bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cytologic screening for esophageal cancer: Results from 12,877 subjects from a high‐risk population in China
Authors: Shen Q. , Wang D. Y. , Liu S. F. , Cao J. , Zhou B. , Cao S. G. , Zhao H. Z. , Li G. Y. , Guo W. D. , Liu F. S. , Li J. Y. , Li B. , Dawsey S. M. , Taylor P. R. , Blot W. J. 
Published: February 2007

AbstractLinxian, China, has one of the highest esophageal‐cancer mortality rates in the world. In 1983, esophageal balloon‐cytology screening was performed to identify subjects eligible for 2 nutrition‐intervention trials in Linxian; 12,877 subjects had cytology slides which were satisfactory for diagnosis. Of the 12,649 subjects with squamous‐cell diagnoses, 31% were normal by Chinese cytologic criteria; 38% showed hyperplasia; 21% showed dysplasia 1; 6% showed dysplasia 2; 2% showed near‐cancer; and 2% showed cancer. Of the 1,471 subjects with columnar‐cell diagnoses, 31 % were normal; 44% showed hyperplasia; 16% showed dysplasia 1; 4% showed dysplasia 2; 2% showed near‐cancer; and 3% showed cancer. Squamous dysplasia and cancer were more common among females than males, while columnar dysplasia and cancer showed male predominance. The prevalence of dysplasia and cancer of both cell types increased with age. The prevalence of squamous dysplasia was significantly higher than in earlier balloon‐cytology screenings in Linxian, probably reflecting changes in cytologic classification.
Amplification and over‐expression of the EGFR and erbB‐2 genes in human esophageal adenocarcinomas
Authors: Al‐Kasspooles Mazin , Moore Jason H. , Orringer Mark B. , Beer David G. 
Published: February 2007

AbstractEsophageal cancer is one of the 10 most prevalent human cancers worldwide. The incidence of esophageal adenocarcinoma is on the rise and patients with this disease typically have very poor prognosis. Informative biomarkers would benefit the clinical management of this disease. We examined 13 cases with esophageal adenocarcinomas and 5 cases with Barrett's esophagus for amplification of the EGFR and erbB‐2 genes. We detected multiple copies of the EGFR gene in 30.8% of the tumors and multiple copies of the erbB‐2 gene in 15.4% of the tumors. Of the cases with amplification of the erbB‐2 gene, co‐amplification of the EGFR gene was found. Multiple copies of the EGFR gene were also found in one case of Barrett's esophagus. Immunohistochemical staining of the tissues revealed increased expression of the erbB‐2 protein in Barrett's mucosa and adenocarcinoma, but no associations between staining intensity and degree of EGFR or erbB‐2 gene amplification, histology, or tumor stage were found. Differential polymerase chain reaction was examined as a method for pre‐operative detection of gene amplification in esophageal tumors and Barrett's mucosa.
Polarization of the α6β4 integrin in ovarian carcinomas
Authors: Bottini C. , Miotti S. , Fiorucci S. , Facheris P. , Ménard S. , Colnaghi M. I. 
Published: February 2007

AbstractBy immunizing a BALB/c mouse with a human ovary‐carcinoma cell line (IGROVI), grown intraperitoneally in nude mice, a monoclonal antibody (MAb), designated MAR6, was produced and characterized. Immunofluorescence on the immunizing cell fine showed a specific labelling by MAR6 at the cell‐to‐cell contact points. In addition, MAR6 was found to immunoprecipitate the α6β4 integrin complex. Competition tests with MAbs anti‐α6, anti‐β4, anti‐β1 sub‐units demonstrated that the recognized sub‐unit is α6. Indirect immunofluorescence on various cell lines gave MAR6 as positive only on α6‐positive lines (IGROVI, OVCAR3, SW626, SKOV3, ME4405, Calu3, N592, MDA468, A431 and HT29). Moreover, on IGROVI and OVCAR3 ovary‐carcinoma cells, which normally grow either adhering to the culture flask or forming clumps in suspension in the medium, MAR6 selectively stained the connection points between the cells in clumps, where, in the same position, the presence of the β4 sub‐unit, laminin and fibronectin was detected. On the contrary, the β1 sub‐unit was distributed over the whole cell membrane. The same pattern of labelling by these MAbs was observed in 2 cases of ovarian‐carcinoma cells present in ascitic fluids obtained from patients. Immunoperoxidase tests performed on cryosections of various normal tissues showed specific reactivity of MAR6 on basal or basolateral membranes of epithelial cells. On cryosections of ovarian tumors, MAR6 reactivity correlated with the degree of tumor differentiation. Indeed, in benign and well‐differentiated tumors, a strong basal or basolateral labelling only of cells surrounding the neoplastic nodules was found. On the contrary, on undifferentiated tumors the inner part of the tumor nodules was also progressively labelled, whereas the staining on the border was weak and discontinuous as a result of the α6 sub‐unit dispersion on the tumor cell surface.
Regulation of integrin‐mediated adhesion to laminin and collagen in human melanocytes and in non‐metastatic and highly metastatic human melanoma cells
Authors: Danen Erik H. J. , Van Muijen Goos N. P. , Jansen Kees F. J. , Ruiter Dirk J. , Van De Wiel‐van Kemenade Elly , Figdor Carl G. 
Published: February 2007

AbstractWe compared integrin‐mediated adhesion to extracellular matrix (ECM) components of cultured human melanocytes and 6 human melanoma cell lines with different metastatic capacities in nude mice. Cultured melanocytes and most melanoma cell lines adhered strongly to fibronectin (FN), whereas only highly metastatic cell lines adhered to laminin (LM), collagen type I (COI) and type IV (COIV). Adhesion to LM and CO could be blocked by anti‐α6 and anti‐α2 monoclonal antibodies (MAbs) respectively. This observation is consistent with the finding that expression of LM receptor α6β1 and LM/CO receptor α2β1 was low on melanocytes and non‐ or poorly metastatic cell lines, whereas these integrins were strongly expressed on highly metastatic cell lines. In addition, immunoprecipitation from [35S]‐methionine‐labeled cells demonstrated increased synthesis of α6, α2 and β1 in highly metastatic cell lines and immunohis‐tochemistry showed expression of α6β1 and α2β1 only in xenograft lesions from highly metastatic cell lines. Furthermore, the observation that adhesion of melanocytes and non‐ or poorly metastatic cell lines could be stimulated with anti β1 MAbs demonstrates that these receptors, on these cells, are expressed in an inactive state. Our results suggest that α2β1 and α6β1 play a role in human melanoma metastasis in nude mice and demonstrate that interactions of these integrins with their ligands can be regulated at the level of surface expression and activation state of the receptor.
Expression of the MuLV‐tumor‐associated antigen is restricted to MuLV‐transformed cells
Authors: Flyer David C. , Sucheski Brian 
Published: February 2007

AbstractImmunization of mice with Moloney murine leukemia virus (MoMuLV) induces the generation of a population of CTL which recognizes a non‐viral, tumor‐associated antigen (TAA) expressed on MuLV‐induced tumors. To determine whether this TAA could be used as a pre‐leukemic or leukemic cell marker, CTL clones directed against Moloney viral and TAA antigen were used to analyze viral and TAA antigen expression on chronically infected and leukemic lymphoid cells obtained from mice inoculated neonatally with MoMuLV. Although both sets of cells could be recognized and lysed by viral antigen specific CTL, they are not recognized by TAA‐specific CTL. Only after transformed cell lines were established from leukemic spleen cells could susceptibility to TAA‐specific CTL be observed. Thus, the appearance of the MoMuLV‐TAA was restricted to MoMuLV‐transformed cells.
A monoclonal antibody detects heterogeneity in vascular endothelium of tumours and normal tissues
Authors: Wang J. M. , Kumar S. , Pye D. , Krupinski J. , Hunter R. D. , Van Agthoven A. J. 
Published: February 2007

AbstractA new murine monoclonal antibody (MAb), E‐9, has been raised using tissue‐cultured human umbilical vein endothelial cells. The antigen recognized by this MAb is a peptide of 170 kDa under non‐reducing conditions and 96 kDa under reducing conditions. MAb E‐9 showed marked heterogeneity in its distribution in various tissues. The antigen recognized by it was present in vascular endothelial cells of all tumours, foetal organs and in regenerating and inflamed tissues. It stained a few normal tissues. However, with the exception of tonsils, staining tended to be weak and limited to a few blood vessels, as revealed by double staining using pan‐endothelial antibody (CD31) and antibody to von Willebrand factor, another marker of vascular endothelium. Surprisingly, blood vessels within the placental villi were completely negative. The function of the antigen recognized by MAb E‐9 is not known, but its evaluation and use should increase our understanding of angiogenesis.
Tumour spectrum in hereditary non‐polyposis colorectal cancer (HNPCC) and in families with “suspected hnpcc”. A population‐based study in northern Italy
Authors: Benatti Picro , Sassatelli Romano , Roncucci Luca , De Leon Maurizio Ponz , Pedroni Monica , Fante Rossella , Gregorio Carmela Di , Losi Lorcna , Gelmini Roberta 
Published: February 2007

AbstractHereditary non‐polyposis colorectal cancer (HNPCC or Lynch syndrome) is characterized by the early onset of colorectal neoplasms, frequently localized in the right colon, increased occurrence of multiple primaries, vertical transmission and aggregation of tumours in families in accordance to a Mendelian dominant type of inheritance. The syndrome accounts for approximately 5% of all colorectal cancers. The purpose of the present study was to describe the tumour spectrum and the most relevant clinical features of 28 kindreds with HNPCC, classified according to the guidelines of the International Collaborative Study Group, and of 61 “suspected” HNPCC. These families were observed during a 6‐year registration of colorectal neoplasms in a health‐care district of Northern Italy. Colorectal cancer was by far the most frequent malignancy; gastric cancer was the second. Uterine carcinoma was only slightly more frequent than expected. Lung‐ and breast‐tumour rates were lower than expected. Cancer distribution in the large bowel showed that about two fifths of the tumours developed in the right colon. The occurrence of cancer before the age of 50 to 60 was much more frequent in HNPCC. Multiple tumours developed in 25 patients with HNPCC and in 32 with “suspected” HNPCC. Pancolonoscopy remains the procedure of choice for surveillance; other examinations, such as gastroscopy, gynaecological investigations, urography and cholangiography, are suggested only to selected families. One of the main features of the study was the inclusion of 61 “suspected” HNPCC, a heterogeneous group of families which nonetheless deserves careful follow‐up.
Amplification of fgfr4 gene in human breast and gynecological cancers
Authors: Jaakkola Susanna , Salmikangas Paula , Nylund Stella , Lehtovirta Pentti , Nevanlinna Heli , Partanen Juha , Armstrong Elina , Pyrhönen Seppo 
Published: February 2007

AbstractWe have investigated gene amplification of fibroblast growth factor receptor‐4 (FGFR4) gene in 30 primary breast tumor samples and 15 gynecological tumor samples. Ten percent of the breast tumors showed 2‐ to 4‐fold amplification. Amplification was found more frequently in estrogen‐ and progesterone‐receptor‐positive tumors and in tumors with high lymph‐node involvement. Breast tumor samples were also analyzed for the amplification of fgfr3 and erbB2 genes and the chromosome I Iq 13 located genes hst I Iint2lbci1 /sea. erbB2 gene was amplified 2‐ to 13‐fold in 13% of the cases, but no amplification of int2/hst I/be/1/sea amplicon was found. Gynecological tumors were also analyzed for the amplification of fgfr4 and fgfr3 genes and for int2 and hst I oncogenes. Eleven of the 15 gynecological tumors were ovarian neoplasms including 2 benign tumors; the remainder comprised I ovarian metastasis of breast cancer; I endometrial cancer; I uterine leiomyosarcoma and I carcinosarcoma of the fallopian tube. In gynecological tumors, fgfr4 gene was found to be amplified in 2 ovarian tumors. Amplification of hst I was found in I benign ovarian tumor. Thus, the fgfr4 gene may be involved in breast and ovarian tumorigenesis.
Differential chemosensitivity of local and metastatic human gastric cancer after orthotopic transplantation of histologically intact tumor tissue in nude mice
Authors: Furukawa Toshiharu , Kubota Tetsuro , Watanabe Masahiko , Kuo Tsong‐Hong , Kitajima Masaki , Hoffman Robert M. 
Published: February 2007

AbstractWe have established a metastatic model of human gastric cancer using orthotopic transplantation of histologically intact tissue in nude mice, and have used this model to evaluate the effects of immunochemotherapy using OK‐432, 5‐fluorouracil (5‐FU) and mitomycin C (MMC) against SC‐I‐NU, a human stomach cancer line. One‐quarter or one‐half maximum tolerated doses (MTDs) of S‐FU or MMC resulted in a significant reduction of stomach tumor growth, while liver metastases were not reduced, possibly due to suppression of natural killer (NK)‐cell activity by both drugs. On the other hand, when combined with OK‐432, half MTDs of 5‐FU and MMC significantly reduced liver metastases, with synergistic reduction of stomach tumor growth, possibly reflecting a rescue of NK‐cell activity by treatment with OK‐432. This metastatic model of human stomach cancer shows that locally growing and metastatic tumors may have different chemosensitivities, and provides the opportunity to test both with various treatment regimens.
Generation and control of metastasis in experimental tumor systems; inhibition of experimental metastases by a tilorone analogue
Authors: Algarra Ignacio , Pérez Matías , Garrido Federico , Gaforio Jose Juan , Höglund Petter , Ljunggren Hans‐Gustaf 
Published: February 2007

AbstractThe role of the chemical compound RMI 10,874DA (3,6‐bis[2‐(dimethylamino)‐ethoxyl]‐9H‐xanthene‐9‐onedihydrochloride) in the abrogation of the metastatic spread of tumor cells was studied. Pre‐treatment of BALB/c mice with the RMI 10,874DA compound (referred to below as tilorone analogue) completely eliminated lung colonization of an H‐2‐negative (GR9.B9) MCA‐induced fibrosarcoma clone in an experimental metastasis assay. Other murine tumors, including H‐2‐positive and H‐2‐negative chemically induced fibrosarcoma clones and B16 melanoma, were also sensitive to the treatment; orally administered tilorone analogue given one day before the i.v. injection of tumor cells markedly inhibited lung colonization. The effect was not due to direct toxicity of tilorone analogue on tumor cells, but instead it was dependent on NK cells; this was suggested by the finding that anti‐asialo GM1 treatment of mice abrogated the effect of tilorone analogue. Kinetic studies of splenic NK activity in tilorone‐treated mice showed a rapid boosting of NK‐cell activity, the greatest stimulation occurring the day before removal of splenocytes for 51Cr‐release assay against YAC‐1 target cells. These kinetics correlated with the inhibition of in vivo lung colonization after tilorone analogue treatment. Inhibition of experimental tumor metastasis was dose‐dependent and was observed when animals were treated the day before or the day after tumor‐cell injection. Furthermore, repeated treatment of mice with this tilorone analogue significantly reduced lung colonization.
Tumor‐suppressor p53 gene in hepatitis C and B virus‐associated human hepatocellular carcinoma
Authors: Carol Shieh Y. S. , Nguyen Chau , Vocal Maria V. , Chu Hoi‐Weng 
Published: February 2007

AbstractAbnormalities of the tumor‐suppressor pS3 gene have been discovered in human hepatocellular carcinoma (HCC). It is unclear, however, whether HCC related to chronic viral hepatitis is associated with p53 gene alterations. In this study, we have examined pS3 abnormalities in HCC associated with hepatitis C and B virus (HCV and HBV) infections. Tissues from 18 HCC patients from several hospitals throughout the United States were collected (9 were HCV‐infected, 5 were HBV‐infected, I was HCV/HBV‐infected, and 3 were non‐virus‐associated). Immunostaining with monoclonal pAb1801 revealed expression of p53 protein in tumor‐cell nuclei in one HCV‐associated HCC, and in no case of HBV‐associated HCC, while the nuclei of adjacent hepatocytes were negative. Using Hae Ill‐digestion of chromosomal DNA, mutations at codon 249 were not found in any of 18 HCC tissues studied. Direct sequencing demonstrated a mutated codon 244 and a wild‐type codon 249 in the conserved regions (exon 5–8) of p53 gene from the tumor tissue with nuclear p53 expression. By reverse‐transcription‐polymer‐ase chain reaction (RT‐PCR), the expression of p53 mRNA was demonstrated in tumor cells from 10 out of 16 HCC tissues. In conclusion, the specific mutation at codon 249 with G to T transversion was not observed in the HCCs associated with HCV or HBV infections. In HBV or non‐virus‐associated HCCs studied, no other p53 gene abnormalities were found. A point mutation at codon 244 with G to A transition of p53 gene was detected in only one of 10 HCV‐associated HCCs, which suggests that p53 mutations may not play a significant role in HCV‐ or HBV‐associated hepatocarcinogenesis.
Novel protein kinases expressed in human breast cancer
Authors: Cance William G. , Craven Rolf J. , Weiner Timothy M. , Liu Edison T. 
Published: February 2007

AbstractThe family of protein kinases includes many oncogenes and growth‐factor receptors, as well as genes that are involved in cell‐cycle regulation. We have identified protein kinases expressed in a human breast‐cancer cell line, 600PEI, and a primary human breast carcinoma, using PCR cloning techniques based on consensus sequences in the kinase domain. Twenty‐five different protein kinases were isolated, including 3 novel putative tyrosine kinases (designated TKI, TK2, and TK5), and 2 novel putative cell‐cycle‐associated serine/threonine kinases (designated STKI and STK2). TKI is a new member of the src family of kinases that is expressed predominantly in epithelial cells. TK2 is homologous to the receptor kinase, HEK, and TK5 appears to be another member of the J AK family of kinases. The novel serine/threonine kinases, designated STKI and STK2, were homologous to the human cdc2 and the Aspergillus nimA genes. We subsequently analyzed the levels of expression of all of these protein kinases in a panel of human breast carcinomas, using PCR‐based methods. This analysis revealed different expression profiles in different primary breast carcinomas and, therefore, may determine new molecular sub‐sets of human.
Malignant mesothelioma after environmental exposure to blue asbestos
Authors: Hansen Janice , De Klerk Nicholas H. , Eccles Jan L. , William Musk A. , Hobbs Michael S. T. 
Published: February 2007

AbstractTo determine the magnitude of the population at risk from non‐occupational exposure to crocidolite at Wittenoom, West ern Australia (WA), a cohort of 4,890 residents who never worked for the mining company Australian Blue Asbestos (ABA) has been assembled from all 18,553 available records: the local school register, hospital attendances, the WA electoral roll, birth certificates, workers who answered a mailed question naire in 1979, participants in a cancer‐prevention programme using vitamin‐A dietary supplements, and other sources. The majority of subjects were relatives and friends of ABA employ ees, and nearly half the cohort were either born at Wittenoom or first went there as children under 10 years of age. As most residents were at Wittenoom when the mine and mill were in operation during the period 1943 to 1966, 82% were first exposed to crocidolite 20 or more years ago. The proportion of other workers (i.e., not employed by ABA) and their families increased once the mining operations ceased. To date, 24 cases of mesothelioma have been reported in this cohort: 9 males and 15 females. Time from first exposure to diagnosis ranged from 23 to 44 years and residence in Wittenoom ranged from 6 weeks to 11 years.
X‐ray‐induced chromatid damage in relation to dna repair and cancer incidence in family members
Authors: Knight Robert D. , Parshad Ram , Price Floyd M. , Tarone Robert E. , Sanford Katherine K. 
Published: February 2007

AbstractThe cytogenetic response to G2‐phase X‐irradiation was examined in phytohemagglutinin‐stimulated peripheral‐blood lymphocytes from 69 individuals, a few of whom were cancer patients. The cancer patients had not received radiation or chemotherapy. The responses of cells arrested by Colcemid 30 to 90 min after X‐irradiation (58R) could be divided into 2 distinct categories: 51 individuals had aberration frequencies typical of normal individuals in previous studies, while 18 others had a 2‐ to 3‐fold higher frequency of chromatid breaks and gaps. Because chromatid breaks and gaps result from unre paired DNA strand breaks, the first category may represent an efficient DNA repair phenotype, while the second may repre sent a deficient repair phenotype. The individuals with the deficient G2 response reported having first‐ and second‐degree relatives with a 3.6‐ and 2.2‐fold higher mean frequency of cancer, respectively. The present results, together with those from earlier studies of families with a genetic disorder predispos ing to cancer, suggest that this deficient cytogenetic response to G2 phase X‐irradiation is associated with a high risk of cancer.
Prediction of response to endocrine therapy in breast cancer using immunocytochemical assays for pS2, oestrogen receptor and progesterone receptor
Authors: Luqmani Y. A. , Ricketts D. , Ryall G. , Turnbull L. , Law M. , Coombes R. C. 
Published: February 2007

AbstractHistological sections obtained from 70 patients with breast cancer, all of whom had received endocrine therapy for meta‐static or locally advanced disease, were assessed for specific immunocytochemical staining of oestrogen receptor and the oestrogen‐induced protein pS2. There was also sufficient material from 25 patients for an assessment of progesterone receptor by immunocytochemistry. We found that, when using a „cut‐off”︁ point of 50% for ER and PR, and of 25% for pS2, ER was positive in 22/29 responders and in 12/41 non‐responders, and thus was significantly associated with response to endocrine therapy. Similarly, in those subjects in whom PR was measured, PR was positive in 5/14 responders and negative in all II non‐responders, again being significantly correlated with response. However, pS2 did not relate to response, being only positive in 10/29 responders and negative in 26/41 non‐responders. The different response categories varied in their „percentage of positivity”︁ as determined by the 2 tests. Thus, for ER and pS2 we observed: complete response—71 % for ER compared with 14% for pS2; partial response—77% compared with 41%; stable disease—36% compared with 64%; and progressive disease—27% compared with 27%. We conclude that at the present time ER appears to be the most reliable indicator for predicting response to endocrine therapy in patients with breast cancer.