bluuebunny/crossref_metadata_2025_split huggingface dataset:
A case‐control study for evaluating lung‐cancer screening in Japan
Authors: Sobue Tomotaka , Suzuki Takaichiro , Naruke Tsuguo 
Published: February 2007

AbstractIn order to evaluate the efficacy of lung‐cancer screening, a case‐control study was conducted using the data from 50 areas where population‐based lung‐cancer screening programmes have been operated by local municipalities. In most areas, chest X‐ray examinations for all participants and sputum cytology for high‐risk participants were offered annually. Case series consisted of 273 deceased lung‐cancer cases. For each case, 2 to 5 controls (a total of 1, 269 controls) were collected from those who were alive at the time of diagnosis of the corresponding case, matched by sex, age, smoking status and type of health insurance. Cases and controls were limited to a high‐risk group for males and a non‐high‐risk group for females. Screening histories, which were obtained from the list of screenees, were compared between case and matched controls for the identical calendar period before the time of diagnosis of the case. The odds ratio of dying from lung cancer for those screened within 12 months vs. those not screened was 0.72 (95% confidence interval 0.50–1.03; p = 0.07). The odds ratios increased towards unity, as the length of time in which screening histories were compared increased. After adjusting for some other variables, which appeared to be associated with the opportunities of chest X‐ray examination, the estimated odds ratio did not change. These results suggest some benefits from lung‐cancer screening in terms of reduction of lung‐cancer mortality and should be subject to further research.
Spontaneous metastatic potential of rat hepatocarcinoma cells after cell fusion or DNA transfection
Authors: Cassingena Roland , Lafarge‐Frayssinet Christiane , Frayssinet Charles , Nardeux Pierre , Estrade Simone , Viegas‐Pequignot Evani , Dutrillaux Bernard 
Published: February 2007

AbstractEight LF × ICIG cell hybrid clones, isolated upon fusion of normal ICIG‐7 human fibroblasts with tumorigenic, non‐metastatic LF CI.2A cells derived from a DAB‐induced rat hepatocarcinoma, were studied. 'They were all highly tumorigenic and were capable of developing spontaneous lung metastases in syngeneic animals. All the hybrids were characterized by a rapid loss of human chromosomes. However, in long‐term culture, they all revealed a persistence of human genetic information as assessed by Southern blotting. In hybrid lines in which human chromosomes were still visible, the most recurrent were numbers 7 and 9. Neither chromosome 7, previously reported to bear some of the genes controlling metastasis in human × mouse T‐cell hybrids, nor chromosome 9 appeared to be correlated with the metastatic potential of LF × ICIG hybrids. The same conclusion applied (I) to a human 3.3‐kb EcoRI DNA fragment which was amplified (approx. 10‐fold) only in metastases induced by one out of 3 metastatic hybrids tested; (2) to the transcription level of c‐Ha‐ras and c‐Ki‐ras genes which was enhanced (approx. 4‐fold) in metastatic and non‐metastatic lines as well. Co‐transfection of LF CI.2A cells with pHSG 272 selectable marker DNA and genomic DNA from normal ICIG‐7 human cells or from a hybrid‐induced metastasis, reproducibly gave rise to geneticin‐resistant transfectants capable of producing spontaneous lung metastases. Neither transfectants nortransfectant‐induced metastases harbored detectable human DNA sequences but all harbored pHSG 272 DNA. These results again call for caution in gene transfer studies of the metastatic process.
Precursor frequency analysis of human cytolytic T lymphocytes directed against autologous melanoma cells
Authors: Coulie Pierre G. , Somville Michel , Lehmann Frédéric , Hainaut Philippe , Brasseur Francis , Devos René , Boon Thierry 
Published: February 2007

AbstractLimiting numbers of peripheral‐blood mononuclear cells (PBMC) from melanoma patients were stimulated with irradiated autologous tumor cells in the presence of interleukins‐2 and −4 and in the absence of feeder cells. The responder cells were restimulated every week. After 2 to 4 weeks, the micro‐ cultures were tested for their lytic activity against the autologous tumor cells. Significant lysis of the tumor cells was observed with a fraction of these microcultures, whereas no lysis was observed with control microcultures seeded without stimulator melanoma cells. Because our aim was to measure the precursor frequency of CTL showing specificity for the tumor, and not that of NK‐like effectors that were also capable of lysing the melanoma cells, we used cold‐target inhibition with an excess of NK target K562 to inhibit the NK‐like activity. Microcultures whose lysis on the tumor cells was not abolished by K562 competition were observed. The specificity of these CTL clones was confirmed by the absence of lytic activity on autologous T‐cell blasts. The numbers of microcultures with anti‐tumor CTL activity fitted the zero‐order of the Poisson distribution equation, indicating that they resulted from the activity of single T‐cell clones. The frequency of anti‐tumor CTL precursor cells (CTL‐P) of 7 melanoma patients ranged from 1/900 to 1/33,000. Frequencies of anti‐tumoral CTL‐P were higher and NK‐like effectors were less frequent when sorted CDS+ T lymphocytes were used as responder cells.
An immunohistochemical survey of pS2 expression in human epithelial cancers
Authors: Luqmani Yunus A. , Ryall Glenys , Shousha S. , Coombes R. Charles 
Published: February 2007

AbstractThe oestrogen‐inducible pS2 protein isolated from human breast‐cancer cells appears to have prognostic significance in breast‐cancer patients. Using both monoclonal and polyclonal pS2 anti‐sera, we have carried out an immunocytochemical survey of 9 epithelial cancers. Some degree of specific tumour staining was observed in 4 tissues, the extent varying greatly between specimens. Most (11/13) of the colorectal cancers showed immunoreactivity, as did 4/5 pancreatic carcinomas. In some of these cases, patchy staining was also observed in adjacent non‐tumour cells. Two bronchio‐alveolar carcinomas showed positivity, but 5 poorly differentiated adenocarcinomas of the lung did not. In the ovary, staining was observed in 3/3 mucinous cystadenocarcinomas but only in 1 /8 of the serous type. No reactivity was seen in specimens of salivary gland, kidney, liver, prostate or uterus. This pilot study indicates that pS2 may be a useful marker of adenocarcinomas in human neoplasms apart from those in the breast, and suggests that more extensive surveys might be worthwhile.
Attenuating effect of ornithine decarboxylase inhibitor (1,3‐diaminopropane) on bombesin enhancement of gastric carcinogenesis induced by N‐methyl‐N'‐nitro‐N‐ nitrosoguanidine
Authors: Iishi Hiroyasu , Tatsuta Masaharu , Baba Miyako , Okuda Shigeru , Taniguchi Haruo 
Published: February 2007

AbstractThe effects of combined administration of bombesin and the ornithine decarboxylase (ODC) inhibitor 1,3‐diaminopropane (DAP) on the incidence and number of gastric tumors induced by N‐methyl‐N'‐nitro‐N‐nitrosoguanidine (MNNG), the ODC activity of the gastric wall and the labelling index of the gastric mucosa were investigated in inbred Wistar rats. Rats were given drinking water containing MNNG (50 μg/ml) for 25 weeks and then drinking water containing DAP (2.5 g/l) and/or injections of 40 (μg/kg) body weight of bombesin in depot form every other day. Administration of bombesin alone resulted in significant increases in the incidence of gastric cancers, the ODC activity of the antral portion of the gastric wall and the labelling index of the antral mucosa. Administration of DAP with bombesin significantly reduced enhancement by the latter of gastric carcinogenesis, ODC activity of the antral portion of the gastric wall and the labelling index of the antral mucosa. Our results suggest that ODC inhibition attenuated the enhancement of gastric carcinogenesis by bombesin, and that this enhancement by bombesin was mediated by polyamine biosynthesis.
Identification and characterization of a rat protein (P 105) auto‐antigenic in rats bearing a progressive syngeneic colon carcinoma
Authors: Blottière Hervé M. , Menoret Antoine , Burg Cédric , Douillard Jean Yves , Pendu Jacques Le 
Published: February 2007

AbstractSera from BDIX rats inoculated with 2 tumor clones derived from a single syngeneic colon carcinoma were assayed by Western blotting for the presence of antibodies against the grafted tumor. The PROb clone is progressive and produces metastases. We observed that rats bearing this tumor developed antibodies against an unglycosylated water‐soluble protein of 105 kDa. The magnitude of this humoral response, as assessed by the intensity of the signal on immunoblots, was inversely correlated with survival of the rats. Furthermore, rats inoculated with the REGb clone, which is immunologically rejected, never developed detectable antibodies against the tumor. Antisera from rats injected with PROb tumor detected p 105 antigen in cellular extracts from the REGb clone and from a series of rat and human cell lines. This protein was also detected in variable amounts in some normal adult and fetal tissues. Treatment of PROb or REGb cells by either interferon‐γ or heat shock did not significantly alter the expression of the p 105 auto‐antigen.
Comparison of spontaneous mutagenesis in early‐passage human mammary cells from normal and malignant tissues
Authors: Eldridge Sandra R. , Gould Michael N. 
Published: February 2007

AbstractSpontaneous mutant frequencies were determined in early‐ passage epithelial‐cell strains derived from either normal or malignant human breast tissues, as well as a non‐tumorigenic immortalized human mammary epithelial cell line (I84BS) derived from normal cells. Mutations at the hypoxanthine‐ guanine phosphoribosyltransferase (HPRT) locus were quantified by determining the 6‐thioguanine resistance. Mutant frequencies in human mammary epithelial cells (HMEC) from 4 normal and 5 carcinoma tissue samples did not differ significantly. In contrast, the mutant frequency in the immortalized HMEC was approximately 10 times higher than in average normal HMEC and normal non‐immortalized cells from early‐passage cultures of the same cell lineage. Our data suggest that the progression of normal breast cells to invasive carcinoma cells does not necessarily involve the establishment of a general genetic instability during this progression.
Enhanced CMP‐NeuAc:Galβ1, 4GlcNAc‐R α2, 6 sialyltransferase activity of human colon cancer xenografts in athymic nude mice and of xenograft‐derived cell lines
Authors: Olio Fabio Dall' , Malagolini Nadia , Serafini‐Cessi Franca 
Published: February 2007

AbstractThe activity of an α2,6 sialyltransferase acting on N‐acetyllac‐tosaminic sequences (α2,6 ST E.G. 2.4.99.1) has previously been found to be increased in 90% of human colon cancer specimens. In the present study, the α2,6 ST activity of 6 human colon cancer cell lines grown in culture was compared with that expressed by the corresponding nude mice xenografts and by the cell lines derived from the xenografts. We found that xenografts of COLO 205, HT‐29, SW 620, SW 948 and SW 948 FL (a non‐adherent sub‐line of SW 948) cells express an α2,6 ST activity much higher than that of the in vitro‐grown cells. SW 48 cells grown either in culture or as xenografts lack the enzyme activity. All the xenograft‐derived cell lines except HT‐29 retained the increased α2,6 ST activity at least for the first 6 passages. Those derived from SW 948 xenografts showed an enrichment of round, non‐adherent cells, strongly reactive with the NeuAcα2,6Gal/GalNAc‐specific lectin from Sambucus nigra (SNA), thus indicating that a selection of these cells has occurred.
Sister chromatid exchanges and chromosome aberrations in lymphocytes of nurses handling antineoplastic drugs
Authors: Goloni‐Bertollo Eny Maria , Tajara Eloiza Helena , Manzato Antonio José , Varella‐Garcia Marileila 
Published: February 2007

AbstractChromosomal aberrations (CA) and sister‐chromatid exchanges (SCE) were investigated in peripheral lymphocytes of 15 nurses and nurse's aides handling cytostatic agents in hospital oncology units. Significantly increased frequencies were noted for both CA and SCE rates when the exposed individuals were compared with 15 nurses working in other hospital units and to a control sample matched by sex and age. This points to the need for emphasizing protective measures in the handling of anti‐neoplastic agents.
Plasminogen activator system in human breast cancer
Authors: Sumiyoshi K. , Serizawa K. , Urano T. , Takada Y. , Takada A. , Baba S. 
Published: February 2007

AbstractWe measured antigen levels of 2 kinds of plasminogen activator, tissue‐type plasminogen activator (t‐PA) and uroki‐ nase‐type plasminogen activator (UK), as well as those of their primary inhibitors, type‐1 plasminogen activator inhibitor (PAI‐I) and type‐2 plasminogen activator inhibitor (PAI‐2), in tissue extracts from benign and malignant breast tumors. Tumor tissue samples from 40 fibroadenomas and 40 breast cancers were examined. t‐PA antigen levels were the same in the 2 groups. Malignant tumors contained higher levels of UK antigen than did benign tumors. In the case of breast cancer, UK antigen levels of tumors with axillary lymph‐node involvement were significantly higher than those of tumors without lymph‐ node involvement. PAI‐1 and PAI‐2 antigen levels of breast‐ cancer tissue samples were higher than those of fibroadenoma samples. PAI‐1 antigen levels of carcinomas with lymph‐node involvement were also significantly higher than those of carcinomas without node involvement. PAI‐2 antigen levels, on the contrary, were higher in carcinomas without node involvement. UK, PAI‐1 and PAI‐2 antigen levels are potentially excellent independent factors for prediction of the metastatic potential of breast cancers.
Detection of antibodies to a linear epitope on the major coat protein (L1) of human papillomavirus type‐16 (HPV‐16) in sera from patients with cervical intraepithelial neoplasia and children
Authors: Cason John , Kambo Parminder K. , Best Jennifer M. , McCance Dennis J. 
Published: February 2007

AbstractAntibodies to the major (L1) coat protein of human papilloma‐ virus type 16 (HPV‐16) in sera from patients with cervical intra‐epithelial neoplasia (CIN) have been investigated by means of recombinant proteins and synthetic peptides. When L1‐ HPV‐16 fusion proteins were used in immunoblot assays, no antibody reactivity was found in sera from 52 patients with CIN or from 21 unrelated children. Amino‐acid sequence analyses indicated that L1‐HPV‐16 amino acids 473 to 492 may contain an HPV‐16 type‐restricted epitope since the greatest diversity occurs in this region. In the ELISA, seropositivity to peptides 473 to 492 was more common among CIN patients whose biopsies contained HPV‐16 DNA (91%, 21 of 23) than among their children (24%, 5 of 21; p < 0.001) or other CIN patients with HPV‐16 DNA‐negative biopsies (66%, 19 of 29; p < 0.05), but was unrelated to the severity of the CIN lesion. Antibodies to L1‐HPV‐16 peptide 473 to 492 among seropositive CIN patients cross‐reacted with the analagous L1‐HPV‐33, but not with the L1‐HPV‐6b peptide, and were predominantly IgM. In contrast, antibodies which recognized a less variable region of L1 ‐HPV‐16 (amino acids 279 to 293) showed no association with HPV‐16 DNA status. Seropositivity to the L1‐HPV‐6b (amino acids 473–492) was less frequent (33%) among CIN patients and unassociated with HPV‐16 DNA status (p > 0.1); however 51% (37 of 72) of patients with genital warts had antibodies to this peptide.
Expression and splicing patterns of human papillomavirus type‐16 mrnas in pre‐cancerous lesions and carcinomas of the cervix, in human keratinocytes immortalized by HPV 16, and in cell lines established from cervical cancers
Authors: Sherman L. , Alloul N. , Golan I. , Durst M. , Baram A. 
Published: February 2007

AbstractWe have analysed the splicing patterns of human papillomavirus (HPV) type‐16 mRNAs in a human epithelial cell line immortalized by HPV 16 (HPKII), in cell lines established from cervical carcinomas (SiHa and CaSki) and in pre‐invasive and invasive carcinomas of the cervix. The presence of mRNA species previously described, which could encode the E6, E6I, E6II, E6III, E7, E2, E2C, E4, E5 and L1 proteins, was determined, using the RNA polymerase chain reaction (PCR) technique with primers that flank unique splice sites. The state of the viral DNA in the tumor biopsies was established by Southern blot analysis. The various HPV 16 transcripts could be detected in cell lines and in tumor biopsies. The size of the RNA PCR products were in agreement with the previously mapped splice sites. The full range of transcripts was revealed in the HPKII cell line and in a number of pre‐invasive carcinomas. Messenger RNAs which could encode the E6III, E4 and E5 proteins were most prevalent in all types of tumor. The overall results of DNA and RNA analyses in cell lines and tumor specimens indicate that (1) expression of either of the early or late transcripts studied is not specifically related to (a) tumor stage or (b) the physical state of the viral genome; and (2) alterations in the splicing patterns of HPV 16 transcripts may not be involved in tumor progression.
Association between childhood rhabdomyosarcoma and maternal history of stillbirths
Authors: Ghali Mohammad H. , Yoo Keun‐Young , Flannery John T. , Dubrow Robert 
Published: February 2007

AbstractA case/control study of childhood rhabdomyosarcoma (RMS) was conducted utilizing information from birth records. Cases among Connecticut residents age 19 and younger diagnosed between 1960 and 1988 were identified from the Connecticut Tumor Registry files. Connecticut birth certificates were located for 103 of the 130 cases identified. A random sample of control birth certificates was frequency‐matched to the cases by year of birth, sex, and ethnic origin, with a control:case ratio of 2:1. Information abstracted from birth certificates included birth weight, length of pregnancy, plurality, birth order, mother's prior stillbirths, mother's age, father's age, and father's occupation. Data were analyzed by conditional logistic regression. The major finding was an association between RMS and the mother having had one prior stillbirth or more (odds ratio = 3.7; 95% confidence interval = 1.5 to 8.9). Particularly noteworthy was the observation that 6 mothers of cases, but no mothers of controls, had had 2 or more prior stillbirths. The trend for increasing risk of RMS with increasing number of mother's prior stillbirths was highly significant (p = 0.0004). This association suggests that RMS and a class of stillbirths share a common etiologic factor. This factor may be genetic or may involve in utero exposure to an exogenous or endogenous agent.
Smoking and colorectal cancer risk: Data from the Melbourne colorectal cancer study and brief review of literature
Authors: Kune Gabriel A. , Kune Susan , Vitetta Luis , Watson Lyndsey F. 
Published: February 2007

AbstractLifetime smoking data were obtained from 715 colorectal cancer cases and 727 age/sex matched community controls as one part of a large, comprehensive, population‐based study of colorectal cancer aetiology and survival in Melbourne, Australia, The Melbourne Colorectal Cancer Study. Statistically significant associations were found for those males smoking hand‐ rolled cigarettes and for cigar‐/pipe‐smoking males with colon cancer. Review of 18 previous case control studies of colorectal cancer showed an elevated risk for cigar‐smoking black males in one study, a statistically non‐significant increased risk for current smokers in one of 3 cohort studies and a statistically significant elevation of risk for smokers in 2 of 3 studies of adenomatous large‐bowel polyps. Although at present there is insufficient evidence to link smoking with large‐bowel cancer, the possibility that ingested tobacco is in some way carcinogenic for the colorectal mucosa may be worth further study.
Immunological analysis of 17β‐hydroxysteroid dehydrogenase in benign and malignant human breast tissue
Authors: Poutanen M. , Isomaa V. , Lehto V.‐P. , Vihko R. 
Published: February 2007

AbstractThe expression of 17β‐hydroxysteroid dehydrogenase (17‐ HSD) enzyme protein was studied in benign and malignant human breast tissue using the time‐resolved immunofluorometric assay (IFMA), immunoblotting and immunohistochemistry. The presence and distribution of estrogen and progestin receptors was also analyzed immunohistochemically. Cytosolic 17‐HSD concentrations in malignant breast specimens were highly variable (⩽ 0.2–311 ng/mg protein). As was previously found for the placental enzyme, the molecular weight of the 17‐HSD expressed in malignant breast tissue was 35 kDa, estimated following polyacrylamide gel electrophoresis and immunoblotting. The cellular distribution of 17‐HSD was further studied by immunohistochemistry. Immunostaining for 17‐HSD was observed in 71% of the benign breast lesions (fibroadenomas and cases of mastopathia chronica) and in 47% of the cancer specimens (intra‐ductal carcinomas, invasive ductal carcinomas). In benign lesions, the staining was exclusively localized in the cytoplasm of epithelial cells, with no immunoreactivity in the stromal cells. The staining in the cancer specimens was also detected only in the cytoplasm of malignant epithelial cells. A strong or moderate expression of 17‐HSD was related to the presence of PR in the specimen (x2 ‐ 4.657, p = 0.031). However, the expression of PR was not a prerequisite for expression of 17‐HSD in all the cancer specimens. Our data suggest that, in addition to the reported regulation of 17‐HSD by progestins, other factors are also involved in this process in breast tissue.
Clinical and biological significance of HSP89 alpha in human breast cancer
Authors: Jameel A. , Skilton R. A. , Campbell T. A. , Chander S. K. , Coombes R. C. , Luqmani Y. A. 
Published: February 2007

AbstractIn order to isolate and characterize genes whose expression may be altered in breast malignancy, we screened a cDNA library with a polyclonal anti‐serum against breast‐cancer‐ metastasis membranes and isolated several immunopositive clones. One of these, AJ I, was analyzed in detail and found to be expressed at varying levels as a 3.3‐kb mRNA in all of 143 breast cancers. High expression was associated with lymph‐node involvement (p = 0.03). Comparison between high‐ and low‐ expressing groups showed a significant difference at 4 and 6 years for both overall (p = 0.004 and p = 0.002 respectively) and disease‐free (p = 0.0001 and p = 0.04 respectively) survival, but not at 11 years. AJ I was expressed at much lower levels in non‐malignant biopsies as compared with malignant tissue (p = 0.001). Expression was observed in breast‐cancer cell lines MCF‐7, ZR‐75‐1, T47D, MDA‐MB‐231 and HBL 100. Partial sequence analysis of the 620 bp clone showed complete homology with human heat‐shock protein 89 alpha. In addition to being heat‐inducible in all the breast cell lines examined, AJ I levels were increased by estradiol (blocked by cyclohexamide and tamoxifen), EGF, oxytocin and vasopressin in a time‐ dependent manner in MCF‐7 cells and by estradiol, EGF, prolactin and hydrocortisone in T47D cells. In MDA‐MB‐231 cells, EGF caused down‐regulation of AJ I mRNA levels. The increasing evidence for the association of heat‐shock proteins with steroid receptors suggests that Aj I may play an important role in the control of estrogen‐receptor transcriptional activity in breast cancers.