bluuebunny/crossref_metadata_2025_split huggingface dataset:
Somatostatin analogue rc‐160 inhibits the growth of transplanted colon cancer in rats
Authors: Qin Yunfeng , Schally Andrew V. , Willems Gerard 
Published: February 2007

AbstractThe effect of somatostatin analogue RC‐160 on the growth of DHD/K12 rat colon cancer has been investigatedin vivoas well asin vitro.Twenty syngeneic BDIX rats with s.c. implanted tumors were divided randomly into 2 groups. The rats from each group received a daily s.c. injection of either RC‐160 (100 μg/kg/day) or injection vehicle as control for 37 days starting from the day of tumor inoculation. Tumor volumes were measured every 3‐4 days. At the end of the treatment, the mean tumor volume was 504.5 ± 97.0 mm3in the control group and 177.8 ± 60.5 mm3in the RC‐160 treated group (p< 0.01). The tumor volume doubling time was calculated to be 11 days in the control group and 13.5 days in the RC‐160 group, respectively. The tumor growth delay time was 18 days. Using bromodeoxyuridine labellingin vivo, the mean labelling index in the tumors was decreased by 35% (p<0.01) after RC‐160 treatment. Total protein and total DNA contents in the tumors were decreased by 70.1% (p< 0.05) and 68.7% (p< 0.05), respectively. The data indicate that somatostatin analogue RC‐160 inhibits the growth of DHD/K12 colon cancerin vivo.In 2 studiesin vitro, DHD/K12 cells were cultured for 72 hr with RC‐160 and natural somatostatin‐14 (S‐S‐14) at concentrations ranging from 62.5 ng/ml to 2,000 ng/ml. Tumor‐cell growth was measured spectrophotometrically by the crystal violet staining assay. No direct effect on tumor cell growthin vitrowas observed with either RC‐160 or S‐S‐14, possibly because of the loss of somatostatin receptors in previous passages of the DHD/K12 cell line.
Differences in patterns of allelic loss between two common types of adult cancer, breast and colon carcinoma, and Wilms' tumor of childhood
Authors: Devilee P. , Van Den Broek M. , Mannens M. , Slater R. , Cornelisse C. J. , Westerveld A. , Khan P. Meera 
Published: February 2007

AbstractSeveral chromosomal regions exhibit loss of heterozygosity (LOH) in different types of human tumor, and on this basis are presumed to carry‐suppressor genes. We studied 7 of such chromosome regions, including 3p, 5q, 11p, 13q, 17p, 18q and 22q, using a selected set of DNA markers in 44 Wilms' tumors, 64 breast and 83 colon carcinomas. In Wilms' tumor only the short arm of chromosome II was preferentially involved (38% of the informative cases), whereas in breast and colorectal carcinomas all investigated chromosome regions showed allelic loss at frequencies ranging from 19‐61% and 12‐55%, respectively. We tried to explain this difference in terms of developmental stages and tissue homeostasis of the organs involved. We postulate that more widespread occurrence of allele loss in colorectal and breast carcinomas compared to Wilms' tumor is associated with a difference in the differentiation status of the tissues at the time of tumor initiation.
Hodgkin's disease in adults in Saudi Arabia. Clinical features, prognostic factors and an analysis of therapy. Outcome of combination chemotherapy only, for both localized and advanced disease
Authors: Al‐Idrissi Hassan Y. , Ibrahim Ezzeldin M. 
Published: February 2007

AbstractFifty evaluable, previously untreated, adult patients with clinically staged (CS) early and advanced Hodgkin's disease were treated with chemotherapy alone, using various regimens. Their mean age was 31.9 years. Fifteen patients (30%) had CS I or II and 35 (70%) had CS III or IV Eighty‐eight per cent of patients had one or more of the B symptoms and 64% had an unfavorable histology. Complete remission (CR) was achieved in 43 out of 50 patients (86% with 95% confidence interval of 76% to 96%), partial remission in 3 (6%) and treatment failure in 4. Adjusted analysis, using all possible subset regression, showed that unfavorable histology, bulky disease and receiving a total dose‐intensity (TDI) ⩽ 0.80 were negatively associated with the likelihood of achieving CR. At a median follow‐up of 36 months (range, 6‐90), 84% of patients were alive and 82% were disease‐free. The overall median survival has not been reached, but the projected 5‐year survival probability was 79%. Time‐to‐relapse was also estimated for those who achieved initial CR. The estimated 5‐year relapse‐free survival was 87%. The Cox proportional hazards model predicted that unfavorable histology, bulky disease and TDI ⩽ 0.80 had an independent, adverse influence on survival. We conclude that the results of chemotherapy alone are encouraging and the rationale is practical and acceptable in those countries where the availability of radiotherapy units is limited.
Intracellular localization of metaiodobenzyl guanidine in human neuroblastoma cells by electron spectroscopic imaging
Authors: Gaze M. N. , Huxham I. M. , Mairs R. J. , Barrett Ann 
Published: February 2007

AbstractThe targeted radiotherapy of neuroblastoma with 131I‐labelled metaiodobenzyl guanidine (mIBG) is now the subject of several clinical studies. The precise intracellular localization of mlBG, necessary for nuclear microdosimetry, has not previously been described. We report the use of electron‐energy‐loss spectroscopy and electron spectroscopic imaging to establish the intracellular distribution of mlBG in cells from the human neuroblastoma line NBI‐G which had been incubated with the drug by mapping iodine in ultra‐thin sections of tumours. Most of the iodine is found within the mitochondria, with lesser amounts in the vesicles and on the nuclear membrane. The use of alternative radionuclides with different physical characteristics has been suggested to optimize the efficacy of this therapeutic strategy. The lack of penetration of mIBG into the nucleoplasm means that ultra‐short‐range Auger electron emitters such as 125I are not likely to prove more cytotoxic than 131I.
Characterization, isolation and amino terminal sequencing of a rat colon carcinoma‐associated antigen
Authors: Chadeneau Corinne , Denis Marc G. , Blottière Hervé M. , Grégoire Marc , Douillard Jean‐Yves , Meflah Khaled 
Published: February 2007

AbstractMonoclonal antibodies have been raised against a cell line derived from a dimethylhydrazine‐induced rat colon carcinoma. One of these antibodies (MAb E4) has previously been shown to react slightly with normal small intestine and colon, and not with other normal tissues as determined by immunohistochemistry. Using Western immunoblotting we confirmed this tumor specificity. Therefore, the Mr of approx. 66,000 glycosylated antigen (pE4) recognized by MAb E4 appeared to be a potential marker of colon carcinoma. Fifteen human tumor cell lines were tested by flow cytometry for the expression of pE4. This antigen was not detected on these cells. In the rat colon carcinoma cell, pE4 was exclusively found on the cell membrane. pE4 was purified to near homogeneity by immunoaffinity chromatography. The first 20 N‐terminal amino acids were identified. Comparison with the NBRF data bank did not reveal a complete homology with known sequenced proteins but similarities were found with the mouse L3T4 precursor, the env polyprotein of human immunodeficiency virus type I, flagellin from Halobacterium halobium and the gp30 from hepatitis B surface antigen. Homology was always found in transmembranous or hydrophobic domains of these proteins. By indirect immunofluorescence analysis of adherent cells and size exclusion chromatography under native conditions, pE4 was found to interact with other molecules and perhaps to be involved in intercellular contact.
Prognostic value of morphometry and DNA flow‐cytometry features of invasive breast cancers detected by population screening: Comparison with control group of hospital patients
Authors: Uyterlinde Anne M. , Baak Jan P. A. , Schipper Nellie W. , Peterse Hans J. , Meijer Jos W. R. , Vooys Peter G. , Matze Erna 
Published: February 2007

AbstractUsing the prognostic value of morphometric and flow‐cytometric features, a group of patients with invasive breast cancers detected with population screening (PS, n = 70) has been evaluated and compared with a random control group in 2 hospitals (H group, n = 225) diagnosed in the same period. The results show that the PS patients had smaller tumors, less positive lymph nodes, better differentiated tumors with a lower mitotic activity index (MAI) and lower values of the morphometric prognostic index (MPI). Furthermore, the women more frequently had diploid tumors and tumors with small nuclei. The second purpose was to evaluate whether quantitative microscopical features, in comparison with other prognostic features such as size of primary tumor, nodal status and histologic grade, are as strong prognosticators in PS tumors as in H‐detected breast cancers. In comparison with H tumors, morphometric and flow‐cytometric features, as well as tumor size, had the same prognostic value for the PS tumors. In contrast, nodal status was not significant within the PS group, and the same phenomenon was found in a sub‐group of H patients with similar sized tumors. Of all quantitative microscopical features (MPI, MAI, mean nuclear area (MNA) and DNA Index (DI)), the MAI had the strongest prognostic value. Dl showed additional prognostic value to the MAI for patients with small tumors and with small tumor‐cell nuclei, because a diploid pattern in these cases (this combination occurred in 21 patients of the total group = 30%) was correlated with a 95% 10‐year survival rate. Histologic grade, although significant within the large H group, was of no prognostic value within the PS group, and also not as in the H sub‐group with small tumors. It is concluded from morphometric and DNA flow‐cytometric criteria that these prognostic features in invasive breast cancers detected by PS were all more favorable than in randomly detected hospital breast cancers. This may account for the reported better survival rate of PS patients. Furthermore, the prognosis of patients with small invasive breast cancers detected by population screening can be more accurately deduced by quantitative microscopical features than by axillary‐lymph‐node status.
Clustering of aberrations to specific chromosome regions in benign neoplasms
Authors: Sreekantaiah Chandrika , Sandberg Avery A. 
Published: February 2007

AbstractCytogenetic analyses of benign tumors in the past 2 decades have established consistent and recurrent abnormalities in a large proportion of these tumors. In particular, chromosomal analyses of meningiomas, adenomas of the salivary gland, uterine leiomyomas and lipomas have led to the identification of cytogenetic subtypes characterized by specific structural or numerical abnormalities. A comparison of these consistent changes shows a clustering of aberrations to specific regions on chromosomes 12, 1, 2, 6, 11, 13 and 22. The specificity of the involvement of these chromosome regions in the various benign neoplasms suggests that genes of importance in growth regulation rather than those related to malignant transformation are located at these sites.
Dietary factors in cancer of the lower urinary tract
Authors: Nomura Abraham M. Y. , Kolonel Laurence N. , Hankin Jean H. , Yoshizawa Carl N. 
Published: February 2007

AbstractThis dietary study was based on 195 male and 66 female cases of lower urinary tract cancer, identified in Hawaii between 1977 and 1986. Each case was matched for sex, age, and ethnic group (Caucasian or Japanese) to 2 population‐based controls. There was a decrease in risk with increasing levels of consumption of vitamin C in women (p =0.03) and dark green vegetables in men (p =0.02). When examined by quartile, the odds ratios for the highest quartile of intake compared to the lowest quartile were 0.4 for women and 0.6 for men, respectively. Although dark green vegetables are a source of carotenoids, the intake of total carotenoids, retinol and total vitamin A was weakly and inconsistently related to risk in both sexes. Among women only, there was also an inverse association with the consumption of regular ground coffee (p ‐0.02) but not with other types of coffee. Finally, there were no statistically significant or consistent differences between cases and controls in the intake of artificial sweeteners and tea.
Alpha‐smooth‐muscle actin and desmin expressions in human neuroblastoma cell lines
Authors: Sugimoto Tohru , Ueyama Hisao , Hosoi Hajime , Inazawa Johji , Kato Taiji , Kemshead John T. , Reynolds C. Patrick , Gown Allen M. , Mine Hiroshi , Sawada Tadashi 
Published: February 2007

AbstractThe neural crest gives rise to a variety of tissues, including peripheral neurons, Schwann cells, melanocytes and ectomes‐enchymal cells, which include the smooth‐muscle cells of large arteries. Cell lines derived from neuroblastoma (a neural‐crest tumor) exhibit at least 2 distinct morphological cell types, a neuroblastic phenotype (N‐type) and an epithelial‐like phenotype (S‐type) with characteristics of substrate‐adhesiveness. We have analyzed 17 human neuroblastoma cell lines using a panel of monoclonal antibodies (MAbs) against cytoskeletal proteins. Three neuroblastoma cell lines (KP‐N‐SI, KP‐N‐YN and SMS‐KCN) bound an α‐smooth‐muscle actin antibody. In addition, one of these lines (KP‐N‐SI) bound anti‐desmin MAbs as determined by indirect immunofluorescence. A total of 8 cioned cell lines were obtained from the above parent cell lines. These were composed of either N‐or 5‐type cells and were confirmed to have the same neuroblastoma origin as each parent cell line by chromosomal analysis. Alpha‐smooth‐muscle actin and desmin were demonstrated In the 5‐type cloned cells by indirect immunofluorescence, as well as by 2‐dimensional Western blot analysis. These results were confirmed by Northern blot analysis using a specific probe (pSHαSMA‐3′UT) to human α‐smooth‐muscle actin mRNA. These ascertain the presence of α‐smooth‐muscle actin and desmin in neuroblastoma cell lines. These data show that, in addition to giving rise to cells with neural, Schwann‐cell and melanocyte markers, neuroblastoma can also give rise to the cells expressing smooth‐muscle cell markers.
Differentiating effect of sodium butyrate on human hepatoma cell lines PLC/PRF/5, HCC‐M and HCC‐T
Authors: Saito Hidetsugu , Morizane Toshio , Watanabe Tetsu , Kagawa Tatehiro , Miyaguchi Shingo , Kumagai Naoki , Tsuchiya Masaharu 
Published: February 2007

AbstractThe in vitro effect of sodium butyrate (SB) on human hepatoma cell lines PLC/PRF/5, HCC‐M and HCC‐T was investigated. SB was added at the non‐toxic but cytostatic concentration of I mM. In all these cell lines, SB reduced cell proliferation and changed the morphology of the cells into a fibroblast‐like shape. In PLC/PRF/5, alpha‐fetoprotein production and c‐myc expression were inhibited. In contrast, gene expression of albumin, one of the normal liver‐cell products, Mid that of integrated hepatitis B virus genome, was increased. In HCC‐M and HCC‐T, c‐myc expression, which was enhanced In the naive state, was reduced. In HCC‐M, fos expression was inhibited but the expression of N‐ and K‐ras genes did not change. SB seemed to induce normal or mature properties of hepatocytes in human hepatoma cell lines.
Altered protein glycosylation of rat 3Y1 cells induced by activated c‐myc gene
Authors: Hiraizumi Sen , Takakasaki Seiichi , Shiroki Kazuko , Kobata Akira 
Published: February 2007

AbstractN‐linked sugar chains of rat 3Y1 cells and tumorigenic cells derived by transfection with activated c‐myc gene were quantitatively released as oligosaccharides from membrane preparations by hydrazinolysis. Structural analyses revealed that cells of both types contain bi‐, tri‐ and tetra‐antennary complex‐type oligosaccharides as well as high‐mannose‐type oligosaccharides. However, the c‐myc‐transfected cells showed an increase in tri‐ and tetra‐antennary oligosaccharides having the GIcNAcβI→4Manαl→ and/or the GlcNAcβl→ 6Manαl→ linkages with a decrease in biantennary oligosaccharides compared to control 3Y1 cells. The data suggest that c‐myc gene has a potential role in the regulation of cellular protein glycosylation and that an elevated expression of c‐myc gene in the cells leads to increased branch formation of outer chains in N‐linked oligosaccharides concomitant with the acquisition of tumorigeniclty.
A case‐control study of gastric cancer and diet in Italy. III. Risk patterns by histologic type
Authors: Buiatti Eva , Palli Domenico , Bianchi Simonetta , Decarli Adriano , Amadori Dino , Avelum Claudio , Gpriani Francesco , Cocco Pierluigi , Giacosa Attilio , Lorenzini Letizia , Marubini Ettore , Puntoni Riccardo , Saragoni Ariele , Fraumeni Joseph F. , Blot William J. 
Published: February 2007

AbstractIn a case‐control study of gastric cancer (GC) in high‐risk and low‐risk areas of Italy, 923 GCs were systematically categorized by one pathologist according to the Lauren classification distinguishing 2 main histologic types, intestinal (55%) and diffuse (23%). Intestinal types outnumbered diffuse types by a 3 to I margin in high‐risk regions in the north‐central part of the country, while both types occurred at nearly equal rates in low‐risk areas. Intestinal types also occurred relatively more frequently at older ages and among males. Relative risks of each type of GC were evaluated In relation to dietary and other data obtained from interviews with the cancer patients and controls. The risk patterns for intestinal and diffuse types were remarkably similar. Increased risks of both types were associated with high intake of meat, salted/dried fish, seasoned cheeses and traditional soups, while decreased risks of both types were found among heavy consumers of fresh vegetables and fruits. Correspondingly similar patterns were seen with indices of nutrients, with risks of both intestinal and diffuse GC rising with animal protein Intake and declining with consumption of vitamins C and E. Both types were inversely related to socio‐economic status, and neither was associated with cigarette smoking. A familial history of GC was reported more frequently by patients with each type than by controls, although the highest risk was for unclassified GC, a group of poorly differentiated and medullary carcinomas accounting for 15% of all GCs in this study. The findings suggest that, despite differences in geographic and demographic patterns, the intestinal and diffuse types of GC have etiologic factors in common.
Ras mutations in united kingdom examples of oral malignancies are infrequent
Authors: Chang Sidney E. , Bhatia Pradeep , Johnson Newell W. , Morgan Peter R. , McCormick Frank , Young Bryan , Hiorns Lynne 
Published: February 2007

AbstractPoint mutations in codons 12, 13 or 61 of the oncogenes Ha‐ras, Ki‐ras or N‐ras have been identified in human malignancies of many types. Using the PCR (polymerase chain reaction) technique for DNA amplification in vitro and stringent probing of the amplified DNA on dot blots with a library of specific oligonucleotides, we have screened for the presence of ras mutations in oral and para‐oral malignancies and some associated lesions. The material, from UK patients, consisted of 22 oral squamous‐cell carcinomas including 5 neck metastases, I oral mucosal dysplasia, I proliferative verrucous leukoplakia, I antral and I tonsillar carcinoma, I basal‐cell carcinoma, I salivary adenocarcinoma, I salivary adenoid cystic carcinoma and I lung adenocarcinoma metastatic to the gingiva. Genomic DNA was extracted from tissues which were fresh or preserved in liquid nitrogen. Two DNA samples contained point mutations in codon 61 of Ki‐ras. One of these mutations was in the lymphocytes infiltrating a retromolar SCC. The other mutation (CAA to CAU; substitution of glutamine by histidine) was in the lung adenocarcinoma metastasis. The absence of ras mutations in the epithelium of primary oral squamous‐cell carcinomas is of considerable interest as other work in our Department on Indian cases of oral carcinomas associated with chewing tobacco (quid) revealed that 35% of these had a codon 12, 13 or 61 mutation in Ha‐ras. While ras activations arising from point mutations may occur in a high proportion of oral malignancies associated with chewing tobacco (quid), this was not the case in UK oral malignancies, even where tobacco was smoked.
Significance of freshly cultured fibroblasts from different tissues in promoting cancer cell growth
Authors: Mukaida Hidenori , Hirabayashi Naoki , Hirai Toshihiro , Iwata Takashi , Saeki Syuuji , Toge Tetsuya 
Published: February 2007

AbstractThe interactions between human cancer cells and primary cultured human fibroblasts without cell‐to‐cell contact were investigated using double soft‐agar culture. Human fibroblasts obtained from different organs were cultured in monolayers and used after the 3rd or 4th passage. In double softagar culture, colony formations of cancer cells in the ‐over‐layer were stimulated or inhibited by the presence of various kinds of fibroblast in the underlayer. The growth of all cancer cells tested was always stimulated by the presence of fibroblasts obtained from an organ In which cancer cells had already developed, and inhibited by those from skin. However, fibroblast‐conditioned media failed to affect cancer cell growth, either in MTT assay or in soft‐agar culture. These results suggest that mutual growth reliance exists between human cancer cells and primary cultured fibroblasts by diffusible factors secreted by both cells (paracrine growth) and that mutual growth enhancement occurs between cancer cells and fibroblasts derived from tissues in which cancer cells had originated.
The role of both specific cellular adhesion and growth promotion in liver colonization by F9 embryonal carcinoma cells
Authors: Rusciano Dario , Lorenzoni Patrizia , Burger Max M. 
Published: February 2007

AbstractUnselected F9 murine embryonal carcinoma cells preferentially colonize the liver upon injection into tail veins of syngeneic mice, while the lungs are only very rarely colonized. Here we show that F9 cells attach better to fibronectin than to laminin in an adhesion assay, like other liver‐colonizing cell lines. Moreover, assays of adhesion to extracellular matrix (ECM) prepared from rat organs (liver, lung and kidney) demonstrate that, in the absence of serum, F9 cells adhere better to liver‐than to kidney‐or lung‐derived ECM. Even in the presence of FCS, the adhesion to lung ECM remains very low. This very low adhesiveness of F9 cells to lung‐derived ECM correlates well with the finding that, in an organ distribution assay, tail‐vein‐injected F9 cells are very rapidly released from the lungs, when compared to the retention times of the lung‐specific murine melanoma cell line B16‐F10. Yet another property appears to contribute to organ‐specific colonization of these cells: extracts of liver promote the growth of F9 cells, in contrast to extracts of lung or kidney which have no effect. These data suggest that preferential formation of metastases in the liver following the intravenous injection of F9 cells is the result of both their adhesive abilities and their growth response to local microenvironment.