bluuebunny/crossref_metadata_2025_split huggingface dataset:
A staging system for soft‐tissue sarcoma and its evaluation in relation to treatment
Authors: Tomita Y. , Kuratsu S. , Naka N. , Uchida A. , Ono K. , Ohsawa M. , Aozasa K. 
Published: February 2007

AbstractIn order to define the significant factors for a staging system of soft‐tissue sarcomas(STS), histologic and clinical findings in 190 adult patients with localized STS in the extremities and trunk were reviewed. The male‐to‐female ratio was 1.21. The histologic grading of tumors was defined according to the criteria recently proposed by us: tumors were low‐grade in 65 cases, intermediate‐grade in 57 cases and high‐grade in 68 cases. The initial surgical procedure was as follows: intracapsular excision in 9 cases, marginal excision in 104 and wide local excision in 77, including 15 amputations. The mode of treatment was surgery alone (101 patients), surgery and chemotherapy (58), surgery and radiotherapy (22) and surgery and combined chemo‐ and radiotherapy (9). Univariate analysis revealed histologic grade, sex, tumor size and tumor depth to be significant prognostic factors. Multivariate analysis revealed histologic grade to be the only independent factor for prognosis. Significant clinical factors in each histologic grade were then evaluated. In the low‐grade group, local recurrence significantly affected prognosis. Most of the patients with local recurrence had had marginal resection as the initial surgical procedure. No clinical factors affecting prognosis in the intermediate‐grade group could be determined. In the high‐grade group, patients with wide local excision and adjuvant chemotherapy had a better prognosis than those with marginal excision with or without adjuvant chemotherapy and wide local excision without chemotherapy (p=0.09). In conclusion, histologic grade was the only significant factor for the staging of STS. On the basis of our staging system, different modalities of treatment for each grade of STS might be indicated; adequate surgery is essential for the prevention of local recurrence, which resulted in reduced mortality in patients with low‐grade STS. For high‐grade STS, the prevention of distant metastasis by combined extensive surgery and adjuvant chemotherapy may make long‐term survival possible.
International comparison on ras gene mutations in latent prostate carcinoma
Authors: Watanabe Masatoshi , Shiraishi Taizo , Yatani Ryuichi , Nomura Abraham M. Y. , Stemmermann Grant N. 
Published: February 2007

AbstractLatent carcinomas of the prostate, discovered at autopsy in men with no prior treatment for prostatic disease, were studied for ras proto‐oncogene mutations. Subjects included 21 Japanese, 15 U.S. whites, 15 U.S. blacks, 20 Hawaiian Japanese and 10 Colombians. PCR and sequence‐specific oligonucleotide hybridization identified mutations in 5 Japanese, in 1 Hawaiian Japanese, in 1 U.S. black, in 1 U.S. white and in 3 Colombians. The 5 Japanese tumor samples contained 3 point mutations in codon 12 of K‐ras and 2 mutations in codon 12 of N‐ras respectively. One tumor in a Hawaiian Japanese man also showed a K‐ras point mutation at codon 12. Two Colombians and one U.S. black man had tumors with mutations at codon 61 of H‐ras, while 1 Colombian showed an N‐ras mutation at this codon. The overall frequency of ras gene mutations was low, but point mutations in codon 12 were most common in latent tumors of Japanese, who experienced the lowest incidence and mortality from this tumor. Latent tumors in men from ethnic groups with high mortality and incidence rates showed fewer ras mutations than the Japanese, and these were more likely to involve codon 61. This finding is consistent with prior studies of more aggressive clinical cancers in Japanese men that indicated a higher frequency of mutations at codon 61.
Comparative analysis of mutations in the p53 and K‐ras genes in pancreatic cancer
Authors: Berrozpe Georgina , Schaeffer James , Peinado Miguel Angel , Real Francisco X. , Perucho Manuel 
Published: February 2007

AbstractMutations in codon 12 of K‐ras occur in a high proportion of pancreatic cancer cases. Although there is evidence that p53 mutations also occur in this tumor, few studies have been reported to date and no comparison has been made of K‐ras and p53 mutations in the same tissues. Single‐strand conformation polymorphism and sequencing of the PCR products were used to determine mutations in p53 gene; to detect mutations in K‐ras genes, the artificial restriction fragment length polymorphism (RFLP) approach was used. Eight out of 30 tissues from primary pancreas cancer and 3 of 4 samples from metastases showed p53 mutations. Fifteen out of 17 pancreatic cancer cell lines had p53 mutations. In 2 cases, the same p53 mutation was identified in the original tumor and in a tumor‐derived cell line. The majority of p53 mutations were present in exons 5‐9 of the gene. Mutations at codon 12 of the K‐ras gene were identified in 23/32 pancreas cancer tissues and in 14/17 cell lines. There was no relationship between the types of mutation observed in the 2 genes. In conclusion, mutations in K‐ras and p53 genes are common in pancreatic cancer. p53 mutations may occur more frequently in metastatic lesions than in primary tumors, although further work is necessary to investigate this point.
Multiple occurrence of carcinoma in the upper aerodigestive tract associated with esophageal cancer: Reference to smoking, drinking and family history
Authors: Morita Masaru , Kuwano Hiroyuki , Ohno Shinji , Sugimachi Keizo , Seo Yosuke , Tomoda Hirotsugu , Furusawa Motonosuke , Nakashima Tadashi 
Published: February 2007

AbstractSmoking and drinking habits as well as family history were examined in 143 men with esophageal cancer, including 30 who had associated second cancers of the upper aerodigestive tract (UADT) and 113 who did not. The risk of second cancers of UADT associated with the main lesions of the esophagus was evaluated, using odds ratios (ORs). As a result, the ORs of second cancers for current smoking and drinking were 5.3 and 7.6 respectively. The ORs significantly increased to 12.7 and 14.7 in heavy smokers and in heavy drinkers respectively. Furthermore, the risk of second cancer also significantly increased (8‐fold) in patients who had close relatives with UADT cancer, compared to those without family history of any cancer. However, there were no differences in smoking or drinking habits regardless of family history. Our data thus suggest that a family history of UADT cancer as well as heavy smoking and drinking are clearly associated with multiple occurrence of UADT cancer. Therefore, careful and frequent examination for appearance of any second lesions are required for patients in these high‐risk groups.
Metastasis of mouse T lymphoma cells is controlled by the level of major histocompatibility complex class I H‐2DK antigens
Authors: Driessche Thierry Vanden , Geldhof Anja , Bakkus Marleen , Toussaint‐Demylle Dominique , Brijs Lea , Thielemans Kris , Verschueren Hendrik , De Baetselier Patrick 
Published: February 2007

AbstractIn vivo inoculation of a low metastatic BW 5147 derived T‐cell lymphoma variant into syngeneic mice, had led to the generation of a highly metastatic variant. The shift towards a more metastatic phenotype is accompanied by an increase in major histocompatibility class I H‐2Dk antigen expression. This suggests that H‐2Dk antigens may control the metastatic potential of BW T lymphoma cells. Our present findings indicate that H‐2Dk expression is directly correlated with the metastatic potential of BW cells. We have confirmed such correlation by specifically altering the level of H‐2Dk expression by: I) FACS analysis, 2) IFN‐γ treatment, 3) H‐2Dk gene transfection. Cells sorted for low H‐2Dk expression had a significantly reduced metastatic potential. Induction of H‐2Dk expression on these cells by either IFN‐γ treatment or H‐2Dk gene transfection concomitantly led to increased metastasis. We also assessed metastatic potential of BW cells in irradiated, immunocompromised recipients. Our results show that the immune system is implicated and we further tested which immune effectors are involved, In vivo depletion of natural killer (NK) and CD8+ T‐cells revealed that the difference in metastatic potential of the H‐2Dk variants relies upon an NK‐dependent mechanism, whereas CD8+ T‐cells are not implicated. Our observations suggest that highly metastatic cells, expressing a high level of H‐2Dk antigens are more resistant to NK‐cell‐mediated cytotoxicity in vivo. We have confirmed our in vivo results by in vitro cytotoxicity assays using poly I:C induced NK and IL‐2 activated LAK cells. We conclude that a NK‐dependent mechanism accounts for the association between differential H‐2Dk antigen expression and metastasis.
Analysis of gene amplification and overexpression in human esophageal‐carcinoma cell lines
Authors: Kanda Yuji , Nishiyama Yasuyuki , Shimada Yutaka , Imamura Masayuki , Nomura Hiroshi , Hiai Hiroshi , Fukumoto Manabu 
Published: February 2007

AbstractGene amplification/overexpression was analyzed in 23 cell lines derived from human esophageal squamous‐cell‐carcinoma tissues by Southern and Northern hybridizations to c‐myc, c‐erbB, hst‐1 and cyclin‐DI probes. Amplification of the c‐myc gene was observed in 5 cell lines derived from well‐differentiated carcinomas and all of them were accompanied by co‐amplification of other examined oncogenes. The c‐erbB gene was amplified in 3 cell lines. Co‐amplification of hst‐1 and cyclin DI, both of which are located in chromosome 11q13, was found in 9 cell lines. Without exception their amplification was simultaneous and the magnitudes were similar. Their amplification, but not their overexpression, was significantly correlated with poor prognosis in patients from whom the cell lines were established. While hst‐1‐gene expression was not detected, at least 1 of the genes analyzed was overexpressed in 20 cell lines vs. its expression in normal esophageal mucosal tissues. However, gene amplification was not necessarily accompanied by overexpression of the corresponding genes. Expression of the cyclin DI gene, which has been assumed to be a target gene for 11q13 amplification, was not detected in one particular cell line with amplification of 11q13.These results suggest that the amplification/overexpression of more than I oncogene is involved in the carcinogenic process of esophageal carcinoma and that c‐myc‐gene amplification is associated with a well‐differentiated subtype. There remains a possibility that key oncogenes other than cyclin DI are involved in 11q13 amplification.
Proliferating cell nuclear antigen and p53 expression as prognostic factors in T1‐2MO prostatic adenocarcinoma
Authors: Vesalainen Satu L. B. , Lipponen Pertti K. , Talja Martti T. , Alhava Esko M. , Syrjánen Kari J. 
Published: February 2007

AbstractThe expression of proliferating cell nuclear antigen and p53 protein was analysed by immunocytochemical methods (PC10, CMI antisera) in 139 patients with T1‐2MO prostatic adenocarcinomas followed‐up for > 12 years. p53 protein was expressed in 21 (15%) tumours (15%), the fraction of positive nuclei being very low (mean SE, 1% ± 0.7%). Accumulation of p53 protein in epithelial cells was independent of tumour stage and Gleason score, and had no effect on prognosis. In 4 cases, p53 protein was expressed only in stromal cells. The fraction of PCNA‐positive nuclei (evaluable in 116 cases) was higher in T2 than in T1 tumours (p< 0.001); furthermore, high Gleason score was positively correlated with PCNA positivity (p< 0.001). A finding of over 5% of PCNA‐positive nuclei predicted progression in T and M categories and were a sign of poor outcome. The fraction of PCNA‐positive stromal‐cell nuclei was related to T‐category with a borderline significance (p= 0.06). In a multi‐variate analysis of the prognostic factors, independent predictors of survival included Gleason score (p< 0.001), fraction of PCNA‐positive nuclei (p= 0.013), observation before therapy (p= 0.05), and T‐category (p= 0.07) in that order of significance. The results suggest that overexpression of p53 protein is of marginal prognostic value in local prostatic adenocarcinomas, whereas direct measurement of cell proliferation by PCNA immunolabelling provides important prognostic information in T1‐2MO tumours, in addition to the Gleason score.
Ethanol and breast cancer: An association that may be both confounded and causal
Authors: Katsouyanni Klea , Trichopoulou Antonia , Stuver Sherri , Vassilaros Stamatis , Papadiamantis Yannis , Bournas Nicholas , Skarpou Nafsika , Mueller Nancy , Trichopoulos Dimitrios 
Published: February 2007

AbstractWe have examined the association of alcohol intake during various life periods, by beverage category, with breast cancer risk in Greece. A hospital‐based case‐control study was performed in Athens, Involving 820 women with breast cancer as well as 795 orthopedic patients and 753 healthy visitor controls‐Relative risk patterns were very similar with either control series, which were therefore combined to increase precision of the estimates. Drinkers of beer were at significantly elevated risk for breast cancer [odds ratio (OR), 1.34 (95% confidence interval, 1.05‐1.71)]. However, drinkers of other alcoholic beverages were not at increased risk. Among beer drinkers there was no dose‐response, and drinkers of both beer and other beverages had a lower OR compared to drinkers of beer only. By contrast, drinkers of 3 or more glasses of alcohol per day, mostly of spirits, were at elevated risk for breast cancer [OR for 3 ‐ < 4 glasses per day, 3.01 (1.14‐7.95); OR for 4 or more glasses per day, 3.79 (1.05‐13.71)]. Reported frequency of consumption was a stronger predictor of breast cancer risk than either duration‐weighted total consumption or consumption before the age of 30 years. There were no coherent patterns for interaction with menopausal status, obesity or use of menopausal estrogens. The association of very low levels of alcohol intake with breast cancer risk may be due to confounding, whereas drinking 3 or more glasses of alcoholic beverages daily appears to genuinely increase breast cancer risk, perhaps by acting as a late‐stage growth enhancing factor. However, the data also are compatible with a linear relationship that has no threshold.
Differential expression of the cell‐cell adhesion molecule E‐cadherin in ascites and solid human ovarian tumor cells
Authors: Veatch Andrea L. , Carson Linda F. , Ramakrishnan S. 
Published: February 2007

AbstractAdvanced ovarian cancers contain 2 distinct phenotypic populations: (a) free‐floating tumor cells in the ascitic fluid and (b) solid tumors. Ascites cells are derived from the solid tumors and spread throughout the peritoneum. Changes in cell‐cell and cell‐extracellular matrix interactions are thought to be responsible for the origin of ascites cells. Since E‐cadherin molecules play a crucial role in the cell–cell interactions in epithelial cells, we investigated the expression of E‐cadherin in those 2 phenotypic populations. Paired samples of ascites and solid tumors were obtained from patients. Both primary tumors and tumor cells isolated from an experimental model showed a marked decrease in E‐cadherin expression in the ascites cells compared to the respective solid tumors. Semi‐quantitative, reverse transcriptase‐polymerase chain reaction (RT‐PCR) was used to determine the steady‐state levels of E‐cadherin‐specific mRNA. Results indicate that the primary tumors had significantly lower levels of E‐cadherin transcript in ascites cells when compared to their solid tumor counterparts. Changes in E‐cadherin expression were also reflected in the invasion capacity of tumor cells in vitro. Ascites cells were 4‐fold more invasive then solid tumor cells, suggesting that ascites cells are a highly malignant phenotype.
Infection of rats with human T‐cell leukemia virus type‐I: Susceptibility of inbred strains, antibody response and provirus location
Authors: Ibrahim F. , Fiette L. , Gessain A. , Buisson N. , De‐thé G. , Bomford R. 
Published: February 2007

AbstractThe susceptibilities of different strains of inbred rats to infection with the human T‐cell leukemia virus (HTLV‐I) after inoculation of human HTLV‐I producer cell lines were compared. The Fisher F344 and Brown Norway strains developed the highest antibody response to HTLV‐I, while the Lewis and BB strains were low responders. Antibodies against the HTLV‐I gag proteins, and env gp21 but not env gp46, were detected in Western blots with sera from HTLV‐I‐infected Fischer F344 and Brown Norway rats. These sera were inactive in an in vitro syncytium‐formation inhibition test The HTLV‐I provirus was detected by polymerase chain reaction in all Fischer F344, and some Lewis and Brown Norway rats, but not in the BB, which lack CP8+ T lymphocytes. The most frequent locations of the HTLV‐I provirus in the Fischer F344, Lewis and Brown Norway rats at 12 weeks after infection were the peripheral blood mononuclear cells (PBMC) and spinal cord. In a second experiment in Brown Norway rats, the provirus was again detected in the PBMC of rats at 11 weeks, but not at 22 weeks, and among the other organs tested at 22 weeks the sympathetic nerve ganglia were positive. It is concluded that HTLV‐I infection occurs in adult rats, but is suppressed with time.
Blockade of the insulin‐like growth‐factor‐I receptor inhibits growth of human colorectal cancer cells: Evidence of a functional IGF‐II‐mediated autocrine loop
Authors: Lahm Harald , Amstad Paul , Wyniger Josiane , Yilmaz Aysim , Fischer Jürgen R. , Schreyer Magali , Givel Jean‐Claude 
Published: February 2007

AbstractInsulin‐like growth factors (IGFs) are potent proliferation stimulators for numerous tumor cells and often function as autocrine growth factors. We have previously shown that exogenous IGF‐I and IGF‐II enhance proliferation of colorectal carcinoma cells. The biological signal of both factors is transmitted through the IGF‐I receptor (IGF‐I‐R). This receptor was expressed in 12/12 colorectal carcinoma cell lines tested. αIR3, a neutralizing monoclonal antibody (MAb) directed against the human IGF‐I‐R, inhibited proliferation in 7/12 lines (Caco‐2, HT‐29, LS411N, LSS13, LS1034, WiDr and SW620), as reflected by a reduction of MTT conversion (19 to 42%), a decrease in cell number (39 to 72%) and an increase in doubling time (up to 2‐fold). In addition, in 4 cell lines (Caco‐2. LSS13, LS1034, WiDr) αIR3 suppressed colony formation in methylcellulose (40 to 84%). Excess of exogenous IGF completely neutralized αIR3‐mediated inhibitory effects. Northern blot analysis revealed abundant expression of 2 IGF‐II transcripts of 5.0 and 4.3 kb in LS1034 cells. In addition, we observed that growth inhibition by αIR3 was correlated with a more differentiated phenotype. Our results suggest that growth of many colorectal carcinoma cell lines is regulated by autocrine IGF‐II‐mediated stimulation of the IGF‐I‐R.
Progressive B‐cell chronic lymphocytic leukaemia frequently exhibits aberrant p53 expression
Authors: Aguilar‐Santelises Miguel , Magnusson Kristinn P. , Wiman Klas G. , Mellstedt Håkan , Jondal Mikael 
Published: February 2007

AbstractWe have analysed the p53 status in non‐progressive and progressive chronic B‐cell leukaemia (B‐CLL) by ELISA, immunoprecipitation, FACS and cDNA sequencing in relation to in vitro proliferation in response to Staphylococcus aureus strain Cowan I (SAC) and IL‐2. In FACS, cells from progressive leukaemia were found to over‐express p53 with a conformation recognized by PAb240. In a PAb240‐based ELISA, 60% of progressive B‐CLL were positive. DNA sequencing of p53 exons 5 to 9 revealed a codon 179 His to Gln change in one of the ELISA‐positive, progressive B‐CLL but failed to reveal any mutations in 4 other ELISA‐positive, progressive B‐CLL Among progressive B‐CLL populations, 10/14 responded by proliferation in vitro to SAC/IL‐2. In non‐progressive cells, low levels of p53 were found by FACS, none was positive in the PAb240 ELISA and only one case showed a weak proliferative response to SAC/IL‐2. Low p53 expression was also seen in different types of normal B cells, resting and activated, and in EBV‐transformed B‐cell lines, in contrast to the high expression observed in Burkitt lymphoma cell lines with verified p53 mutations. We conclude that progressive B‐CLL is characterized by aberrant p53 expression which may be a significant prognostic factor.
Prevalence of serum antibodies against the p53 tumor suppressor gene protein in various cancers
Authors: Angelopoulou Katerina , Diamandis Eleftherios P. , Sutherland Donald J. A. , Kellen John A. , Bunting Peter S. 
Published: February 2007

AbstractWe have developed 2 new quantitative methods for measuring anti‐p53 antibodies in human serum. Using these methods we analyzed 1,392 sera from patients with various malignancies and 230 sera from individuals without malignancy. Highest prevalence of anti‐p53 antibodies was associated with ovarian and colon cancers (15%), followed by lung (8%) and breast (5%) cancers. Prevalence in other malignancies was lower (<4%). In hospitalized patients and apparently healthy individuals, prevalence was very low (<2 and 1% respectively). Extremely high antibody concentrations (> 105 U/L) were found in 5 ovarian, 2 breast, I lung and I colon cancers. Sequential analysis of 6 positive samples has shown that the p53 antibody test may have potential for patient monitoring. The p53 antibody‐positive sera from breast cancer patients were associated with tumors that were steroid hormone receptor‐negative (p < 0.002). We propose that the measurement of p53 antibodies is a relatively specific serological test for cancer, which can be performed with easily automatable and quantitative methodologies and may be further exploited for patient monitoring, prognosis, diagnosis and probably screening for selected cancers.
Human neurological cancer cells express interleukin‐4 (IL‐4) receptors which are targets for the toxic effects of IL4‐pseudomonas exotoxin chimeric protein
Authors: Puri Raj K. , Leland Pamela , Kreitman Robert J. , Pastan Ira 
Published: February 2007

AbstractGlioblastoma, glioma or neuroblastoma cells were examined for the expression of IL‐4 receptors (IL‐4R) by flow cytometric analysis and 125I‐IL‐4 binding. These cancer cell lines expressed IL‐4R which were of high affinity (KD = 700 × 10−12 M) on glioblastoma cells. To investigate the function of these receptors and to target potent cytotoxic antitumor agents to human neurological cancers, we utilized IL4‐PE4E, which is composed of IL‐4 and mutant Pseudomonas exotoxin (IL4‐PE4E). This chimeric molecule was cytotoxic toward human glioblastoma, neuroblastoma and glioma tumor cells in a dose‐dependent manner. The cytotoxicity of IL4‐PE4E was specific, since it was neutralized by excess IL‐4, and by an anti‐IL‐4 monoclonal antibody in all types of brain tumor tested. IL2‐PE4E and IL6‐PE4E were not cytotoxic, nor was an IL4‐PE4E mutant lacking ADP‐ribosylating activity, indicating the IL4‐PE4E‐mediated cytotoxicity of the brain tumor cells required both IL‐4R binding and enzymatic toxin activity. These data indicate that human neurological cancer cells express IL‐4R which are targets for the cytotoxic effects of IL4‐toxin. In addition, our data also suggest that IL4‐PE4E should be studied further as a potential treatment for human neurological cancers.