bluuebunny/crossref_metadata_2025_split huggingface dataset:
High levels of NM23‐H1 and NM23‐H2 messenger RNA in human squamous‐cell lung carcinoma are associated with poor differentiation and advanced tumor stages
Authors: Engel Matthias , Theisinger Birgit , Seib Thomas , Zang Klaus D. , Welter Cornelius , Dooley Steven , Seitz Gerhard , Huwer Hanno 
Published: February 2007

AbstractExpression of the candidate metastasis‐suppressor gene nm23‐H1 has been shown to correlate inversely with metastatic potential in some human tumors, but not in all. Until now, few studies have been carried out on the activity of the homologous nm23‐H2 gene in human cancer. No nm23 transcription studies exist for human lung cancer so far. To determine whether the nm23 genes could have a metastasis‐suppressor function in non‐small‐cell lung carcinoma (NSCLC), pulmonary sarcoma and carcinoids, we analysed both nm23‐H1 and nm23‐H2 mRNA levels in 37 tumor samples obtained from patients who underwent potentially curative resection between 1986 and 1990, and in 4 metastatic tumors obtained from autopsy. As compared to corresponding healthy lung parenchyma, both nm23‐H I and nm23‐H2 transcript levels were elevated in 37 of 41 tumors. The increases in nm23 mRNA expression were stronger in advanced stages of squamous‐cell carcinoma, large‐cell carcinoma, sarcoma and carcinoids than in early stages of the respective tumor types. Within stages I and II of squamous‐cell carcinoma, significantly higher nm23 mRNA levels were found in poorly differentiated tumors than in moderately differentiated ones. Moreover, an inverse correlation between nm23 expression and disease‐free survival of the patients was observed. In conclusion, our results indicate that the increased nm23 expression in the analysed tumors is not consistent with the proposed metastasis‐suppressor function, but the 2 nm23 genes nevertheless may be implicated in the mechanism of tumor progression.
Refined‐sugar intake and the risk of colorectal cancer in humans
Authors: Vecchia Carlo La , Franceschi Silvia , Bidoli Ettore , Barbone Fabio , Dolara Piero 
Published: February 2007

AbstractThe relationship between sugar added to coffee and other hot beverages‐‐as an indicator of taste for sugar and sugar intake outside main meals‐‐and the risk of colorectal cancer was investigated using data from a case‐control study conducted in Northern Italy on 953 cases of histologically confirmed colon cancer, 633 of rectal cancer and 2845 controls admitted to hospital for acute, non‐neoplastic, non‐digestive tract disorders. Compared with subjects who reported adding no sugar to their beverages, the multivariate relative risks (RR) of colon cancer were 1.4 for those adding one spoonful of sugar, 1.6 for those adding 2 spoonsful, and 2.0 for those adding 3 or more. The corresponding RRs for rectal cancer were 1.3, 1.5 and 1.4. For combination of colorectal cancer the RRs were 1.4, 1.5 and 1.8. All the trends in risk were significant, and the results were consistent across strata of study centre, sex and age, and were not appreciably modified by allowance for a number of major identified potential distorting factors, including an estimate of total calorie intake. These findings, if confirmed, would suggest that taste for sugar is a relevant indicator of colorectal cancer risk, and could be interpreted either in terms of a role of sugar in colorectal carcinogens, or of a specific influence of even limited amounts of sugar taken outside meals, which may stimulate the proliferation of the bowel epithelium, and hence enhance colorectal carcinogenesis.
Y chromosome loss and rearrangement in non‐small‐cell lung cancer
Authors: Center Rob , Lukeis Robyn , Vrazas Vickie , Garson O. Margaret 
Published: February 2007

AbstractWhile loss of the Y chromosome from the karyotype of tumor cells has frequently been found in a number of human malignancies of different types, structural alterations are a much less common finding. Prompted by the high frequency of cytogenetic Y chromosome loss found in primary non‐small‐cell lung cancer (NSCLC), and the fact that NSCLC karyotypes usually contain marker chromosomes of unidentified origin, we have determined the Y chromosome status of 12 NSCLC samples (7 cell lines and 5 primary tumors) at a molecular level. Of the 9 cases which did not have a cvtogenetically detectable Y chromosome, 4 were negative for all the Y sequences tested. The other 5, in contrast, retained some Y chromosome sequences. In I case (H520), only Yq heterochromatic sequences were detected, whereas in the remaining 4 (L162, L93, L125 and L71) both Yq heterochromatic sequences and Y euchromatic sequences were retained. The region of common overlap for loss of Y euchromatin was Yp distal to the Y centromere. We hypothesize that deletion of Yp sequences may play a role in tumor progression in NSCLC due to loss of a tumor‐suppressor gene.
Incidence of colorectal cancer following adenomatous polyps of the large intestine
Authors: Levi Fabio , Randimbison Lalao , Vecchia Carlo La 
Published: February 2007

AbstractAn association between adenomatous polyps of the large bowel and colorectal cancer has been reported, in the absence, however, of population‐based estimates of risk. Subjects with histologically confirmed first diagnosis of large‐bowel polyps notified to the population‐based Cancer Registry of the Swiss Canton of Vaud (about 600,000 inhabitants) during the calendar period 1979‐1990 were actively followed up to the end of 1990 for the subsequent occurrence of malignant neoplasms. Among 2,496 individuals with intestinal polyps, followed for a total of 10,310 person‐years at risk (6,201 among males and 4,109 among females), 150 malignant neoplasms were registered versus 152 expected. Thus, the standardized incidence ratio (SIR) for all cancers combined was 0.99. A significant excess was observed for colorectal cancer, with 35 cases observed (19 males, 16 females) versus 17.0 expected (SIR = 2.1; 95% CI: 1.5–3.0). There was also an excess, although not significant, for small‐bowel cancer (2 cases observed vs. 0.4 expected; SIR = 5.4). In none of the other cancer sites was SIR significantly or appreciably elevated: in subjects with colorectal polyps the SIR was 1.6 for stomach, 1.0 for lung, 0.9 for breast and 1.2 for prostate. The SIR of colorectal cancer was 3.1 in the first year since polyp registration, and declined thereafter to 1.8, in the absence, however, of any further trend with time since diagnosis. The cumulative risk of colorectal cancer in subjects with colorectal polyps was 2% at 5 years and 3% at 10 years. The quantitative estimates of this study are of interest for their population‐based nature, and are potentially useful for defining and targeting screening colonoscopy programmes.
Cytogenetic analysis of 52 colorectal carcinomas‐‐non‐random aberration pattern and correlation with pathologic parameters
Authors: Bardi Georgia , Johansson Bertil , Pandis Nikos , Mandahl Nils , Mitelman Felix , Heim Sverre , Bak‐Jensen Elisabeth , Lindström Clas , Törnqvist Anders , Frederiksen Hans , Andrén‐Sandberg Åke 
Published: February 2007

AbstractCytogenetic analysis of short‐term cultures from 52 colorectal carcinomas revealed a normal karyotype in 13 and clonal chromosome aberrations in 39 tumors. In the abnormal group, 13 tumors had simple numerical changes only, whereas 26 had at least one structural rearrangement with or without concomitant numerical changes. The most common numerical abnormalities were, in order of decreasing frequency, +7, −18, −Y, +8, +13 and −14. The most common structural rearrangements affected, again in order of decreasing frequency, chromosomes 8, 1, 6, 7, 17, 3, 11, 13, 14, 16, 2 and 10. The chromosome bands most frequently involved in the structural changes were 8q 10, 17p11, 11q13, 8p11, 6q21, 7p15, 7q36, 12q13, 13q10, and 16q13. The most frequent genomic imbalances brought about by the structural rearrangements were losses from chromosome arms 8p, 1 p, 6q, 17p, 7p, and 16q, as well as gains of 7q, 8q, 13q, and 11 q. A statistically significant (p < 0.05) correlation between the karyotypic pattern and tumor grade was found, with the poorly differentiated carcinomas generally having more massive chromosomal abnormalities.
Enhancement of cisplatin and etoposide cytotoxicity after all‐trans retinoic‐acid‐induced cellular differentiation of a murine embryonal carcinoma cell line
Authors: Guchelaar H.‐J. , Uges D. R. A. , Timmer‐Bosscha H. , De Vries E. G. E. , Mulder N. H. , Dam‐Meiring A. , Oosterhuis J. W. 
Published: February 2007

AbstractThe potential of a combination of differentiation induction and chemotherapy was analyzed. Treatment of the murine embryonal carcinoma (EC) cell line PCC4 in vitro with all‐transretinoic acid (RA) was followed by exposure to cisplatin (CDDP) or etoposide (VP‐16). The expression of EC‐cell‐specific markers decreased upon 96 hr exposure to 10−9, 10−8, 10−7and 10−6M RA, indicating a loss of embryonal phenotype of the cells, whereas expression of markers specific for cytokeratins and neurofilaments was increased after this treatment. These data suggest early somatic differentiation of PCC4 cells upon treatment with RA. Cellular growth rate of PCC4 cells was not affected by preincubation with RA at 10−9 M for 96 hr, but was reduced at 10−8 and 10−7 M RA and inhibited at 10−6 M RA. Culture of PCC4 cells in the presence of 10−7 M RA for 96 hr led to accumulation in G1 of the cell cycle, whereas at 10−8 M RA cell‐cycle distribution was not affected. RA‐treated and ‐untreated PCC4 cells were compared for CDDP and VP‐16 sensitivity. Pre‐treatment with 10−9, 10−8 and 10−7 M RA increased CDDP sensitivity, resulting in a 1.9‐, 2.7‐ and 2.6‐fold decrease in the concentrations inhibiting survival by 50% (IC50s) respectively. Pre‐treatment with 10−8 and 10−7 M RA increased VP‐16 sensitivity 2.5‐ and 3.0‐fold, respectively. Enhanced CDDP sensitivity at RA concentrations not affecting cell‐cycle distribution was not attributable to changes in cellular platinum (Pt) accumulation, or to changes of Pt‐DNA binding. Enhanced VP‐16 sensitivity also occurred while topoisomerase‐II activity was unchanged and topoisomerase‐I activity was increased 2‐fold. Furthermore, there was a 2.0‐ to 4.5‐fold increase in the cellular concentration of VP‐16 after 10−8 and 10−7 M RA pre‐treatment. In conclusion, this study shows that in PCC4 cells the rationale for combining RA and VP‐16 or CDDP is 2‐fold: RA induces differentiation and increases CDDP and VP‐16 sensitivity.
Epidermal growth factor elevates the activity levels of glycolipid sulfotransferases in renal‐cell‐carcinoma cells
Authors: Kobayashi Takahiko , Honke Koichi , Gasa Shinsei , Kato Naoyuki , Makita Akira , Miyazaki Tamotsu 
Published: February 2007

AbstractAccumulation of sulfoglycolipids associated with markedly elevated levels of glycolipid‐sulfotransferase activity was previously demonstrated in human renal‐cell‐carcinoma cells. To elucidate the regulatory mechanisms of sulfoglycolipid metabolism in renal‐cell carcinoma, effects of various growth factors on the sulfotransferase‐activity levels were investigated using a human renal‐cell‐carcinoma cell line, SMKT‐R3. Exogenous epidermal growth factor (EGF) significantly increased the activity levels of the sulfotransferases in a dose‐dependent manner, but did not change that of arylsulfatase A, which hydrolyzes sulfoglycolipids. Furthermore, metabolic labeling with 35S‐sulfate revealed that the addition of EGF to the culture medium of the cells resulted in an increment of sulfoglycolipid synthesis. The expression of the EGF receptor on SMKT‐R3 cells was demonstrated by affinity cross‐linking with 125l‐EGF. These observations suggest that EGF can regulate sulfotransferase‐activity levels in renal‐cell‐carcinoma cells, and function as one of the regulatory factors of sulfoglycolipid synthesis in these carcinoma cells.
Induction of tumor‐cell lysis by bi‐specific antibody recognizing ganglioside GD2 and T‐cell antigen CD3
Authors: Bernhard Helga , Karbach Julia , Büschenfelde Karl‐Hermann Meyer Zum , Strittmatter Wolfgang , Knuth Alexander 
Published: February 2007

AbstractHuman tumor cells expressing ganglioside GD2 were lysed by various effector populations targeted with an anti‐CD3‐anti‐GD2 bi‐specific antibody (BAb CD3 x GD2). This antibodyheteroconjugate was prepared by chemically cross‐linking the OKT‐3 monoclonal antibody (MAb) reactive with CD3 antigen on T lymphocytes with the ganglioside MAb ME 361, which binds preferentially to the tumor‐associated ganglioside GD2. The specificity of target‐cell lysis by the cytotoxic T cells (CTL) was mediated by the specificity of the targeting antibody: GD2‐negative cells were not lysed in the presence of the CD3 x GD2 BAb. A dose‐dependent response was observed in a range of 10 to 10,000 ng/ml. In contrast, 2 other BAbs recognizing the tumor‐associated antigens EGF‐R and TKB‐2 had greater potency to mediate tumor‐cell lysis than the GD2 x CD3 BAb. Peripheral‐blood cells (PBL) stimulated with OKT‐3 MAb or with irradiated tumor cells in a mixed lymphocyte culture (MLTC) could be induced to lyse GD2‐positive tumor cells in the presence of CD3 x GD2 BAb. The tumor‐cell lysis could be mediated by autologous or allogeneic effector cells. NK cells had no influence on the BAb‐induced cytotoxicity.
The anti‐tumor arotinoid RO 40‐8757 protects bone marrow from the toxic effects of cyclophosphamide
Authors: Eliason James F. , Inoue Tomoaki , Kubota Akiko , Horii Ikuo , Teelmann Kampe , Hartmann Diethelm 
Published: February 2007

AbstractThe arotinoid Ro 40‐8757 is a novel compound that has significant therapeutic activity against chemically induced breast tumors in rats. The results of combination therapy with cyclophosphamide, plus the arotinoid showed that the anti‐tumor effects were additive. However, all of the rats given CPA alone died between week 6 and week 10 of treatment. None of the animals in the group treated with the combination died. Administration of a single dose of Ro 40‐8757 to non‐tumor bearing mice resulted in a transient increase in bone‐marrow‐progenitor cells after 2 days and a decrease in splenic progenitors at day 4. Treatment of mice with the combination demonstrated that the marrow progenitors were protected from the toxic effects of CPA by the arotinoid. Direct addition of Ro 40‐8757 to mouse bone‐marrow cells in clonogenic assay cultures containing WEHI‐3‐conditioned medium plus erythropoietin showed no significant enhancement by the arotinoid. The results suggest that this compound may exert its protective effect through the hemopoietic micro‐environment.
Inhibitory effects of 3′‐methyl‐3‐hydroxy‐chalcone on proliferation of human malignant tumor cells and on skin carcinogenesis
Authors: Satomi Yoshiko 
Published: February 2007

Abstract3′‐methyl‐3‐hydroxy‐chalcone (3Me‐3‐C), a derivative of chalcone, inhibited the proliferation of various kinds of human malignant tumor cells, such as HGC‐27 (gastric cancer), HeLa (cervical carcinoma), PANC‐1 (pancreatic cancer) and GOTO (neuroblastoma). Flow‐cytometric analysis of HGC‐27 cells revealed that 3′Me‐3‐C perturbed the cell cycle, i.e., it delayed passage through the S phase, and/or caused arrest in the G0/G1 phase. 3′Me‐3‐C inhibited the binding of [6,7‐3H]estradiol to type‐II estrogen‐binding sites dose‐dependently, and altered the pattern of protein synthesis and phosphorylation, which may explain 3Me‐3‐C‐induced inhibition of cell proliferation. In addition, 3Me‐3‐C also suppressed the promoting activity of 12‐0‐tetradecanoylphorbol‐13‐acetate on skin carcinogenesis in 7,12‐dimethylbenz[a]anthracene‐initiated mice.
Liposarcoma: A population‐based epidemiologic and prognostic study of features of 43 patients, including tumor DNA content
Authors: Gustafson Pelle , Rydholm Anders , Willén Helena , Åkerman Måns , Baldetorp Bo , Fernö Mårten 
Published: February 2007

AbstractDifferent conceptions exist regarding the epidemiology and prognosis of liposarcoma, and several classification systems are in use. We analyzed a population‐based, 25‐year series of 43 patients with liposarcoma of the extremity or trunk wall. Follow‐up was complete. The annual incidence was 0.12/10s. The thigh was the most common location. One of 6 tumors was subcutaneous. Deep‐seated tumors were larger than s.c. tumors. Among the 42 surgically treated patients, grade II (4‐grade scale) was the most common malignancy grade. Four tumors were well‐differentiated, 24 were predominantly myxoid, 4 predominantly round‐cell, and 10 were predominantly of pleomorphic type. The 5‐year metastasis‐free survival rate was 69%. By univariate analysis increasing malignancy grade, tumor necrosis, vascular invasion, mitotic count, subtype other than well‐differentiated, and high cellularity were prognostic for metastatic disease. However, in the multivariate analysis only tumor necrosis was an independent risk factor. Tumor necrosis should be considered when prognosis of liposarcoma of the extremity and trunk wall is evaluated.
Lack of allelic deletion and point mutation as mechanisms of p53 activation in human malignant melanoma
Authors: Castresana Javier S. , Rubio Mari‐Paz , Seizinger Bernd R. , Vàzquez J. Jaime , Idoate Miguel , Sober Arthur J. , Barnhill Raymond L. 
Published: February 2007

AbstractTo investigate the role of the p53 tumor‐suppressor gene in the development of human melanoma, loss of heterozygosity (LOH) of p53 was studied in 46 cases of melanoma by a polymerase‐chain‐reaction/restriction‐fragment‐length polymorphism (PCR/RFLP) analysis, and p53 mutations were assessed in 51 cases of melanoma by a polymerase‐chain‐reaction/ single‐strand‐conformation polymorphism (PCR/SSCP) analysis. Frozen tumors and paraffin samples were used in the study. We were not able to detect any allelic loss in 12 BstU1 informative cases or any single mutation in exons 5 to 8 of the p53 gene. Our results, together with other findings at the DNA level, suggest that the p53 gene appears not to be commonly involved in the development of melanoma, at least by its most frequent mechanisms of deletion of one allele and/or mutation in the other.
Tumor‐cell proliferation and prognosis in renal‐cell carcinoma
Authors: Larsson Per , Ljungberg Börje , Roos Göran , Stenling Roger 
Published: February 2007

AbstractIn the present study the prognostic value of tumor S‐phase fraction was evaluated in 69 patients with renal‐cell carcinoma. The proportion of S‐phase cells was calculated from DNA histograms by flow cytometry in multiple samples from each tumor. The mean tumor S‐phase percentage varied between 1.0 and 17.0%, mean 7.5%, with a significant difference between diploid and non‐diploid tumors. Stage‐I tumors showed significantly lower S‐phase values than tumors of stages II/III and IV. Histopathological grade correlated with fraction of cells in S‐phase. Nineteen tumors were homogeneously diploid, I was tetraploid and 49 were aneuploid. Heterogeneity concerning S‐phase values was found in 46 of the 69 tumors and concerning DNA ploidy in 34 tumors. Survival time was longer for patients with diploid tumors than for those with aneuploid tumors. Patients with S‐phase values <7.5% had a longer survival time than patients having tumors with S‐phase values >7.5%. Within the group of aneuploid tumors, patients with S‐phase values <7.5% had a significantly better prognosis. In multivariate analysis, only tumor stage and S‐phase gave significant independent prognostic information. The S‐phase fraction seems to be an additional prognostic parameter for patients with renal‐cell carcinoma.
Correlation of epithelial proliferation and squamous esophageal histology in 1185 biopsies from linxian, china
Authors: Liu Fu‐Sheng , Wang Guo‐Qing , Li Jun‐Yao , Dawsey Sanford M. , Rao Madhusudan , Taylor Philip R. , Lipkin Martin , Lewin Klaus J. , Li Bing 
Published: February 2007

AbstractEpithelial proliferation is an active area of research in gastrointestinal cancer, but only a few studies have examined the relationship of esophageal epithelial proliferation and squamous histologic findings in populations with high rates of squamous esophageal cancer. In order to study this correlation, tritiated thymidine labeling was performed on 1185 esophageal biopsies from 745 residents of Linxian, China, a county with some of the highest esophageal‐cancer rates in the world. Total labeling index (TLI = total labeled cells/total cells counted) was used to measure the amount of proliferation, and the proportion of labeled cells found in cell layers 4 to 10 (labeled cell fraction 4 plus, LF4+ = labeled cells in layers 4‐10/total labeled cells) was used to measure the vertical distribution of proliferation. Of the biopsies, 979 were histologically normal, 51 showed acanthosis, 35 showed esophagitis, 116 showed squamous dysplasia, and 6 showed invasive squamous cancer. The mean values of both proliferation variables, stratified by histologic diagnosis, showed the following relationships: normal = acanthosis < esophagitis = dysplasia < cancer. The ranges of proliferation values overlapped extensively in all biopsy categories, so that measuring proliferation could not substitute for histologic diagnosis. It remains to be seen whether proliferation values, histologic diagnoses, or some combination of these methods is most predictive of subsequent esophageal cancer.
E‐cadherin expression in head and neck squamous‐cell carcinoma is associated with clinical outcome
Authors: Mattijssen Vera , De Mulder Pieter H. M. , Peters Herman M. , Schalkwijk Lia , Van't Hof‐Grootenboer Bep , Ruiter Dirk J. , Manni Johannes J. 
Published: February 2007

AbstractThe cell‐cell adhesion molecule E‐cadherin has been shown to suppress invasive growth of epithelial cells in vitro, and loss of its expression is thought to be important in invasion and metastatic potential of epithelial tumors in vivo. We retrospectively studied the level of E‐cadherin expression in 50 primary head and neck squamous‐cell carcinomas (HNSCC) by immunohistochemical methods, on frozen sections, using anti‐E‐cadherin monoclonal antibody (MAb) 6F9. It concerned patients with different stages of carcinoma of larynx or oral cavity who had been treated with curative intention 30 months or more before. Percentages of membranous stained tumor cells were scored in 1 of 5 categories. Scores were generally low, as in 11/50 lesions ≤5% cells were stained, and in 19/50 lesions only 6‐25% cells showed membranous staining. In 9 lymph‐node metastases evaluated, E‐cadherin expression was in the same range as in the primary tumors. There was a significant correlation between the level of membranous E‐cadherin expression in the primary tumor and the degree of differentiation. No relation was found with tumor size (pT) or regional lymph‐node classification (pN). Nevertheless, 29 patients surviving ≥30 months without evidence of disease had significantly higher levels of membranous E‐cadherin expression in their primary tumors than 10 patients with unfavorable clinical course clearly related to recurrent and/or metastatic HNSCC. Moreover, this could only partially be explained by distinctions in differentiation grade between both groups. Our results suggest that membranous E‐cadherin expression has prognostic importance in patients with HNSCC.