL patients as compared with those of normal subjects. However, chronic irradiation demonstrated significantly increased radiosensitivity in at least 10‐12 NHL patients with a p value of < 0.05, when the D,10 values of each patient's cell line were compared with the calculated composite values for the normals. When the Dl0 values of the NHL patients and the normal subjects were compared as 2 groups, the former appeared to be significantly more sensitive to chronic gamma irradiation (p < 0.0001). The same level of significant difference in radiosensitivity was found between the 2 groups when their D37 values (radiation dose resulting in 37% survival) were compared. In general, the radiation response of the NHL patients was similar to that of the AT homozygotes and heterozygotes used as a positive control group. Our data thus show that increased radiosensitivity is associated with the NHL patients studied, indicating an underlying abnormality of their DNA repair.
Preparation and characterization of monoclonal antibodies specific to synthetic peptide of carcinoembryonic antigen
Authors: Tsujisaki Masayuki , Imai Kohzoh , Hishikawa Noriyuki , Tokuchi Shigeru , Hinoda Yuji , Matsukawa Hirokazu , Oikawa Shinzo , Nakazato Hiroshi , Yachi Akira 
Published: February 2007

AbstractMonoclonal antibodies (MAbs) were prepared to a synthetic peptide (PI: 119‐140 amino acids) in domain I of the carcino‐embryonic antigen (CEA) molecule. The majority of the amino acids in peptide PI show a hydrophilic character, and similar sequences are repeated in domains I, II and III of this molecule. These MAbs appear to recognize new epitopes of CEA, since representative conventional MAbs to CEA do not show reactivity to synthetic peptide PI. The resulting MAbs were divided into 2 groups; group 1 (MAb PI‐706) reacted with peptide PI, but not with purified CEA preparation, while group 2 (MAb PI‐234 and PI‐255) reacted with either type of antigen, in the immunoblotting assay using purified CEA and in immunostaining of colonic carcinoma tissues. Furthermore, group‐1 MAb PI‐706 was reactive to purified CEA after treatment with periodate.
Detergent extraction and characterization of tumor hemolytic factor from plasma membranes of oncogene transformed fibroblasts
Authors: Zuucker Stanley , Dimassimo Betty I. , Lysik Rita M. , Vuaridel‐Bonanomi Evelyne 
Published: February 2007

AbstractCancer cells have the capacity to lyse erythrocytes by a cell‐contact‐requiring phenomenon. Subcellular fractionation procedures have revealed that the hemolytic principle resides in the cancer cell plasma membrane. In this study we report the detergent extraction of a potent hemolytic factor from the plasma membranes of ras‐oncogene‐transformed fibroblasts. Ammonium‐sulfate partitioning (60‐100%) of detergent‐extracted proteins was used to enrich hemolytic activity. Tumor membrane Hemolytic Factor (mTHF) was inactivated by treatment with papain, suggesting that it is a protein. mTHF was inhibited by serum, but was unaffected by extremes of temperature and pH, also by metal chelation with EDTA. Surface radio‐iodination of tumor cells and isolation of cell organelles was used to characterize the outer plasma membrane localization of mTHF. mTHF retained hemolytic activity when reconstituted into stable phospholipid vesicles. Pre‐incubation of mTHF with red cell ghosts led to an abrogation of hemolytic activity. mTHF‐induced hemolysis consists of a 2‐stage phenomenon: an early binding step, followed by hemolysis after 4 hr.
Oncofetal mucin Ml epitope family: Characterization and expression during colonic carcinogenesis
Authors: Bara J. , Gautier R. , Mouradian P. , Decaens C. , Daher N. 
Published: February 2007

AbstractThe gastric mucin M1 antigens, markers associated with colonic carcinogenesis, have been characterized by new anti‐mucin monoclonal antibodies (MAbs). These MAbs, obtained against mucins isolated from a human ovarian mucinous cyst (MAbs 19M1, 21M1 and 45M1) and from a pancreatic adenocarcinoma (MAb 96RA), were compared with 5 other anti‐M1 mucin MAbs described previously, which characterized the a, b, c, d and e mucin M1 epitopes. Using immunoperoxidase, these new MAbs exclusively stained the surface gastric epithelium of normal human gastro‐intestinal tract and reacted with fetal, precancerous and cancerous colonic mucosa, but not with normal colon. Immunoradiofixation studies showed that these new MAbs are directed against 3 epitopes (f, g and h) which are different from the a, b, c, d and e mucin M1 epitopes, though present on the same a immunoreactive high‐molecular‐weight components (> 1,000 kDa) with a density of 1.4 by CsCl‐density‐gradient ultracentrifugation. M1 antigenicity is characterized by a family of 8 different M1 epitopes which were destroyed with β‐mercaptoethanol (except for the f epitope), sensitive to a 5 hr trypsin treatment and resistant to 5 mM periodate (except for the h epitope). Some epitopes (b, c and d) showed increasing immunoreactivity after 20 mM periodate treatment, suggesting cryptic location. In rat‐colon adenocarcinomas, M1 mucin epitopes were masked but could be decrypted using high periodate treatment, similar to normal rat gastric mucosa, thus suggesting the absence of drastic changes in the saccharide coat of the peptide mucin portion bearing M1 epitopes. Cryptic location, periodate resistance, sensitivity to protease and conformational behavior strongly suggest that the peptidic core of gastric (or fetal colonic) mucin plays a role in M1 immunoreactivity. Indeed, the resurgence of M1 antigens during colonic carcinogenesis is due to re‐expression of the peptide core of gastric (or fetal colonic) mucins.
Cigarette smoking and cancer of the pancreas: Evidence from a population‐based case‐control study in Toronto, Canada
Authors: Howe G. R. , Jain M. , Burch J. D. , Miller A. B. 
Published: February 2007

AbstractResults are reported with respect to smoking data from a population‐based case‐control study of pancreatic cancer conducted in Toronto, Canada, between 1983 and 1986. Lifetime smoking histories were obtained for 249 cases and 505 controls. A statistically highly significant positive association was observed between lifetime cigarette consumption and risk of pancreatic cancer. There was a rapid decrease in risk with time for those who quit cigarette smoking, the risk for ex‐smokers being the same as for lifetime non‐smokers between 10 and 15 years after quitting. Limiting exposure to the 15 years prior to diagnosis considerably strengthens the association and leads to a much more clearly defined dose‐response relationship with relative risks of 1.88, 4.61, and 6.52 for tertiles of consumption for current cigarette smokers compared with lifetime non‐smokers (p trend < 10−5). We conclude that the current data, together with those from previous studies, strongly support a causal relationship between cigarette smoking and risk of pancreatic cancer, and indicate that cessation of smoking is likely to prove a rapidly effective preventive measure for this major type of cancer.
Correlation between cytogenetic data and ganglioside pattern in human meningiomas
Authors: Berra B. , Papi L. , Bigozzi U. , Serino D. , Morichi R. , Mennonna P. , Rapelli S. , Cogliati T. , Montali E. 
Published: February 2007

AbstractPartial or total loss of chromosome 22 is often associated with tumors of the central nervous system and in particular with meningiomas. As in the case of other tumors, the ganglioside pattern is modified in transformed tissues. Cytogenetic analysis of 30 human meningiomas has been performed and the results compared to biochemical analysis of ganglioside distribution on the membrane surface. The meningiomas were divided into 2 groups on the basis of the presence or absence of chromosome 22. Thirteen tumors exhibited partial or total monosomy of the chromosome, whereas 17 were normal or showed other chromosomal anomalies. The GM3 and GD3 content of the meningiomas belonging to the 2 groups revealed a significant correlation between amount and reciprocal ratio of these 2 gangliosides and cytogenetic data. Tumors with monosomy 22 had a higher content of ganglioside GD, than samples without monosomy 22, where the main ganglioside was GM3. Other gangliosides such as GM1, GD1a, GD1b and GT were present in various amounts in the 2 groups. Considering the biosynthetic pathway of gangliosides, we hypothesize the involvement of a gene located on chromosome 22 in the regulation of the enzymes which catalyze either GD3 synthesis (sialyltransferase 2, SAT‐2) or its degradation to GM3 (neuraminidase).
Quantitative measurement of monoclonal antibody distribution and blood flow using positron emission tomography and 124iodine in patients with breast cancer
Authors: Wilson C. B. , Snook D. E. , Dhokia B. , Taylor C. V. J. , Watson I. A. , Lammertsma A. A. , Lambrecht R. , Waxman J. , Jones T. , Epenetos A. A. 
Published: February 2007

AbstractThe uptake and in vivo quantitation of monoclonal antibodies (MAbs) has been measured non‐invasively using positron emission tomography (PET) and 124iodine in 9 patients with breast ductal carcinoma. Blood‐flow measurements were also made using 15oxygen‐labelled water and PET to evaluate antibody delivery; 7 patients were studied with HMFGI antibody and 2 patients with a non‐specific antibody. Tumour uptake ranged from 2‐7.7 × 10−3% of injected dose per gram of tissue. Values for normal tissue including liver, lung and bone were also obtained. In 2 out of 7 patients studied with the specific antibody, uptake was greater than that seen with the non‐specific antibody. There was no correlation between antibody uptake and blood flow. This report exemplifies the potential of PET for the non‐invasive and accurate quantitative assessment of targeted antibody which is a prerequisite to therapy.
Bilateral ovarian carcinoma: Cytogenetic evidence of unicentric origin
Authors: Pejovic Tanja , Heim Sverre , Mandahl Nils , Elmfors Bengt , Furgyik Stefan , Flodérus Ulla‐Maria , Helm GÖRan , Willén Helena , Mitelman Felix 
Published: February 2007

AbstractCytogenetic analyses were performed on the tumors from both ovaries in 15 patients with bilateral ovarian carcinoma. In 4 of them, omental implants were also examined. Abnormal karyotypes were detected in 11 cases. The baseline karyotypes in the 2 tumorous ovaries were identical in each patient, indicating that bilateral ovarian cancer develops by metastatic spreading. There was no clear‐cut evidence of differences in the clonal evolution between the tumors of the 2 ovaries, and hence the side harboring the primary tumor could never be determined. The metastatic nature of the omental implants was proved by the fact that their karyotypes were indistinguishable from those of the ovarian tumor tissue.
Expression of the gastrin‐releasing peptide gene in carcinomas of the breast
Authors: Pagani A. , Papotti M. , Sanfilippo B. , Bussolati G. 
Published: February 2007

AbstractExpression of gastrin‐releasing peptide (GRP), the mammalian homologue of the amphibian bombesin, has been investigated at gene and protein level in a series of 28 primary breast carcinomas, in 6 mammary cancer cell lines and in one transplantable rat mammary carcinoma. Moderate to strong expression of GRP mRNA was detected in 5 breast carcinomas by Northern blot analysis with a pre‐pro‐GRP probe; 4 other cases were weakly reactive. Two of these cases also gave a specific immunocytochemical reaction for GRP, controlled with absorption experiments. Correlation with NE differentiation [as shown by chromogranins (Cg) and/or NSE and/or Grimelius positivity] was low, since only one case of breast carcinoma co‐expressed GRP and Cg mRNAs. Breast cancer cell lines and a rat carcinoma gave negative results. GRP production in breast cancer did not appear to bear prognostic implications, but longer follow‐up periods are needed to confirm these data. As shown in small‐cell lung cancer, GRP might be involved in autocrine growth control mechanisms of a group of breast carcinomas.
Squamous‐cell carcinoma antigen (SCC‐A) values related to clinical outcome of pre‐invasive and invasive cervical carcinoma
Authors: Brioschi P. A. , Bischof P. , Delafosse C. , Krauer F. 
Published: February 2007

AbstractThe serum concentration of squamous‐cell carcinoma antigen (SCC‐A), a subfraction of tumour antigen, was determined by RIA from healthy donors (control group) and from patients with malignant cervical disease. Ninety‐six percent (173/180) of the healthy patients had squamous‐cell carcinoma antigen serum levels below 2ng/ml. Ten of 70 (14.3%) patients with CIN III, 53.8% (34/62) of patients with invasive squamous‐cell carcinoma stage 1, 85.8% (30/35) with stage II and 96.5% (27/28) with stage III/IV had squamous‐cell carcinoma antigen serum levels above 2ng/ml. We observed that 22.5% (11/49) of patients with a tumour volume below 10ml and 92.6% of patients with a tumour volume greater than 10ml had squamous‐cell carcinoma antigen levels above 2ng/ml (p < 0.005). SCC‐A was correlated with recurrence or progressive disease in 90.0% of cases. Other risk factors such as depth of invasion, microscopic parametrial involvement, lymphatic and/or vascular space permeation and histological grade were not correlated with squamous‐cell carcinoma antigen. Furthermore, this marker increased 4.3 ± 2.7 months before clinical evidence of recurrence or progressive disease. We conclude that serial serum levels of squamous‐cell carcinoma antigen provide a means for early detection of recurrence or progressive disease. This tumour marker might also be useful for monitoring the treatment effects and has some prognostic value.
Changes in cell kinetics induced by primary chemotherapy in breast cancer
Authors: Daidone Maria Grazia , Silvestrini Rosella , Valentines Barbara , Ferrari Laura , Bartoli Cesare 
Published: February 2007

AbstractChanges in the 3H‐thymidine labelling index (3H‐TdR LI) of primary tumor induced by cytoreductive chemotherapy were evaluated in 26 patients with locally advanced breast cancer subjected to mastectomy after different systemic therapies. A significant reduction of 3H‐TdR LI by primary chemotherapy was observed in 11 cases. Changes in cell kinetics were related to the pretreatment proliferative activity: significant increases were observed in 70% of tumors with a very low 3H‐TdR LI (<2.5%) and significant decreases in 100% of tumors with a very high 3H‐TdR LI (>7.0%). There was no correlation between pretreatment 3H‐TdR LI and the objective clinical response, which was conversely related to post‐treatment cell kinetics. The 2‐year progression rate was lower for patients whose residual tumors after treatment had remained (2/7) or become (1/8) slowly proliferating than for patients whose tumors had remained (5/7) or become (4/4) rapidly proliferating.
Coffee and alcohol as determinants of risk of pancreas cancer: A case‐control study from toronto
Authors: Jain M. , Howe G. R. , St. Louis P. , Miller A. B. 
Published: February 2007

AbstractResults are reported from a population‐based study of 249 cases of pancreas cancer and 505 controls carried out in Toronto, Canada, between 1983 and 1986. Lifetime consumption of coffee and alcohol and medical histories were assessed by personal interviews. No evidence of any association was found with different types of coffee or alcohol after adjusting for smoking, calories and fibre intake. There was a significant increased risk associated with a history of diabetes mellitus within 5 years of cancer development. A protective effect of a history of some allergic conditions, hay fever, eczema and asthma, was observed, although the relative risks were not significant (p value > 0.10).
Inhibition by neurotensin of azaserine‐induced carcinogenesis in rat pancreas
Authors: Tatsuta Masaharu , Iishi Hiroyasu , Baba Miyako , Nakaizumi Akihiko 
Published: February 2007

AbstractThe effect of neurotensin on pancreatic carcinogenesis induced by azaserine was investigated in Wistar rats. Rats were given weekly injections of 10 mg/kg body weight of azaserine for 25 weeks and 200 μg/kg body weight of neurotensin in depot form every other day for 62 weeks. Carcinogen‐induced pancreatic lesions were examined by histochemical techniques, and were classified as ATPase‐positive or ATPase‐negative. In week 62, quantitative histological analysis showed that prolonged administration of neurotensin significantly reduced the volume (as percent of parenchyma) of ATPase‐positive pancreatic lesions, which are closely correlated with the ultimate development of pancreatic cancer. Histologically, pancreatic adenocarcinomas occurred at a significantly lower rate in rats treated with neurotensin than in untreated rats. Administration of neurotensin also significantly decreased the labelling indices of carcinogen‐induced pancreatic lesions, but not of the surrounding acinar cells. These findings indicate that neurotensin inhibits pancreatic carcinogenesis, and that this may be related to the reduction of ATPase‐positive lesions and to the inhibition of cell proliferation in neoplastic lesions of the pancreas.
Differential role of transforming growth factor‐α in two human colon‐carcinoma cell lines
Authors: Watkins Linda F. , Levine Alan E. 
Published: February 2007

AbstractAntibodies to epidermal‐growth‐factor receptor (EGF) and transforming growth factor‐α (TGF‐α) were used to determine the role of endogenous TGF‐α in the growth of 2 human colon‐carcinoma cell lines. Both the GEO and HCT 116 colon‐carcinoma cell lines secrete similar levels of TGF‐α and have similar numbers of low‐affinity binding sites for EGF. However, the HCT 116 cells lack the high‐affinity EGF binding site present on the GEO cells. The anti‐EGF receptor antibodies effectively blocked the binding of 125I‐EGF to the GEO and HCT 116 cell lines. Growth of the GEO cell line was inhibited 50‐80% by the anti‐EGF receptor and anti‐TGF‐α antibodies. When the same antibodies, in sufficient amounts to block binding of TGF‐α to the cells, were added to the HCT 116 cell line, no effect on growth was seen. These results suggest that while the GEO cell line utilizes TGF‐α in an autocrine manner, the TGF‐α secreted by the HCT 116 cells apparently does not play a role in the growth of these cells.
Retinoic‐acid‐induced differentiation prevents gene amplification in teratocarcinoma stem cells
Authors: Lücke‐Huhle Christine , Herrlich Peter 
Published: February 2007

AbstractIn an attempt to study the regulatory properties of cells required for gene amplification, the capacity for amplification of the dehydrofolate reductase gene (dhfr) was determined in F9 teratocarcinoma stem cells during differentiation. By stepwise selection of surviving cells exposed to progressively increasing concentrations of methotrexate (MTX) up to 1000 μm within 4 months, non‐differentiated F9 cells reached a more than 40‐fold amplification of their dhfr gene, elevated levels of dhfr mRNA and a 5‐log increase in MTX resistance. Exposure to 5 Gy of 40Co‐gamma‐irradiation accelerated the process of amplification. In contrast, F9 cells that had been differentiated to endodermal cells by treatment with retinoic acid (RA) did not grow in MTX concentrations above 0.1 μm, either with or without radiation pretreatment and did not amplify the dhfr gene to any measurable extent over the same period of time. Upon treatment of methotrexate‐resistant (F9‐MTXr) cells with retinoic acid, loss of the amplified DNA in the absence of selection was significantly retarded. The ability to amplify the dhfr gene was correlated with the occurrence of origin binding activity in vitro (early domain of SV40 minimal origin of replication). These data indicate an increase in genomic stability and rigorous control of origin activity by differentiation.