bluuebunny/crossref_metadata_2025_split huggingface dataset:
trk and ret proto‐oncogene expression in human neuroblastoma specimens: High frequency of trk expression in non‐advanced stages
Authors: Borrello M. G. , Bongarzone I. , Plerotti M. A. , Luksch R. , Gasparini M. , Collini P. , Pllotti S. , Rlzzetti M. G. , Mondellini P. , De Bernardi B. , Di Martino D. , Garaventa A. , Brisigotti M. , Tonini G. P. 
Published: February 2007

AbstractForty‐three fresh tumor specimens of human neuroblastoma belonging to different clinical stages were analyzed for the expression of 2 proto‐oncogenes: trk, which encodes a tyrosine‐kinase receptor for nerve growth factor (NGF) and ret, another receptor‐type tyrosine kinase whose ligand is unknown. The mRNA expression of the trk gene was detected in 67.4% of cases, with increased frequency in I, II and IVs Evans' stages and in patients with favorable prognosis according to the Shimada classification. Moreover, trk expression inversely correlated with Nmyc‐gene amplification, ret mRNA was found in 36.8% of cases and equally distributed in the different stages. In addition, ngfR (low‐affinity NGF receptor)‐gene expression was present in 9 out of 25 cases. The simultaneous presence of mRNA related to both forms of the NGF receptor, while not proving the presence of a functional receptor, indicates the existence of a sub‐set of neuroblastoma cells potentially responsive to NGF.
Sulfated proteoglycans in the extracellular matrix of human breast tissues with infiltrating carcinoma
Authors: Losa Gabriele A. , Alini Mauro 
Published: February 2007

AbstractThe size, content and distribution of sulfated proteoglycans, constituents of the extracellular matrix, were investigated in non‐neoplastic human breast tissues and in tissues with infiltrating carcinoma. Sulfated proteoglycans were identified as cupro‐linic‐blue‐positive elements on electron microscopy preparations by the method of the critical electrolyte concentration. Morphometric data indicated that the numerical density of PG per surface area (Na) in normal tissues was about 2 to 7 times higher respectively in dense or loose connective zone then that found in the corresponding zones of malignant tissues. By referring to the unit volume of tissue, the overall PG content (Nv) was found to be increased about 5 fold in nonneoplastic tissues. However, in tissues with carcinoma the average length of sulfated proteoglycans was about twice as long in dense and loose connective layers than in the corresponding connective zones of non‐neoplastic breast tissues. Our findings provide evidence of profound structural alterations of non‐collagenous constituents in the extracellular matrix of human mammary tissues concerned with infiltrating carcinoma.
Effect of organized screening on the risk of cervical cancer. Evaluation of screening activity in iceland, 1964–1991
Authors: Sigurdsson Kristján 
Published: February 2007

AbstractThe Icelandic Cancer Society launched a screening programme for cervical cancer in June 1964. The aim was to lower the incidence and mortality rates by screening the age group 25—69 at 2‐ to 3‐year intervals. This report analyses the trends in invasive and pre‐invasive disease and the distribution of stage and histology, and also evaluates the attendance, the target age group and the screening interval. Before screening, the inci dence and mortality rates were on the increase but both have since fallen significantly. Screening greatly affected the rate of microinvasive and stage ≧11 squamous‐cell carcinomas but not the rate of adeno‐ and adenosquamous carcinoma. The mean age at detection of invasive cancer has decreased significantly and cancer has become practically non‐existent among correctly screened subjects over the age of 69. Among younger women the rates of moderate and severe pre‐invasive lesions at first visit increased significantly after 1980. The rate of these lesions was fairly consistently high only I year after the first normal visit. It is concluded that organized screening, coordinated with spontaneous activity, is effective in reducing the risk of cervical cancer. Regular high attendance and strict follow‐up of abnormal cases is a prerequisite for good screening results. Screening should preferably start at about the age of 20 and extend to 60–69 years of age, depending on the number of negative smears by that age. Screening can safely start with a screening interval of 2 to 3 years, but this interval can probably be extended to 4 or 5 years at older ages.
Expression of the target antigen for cytotoxic T lymphocytes on adult T‐cell‐leukemia cells
Authors: Kannagi Mari , Matsushita Shuzo , Harada Shinji 
Published: February 2007

AbstractAdult T‐cell‐leukemia (ATL) cells were examined for suscep tibility to human T‐cell‐leukemia virus type I (HTLV‐I) tax‐specific cytotoxic T lymphocytes (CTL) derived from a patient with HTLV‐l‐associated myelopathy/tropical spastic parapare sis (HAM/TSP). These CTL efficiently killed HLA‐matched leukemia cells of an ATL patient after overnight incubation. However, ATL cells immediately after isolation from the periph eral blood were only marginally susceptible to the CTL. This is not due to inappropriate expression of major‐histocompatibility‐complex(MHC)‐class‐l antigen on the leukemia cells. Addition of synthetic peptide, corresponding to the CTL epitope, to the assay enabled the CTL to kill the fresh ATL cells. Scarcity of HTLV‐I antigens in the fresh ATL cells and induction of these antigens by in vitro incubation were demonstrated both on the cell surface and in the cytoplasm. Lectin stimulation augmented synthesis of HTLV‐I antigens, but was not essential for the induction. The presence in the culture of human plasma contain ing a high titer of antibodies to HTLV‐I did not affect the induction of HTLV‐I expression in the ATL cells. Furthermore, significantly lower levels of HTLV‐I tax mRNA were present in the fresh ATL cells than in the cultured ATL cells, whereas the levels of HTLV‐I proviral tax gene did not differ among these cells. This suppression of HTLV‐I transcription in fresh ATL cells accounts for resistance to the CTL, and could be a reason for the persistence of HTLV‐I infection in vivo.
A fucose residue can mask the muc‐1 epitopes in normal and cancerous gastric mucosae
Authors: Bara J. , Imberty A. , Pérez S. , Imai K. , Yachi A. , Oriol R. 
Published: February 2007

AbstractMUSE II, DF3 and SM3 MAbs react with a synthetic peptide of 20 amino‐acids: VTSAPDTRPAPGSTAPPAHG. This se quence is a tandem repeat domain of the mucin‐type glycopro tein coded by the muc‐1 gene. MUSE II and DF3 MAbs immuno react strongly with mucus cells of the normal surface gastric epithelium of Le(a+b‐) non‐secretors, but in spite of the peptidic nature of the recognized epitope, the same tissue of Le(a‐b+) secretors reacts only after treatment with α‐fucosi dase. These reactions are inhibited by the PNA lectin, which recognizes the T disaccharide antigen (βGall‐3αGalNAc), sug gesting that the peptide epitope may be close to the T‐saccha ride structure. The SM3 MAb reacted on the surface gastric epithelium of all individuals after a more drastic deglycosylation using 20 mM periodate. Computer modeling of the MUC‐I immunoreactive glycopeptide containing the H type‐3 trisaccha ride αFucl‐2βGall‐3αGalNAc‐ bound to the threonine of the PDTRP‐pentapeptide shows that the peptide epitope might be masked when the fucose is positioned over the arginine. Thus, a single fucose linked to the T structure could mask the MUC‐I epitopes. In gastric adenocarcinomas, MUSEII and SM3 epi topes are expressed in 75% (25/33) and 9% (3/33) respectively, while, after partial deglycosylation by periodate treatment, they are positive in 100% (33/33) and 70% (23/33) of cases, respectively.
In vivo cytokeratin‐expression pattern of stratified squamous epithelium from human papillomavirus‐type‐16–immortalized ectocervical and foreskin keratinocytes
Authors: Sun Qi , Tsutsumi Kouichiro , Yokoyama Masatoshi , Pater Mary M. , Pater Alan 
Published: February 2007

AbstractThe association between human papillomavirus (HPV) type 16 and cervical squamous‐cell carcinoma has been well documented, and HPV 16 DNA has been shown to immortalize human genital keratinocytes in vitro. Using a panel of cytokera‐tin(CK)‐specific antibodies, we examined the CK expression pattern, an important characteristic of epithelia, of the stratified squamous epithelium reconstructed in vivo from monolayer cultures of 2 human ectocervical and 3 human foreskin keratino‐cyte cell lines immortalized by HPV 16 DNA. Whereas the abnormal epithelium formed from these grafts presented certain aspects of mature terminal differentiation, such as morphology and expression of CKIO/II, the expression patterns for CK19, and especially CK13, were more obviously abnormal. CK18 expression was not detectable in any of the epithelia formed from the 5 cell lines. In contrast, for an HPV‐16–immortalized endocervical cell line and the CaSki cervicalcarcinoma cell line there was expression of CK18. Our results indicate that HPV‐16–induced immortalization of keratinocytes is associated with disruption of the normal CK expression pattern in stratified squamous epithelium and that expression of particular CKs can be differentially disrupted.
Characterization and chemosensitivity of a human epithelioid sarcoma cell line (SARCCR 2)
Authors: Roché H. , Julia A. M. , Jozan S. , Muller C. , Dastugue N. , Arquier M. A. , Marques B. , Laurent G. , Canal P. 
Published: February 2007

AbstractA new cell line was derived from the epithelioid sarcoma of a Caucasian woman who had previously received chemotherapy. The cells grew as an adherent monolayer, with a doubling time of 28 hr and had mainly epithelial morphology, but with areas of mesenchymal‐like cytoplasmic extensions. The cells were tumorigenic in nude mice, with a short growth time, and a doubling time of 8 days. The cell line showed over‐expression of P‐glycoprotein by Western blot analysis, and its sensitivity to doxorubicin and vincristine was low. This sensitivity could be enhanced by reversants of multidrug resistance (MDR), such as cyclosporin or verapamil. This cell line constitutes an excellent model for studying compounds able to reverse MDR.
Eradication of spontaneous and experimental adenocarcinoma metastases with chronic indomethacin and intermittent IL‐2 therapy
Authors: Lala Peeyush K. , Parhar Ranjit S. 
Published: February 2007

AbstractWe had earlier shown that tumor‐bearing results in an inactivation of IL‐2–dependent effector cells by host macrophagederived PGE2, and that chronic indomethacin therapy (CIT) aimed at blocking prostaglandin synthesis, combined with multiple rounds of IL‐2, can cure experimental metastases of a variety of tumors in mice. We have now tested the efficacy of this therapy on spontaneous as well as experimental metastasis of C3–L5 mammary adenocarcinoma in C3H/HeJ mice. Mice transplanted s.c. with C3–L5 cells (and showing visible spontaneous lung metastases between days 7 and 10) were given CIT starting on day 15, plus 2 5–day rounds of IL‐2 or IL‐2 alone. Mice injected i.v. with 104 C3–L5 cells (and showing lung micrometas‐tases on day 5) were placed on CIT on day 5 and given 3 5–day rounds of IL‐2 or treated with IL‐2 alone. Control mice received vehicles alone. Results revealed that combined CIT + IL‐2 therapy in the spontaneous metastasis model caused a regression of primary tumors, a marked reduction in lung metastases scored on days 25–35 and a marked prolongation of host survival (79% cured). Survivors rechallenged with 104 tumor cells i.v. on day 210 resisted tumor growth. In the experimental metastasis model, this therapy also markedly reduced lung metastases and prolonged animal survival (50% cured). In both models, the combination therapy led to the presence of highly active tumoricidal (for C3–L5 and YAC‐I lymphoma targets) lymphocytes with AGM‐I+, Lyt‐2‐ and Thy‐l± phenotype and macrophages in the spleen and the lungs, and ADCC‐promoting activity in the serum. CIT + IL‐2 therapy can thus effectively eradicate spontaneous and experimental mammary adenocarcinoma metastasis in mice. It activates natural effector cells in situ, generates ADCC‐promoting activity in the serum and results in resistance to umor take in this moderately immunogenic tumor model.
Consistent chromosomal aberration in cell lines transformed with mareks disease herpesvirus: Evidence of genomic dna amplification
Authors: Moore F. R. , Moore F. R. , Schat K. A. , Hutchison N. , Bloom S. E. 
Published: February 2007

AbstractA specific chromosomal aberration was observed in 14 of 15 avian lymphoblastoid cell lines transformed with Marek's disease herpesvirus. This aberration, designated dup(lp)(p22–p23), appeared as an extra G‐positive band and interband on the short arm of one chromosome I homolog. Using fluorescent in situ hybridization, we identified amplified genomic DNA sequences in this region. This amplification involves sequences linked to an endogenous retrovirus locus and genes in the histone multigene family. This aberration was not observed in cells transformed by reticuloendotheliosis virus or by avian leukosis virus, nor has it been observed in untransformed chicken cells. The induction of the I p+ chromosomal aberration may be an essential event in the transformation of lymphocytes by Marek's disease virus.
Geographic association between urinary excretion of N‐nitroso compounds and oesophageal cancer mortality in china
Authors: Wu Y. , Chen J. , Ohshima H. , Pignatelli B. , Boreham J. , Li J. , Campbell T. C. , Peto R. , Bartsch H. 
Published: February 2007

AbstractOvernight urine samples were collected from approximately 60 male adults in each of 69 counties of China in 1989. Two specimens were collected from each subject—one after a loading dose of proline and ascorbic acid and another after a loading dose of proline only. Levels of N‐nitrosamino acids and nitrate were measured in urine samples and correlated with cumulative mortality rates for subjects aged between 0 and 64 years in the 1970s. Oesophageal cancer mortality rates were positively and significantly associated with (i) urinary levels of excreted N‐nitrosoproline (NPRO) (after proline and ascorbic acid loading or proline loading only), (ii) N‐nitrososarcosine levels, and (iii) nitrosation potential (the decrease in the amount of urinary NPRO after adding ascorbic acid to the proline load). There were also positive correlations between the urinary level of NPRO or other N‐nitrosamino acids and that of nitrate. The urinary excretion of nitrate was associated with consumption of various nitrate‐rich vegetables. The results suggest that N‐nitroso compounds (NOC) or other nitrite‐derived carcinogens are implicated in the aetiology of oesophageal cancer in China.
Intermediate filaments as differentiation markers of exocrine pancreas. II. Expression of cytokeratins of complex and stratified epithelia in normal pancreas and in pancreas cancer
Authors: Real Francisco X. , Vilá Maya R. , Skoudy Anouchka , Ramaekers Frans C. S. , Corominas Josep M. 
Published: February 2007

AbstractCytokeratin (CK) expression in tumors generally reflects the CK pattern of the corresponding normal epithelium. Pancreas cancers express CK of simple epithelia 7,8, 18 and 19, as normal ductal cells. To analyze whether CK of complex or stratified epithelia are abnormally expressed in pancreas cancers, we have used polypeptide‐specific mouse monoclonal antibodies (MAbs) detecting CK 5, CK 10, CK 13, CK 14 and CK 17, and an antibody detecting CK 13, CK 15 and CK 16. The streptavidin‐peroxidase technique was applied on sections of fresh‐frozen specimens of normal pancreas and of pancreas cancer. None of these polypeptides were expressed by normal acinar and centro‐acinar cells. CK 5, CK 14 and CK 17 were expressed by less than 5% of cells in normal ducts, whereas CK 10, CK 13, CK 15 and CK 16 were not expressed at all. In tumors, CK 14, CK 15/16 and CK 17 were detected in the majority of cases studied; CK 5, CK 10 and CK 13 were present in a sub‐population of pancreas cancers. CK of complex/stratified epithelia were detected in areas of glandular differentiation, but expression was more intense in areas of squamous differentiation. In pancreatitis adjacent to cancer, CK of complex/stratified epithelia were weakly detected or undetectable. These results suggest that up‐regulation of these CK takes place in pancreas cancer. The CK phenotype may be of help in the differential diagnosis of this tumor.
Alkylation and oxidative‐DNA damage repair activity in blood leukocytes of smokers and non‐smokers
Authors: Hall Janet , Brésil Henriette , Wild Christopher P. , Loktionova Natalya A. , Kazanova Olga I. , Komyakov Igor P. , Lemekhov Vladimir G. , Likhachev Alexei J. , Montesano Ruggero 
Published: February 2007

AbstractThe levels of 3 DNA repair enzymes involved in alkylation and oxidative DNA damage repair in human peripheral blood leukocytes were measured in 20 smokers and 17 non‐smokers. No differences in O6‐alkylguanine‐DNA‐alkyltransferase (AGT) activity were found between the 2 groups and the AGT distribution within the population appeared to be unimodal. In contrast, the mean activities of both the methylpurine (MeP)‐ and the 2‐6‐diamino‐4‐hydroxy‐5N formamidopyrimidine (FaPy)‐DNA glycosylases were higher in the smokers, although only the difference between the MeP‐DNA glycosylase means was statistically significant. The standard deviations of these 2 enzymes were also higher in the smokers. The MeP‐DNA glycosylase activity showed a bimodal distribution when all subjects were considered. This may in part be due to the smoking habit; 83% of the subjects with enzyme activities higher than 500fmoles/mg protein were current smokers, whilst 85% of the non‐smokers had lower enzyme activities. However, if the smokers were considered separately, a bimodal distribution of this enzyme activity could still be observed. No strong correlation was observed between enzyme activity and age, although the slopes of the regression lines of enzyme activity on age were all negative. The relationship between enzyme activities was studied by bivariate distribution and a strong correlation was only found between the MeP‐DNA glycosylase and the FaPy‐glycosylase, with the highest values of both enzyme activities being observed in the smokers and the lowest in the non‐smokers. Our results suggest that the activity of certain DNA repair enzymes can be modulated by environmental exposure.
Reverse smoking as a risk factor for palatal cancer: A cross‐sectional study in rural andhra pradesh, india
Authors: Van Der Eb M. M. , Leyten E. M. S. , Gavarasana Satyanarayana , Vandenbroucke J. P. , Meera Kahn P. , Cleton F. J. 
Published: February 2007

AbstractA cross‐sectional study of reverse smoking and its association with pre‐malignant and malignant lesions of the palate was conducted in the north coastal areas of Andhra Pradesh, India. A total of 480 randomly selected persons were interviewed. Information about smoking status, diet and access to mass media was obtained in each case and an examination of the oral cavity was performed. Reverse smoking of chutta was practised by 33% of the total rural population. The prevalence rate of all palatal lesions was 55%. The prevalence rates of the separate lesions: leukoplakia palatii, palatal keratosis and palatal cancer, were 9.8%, 18.1% and 1.9%, respectively. The presence of these (pre‐)malignant lesions was strongly associated with reverse smoking and also associated with conventional chutta smoking. Reverse smoking induced significantly more lesions than conventional chutta smoking, and was a major determinant of subsequent palatal cancer: all 9 newly diagnosed palatal cancers were observed within the group of reverse smokers. There was an inverse relationship between the incidence of palatal lesions and vitamin A intake. The study of access to mass media indicated that the most favourable medium for promoting a prevention campaign would be the cinema.
Establishment and characterization of human ocular melanoma cell lines
Authors: Aubert Christian , Rouge Françoise , Reillaudou Monique , Metge Paul 
Published: February 2007

AbstractFive continuous cell lines have been established from 29 ocular melanomas and maintained for periods ranging from 3 to 9 years in medium identical to that in which 3 concomitantly studied lines of cutaneous melanoma cells were cultured as controls. The long‐term problems to be overcome in establishing uveal cell lines are related to cell‐doubling times which ranged from 72 to 432 hr, and plating efficiency, which ranged from 0.5%–6.5%. Tumors and cell lines were found to contain melanosomes. The morphology of uveal cells during the early subcultures exhibited multiple changes. Two different established cell lines were obtained from one ciliary‐body tumor. Biochemical studies revealed markers of melanogenesis and neuroendocrine compounds. Cytogenetic studies revealed chromosomal abnormalities that differed between uveal and conjunctival melanomas.
Thrombin increases the metastatic potential of tumor cells
Authors: Wojtukiewicz Marek Z. , Tang Dean G. , Ciarelli James J. , Nelson Kevin K. , Walz Daniel A. , Diglio Clement A. , Mammen Eberhard F. , Honn Kenneth V. 
Published: February 2007

AbstractInitial arrest of tumor cells in the microvasculature and their attachment to the endothelium and subendothelial matrix (SEM) are essential prerequisites for metastasis to occur. Factors mediating these interactions are viewed as important determinants of the tumor‐cell metastatic phenotype. In this work we have studied the effects of thrombin, its analogs and its precursors on the adhesive properties and metastatic potential of tumor cells. We show that α‐thrombin, the native form of the key coagulation enzyme, is capable of enhancing tumor‐cell adhesion to both the endothelium and SEM components represented by fibronectin. Subclotting, physiological concentrations of α‐thrombin produced a 2‐ to 5‐fold increase in tumor‐cell adhesion. A bell‐shaped dose‐response curve was observed, with maximal effect at 0.1 U/ml. Maximum effect occurred when cells were exposed to the agonist for 15 min and exposure for up to 4 hr resulted in enhanced tumor‐cell adhesion. Prolonged incubation with thrombin resulted in a decline in the thrombin‐enhanced adhesion which reached unstimulated control levels by 24 hr. Thrombin precursors and active‐site‐inhibited thrombin analogs only had minimal adhesion‐enhancing activity; nitro‐ and exosite‐α‐thrombin, which retain a functional active site, mimicked, although to a lesser degree, the action of α‐thrombin. Tumor‐cell incubation with thrombin resulted in an upregulated cell‐surface expression of the αllbβ3 integrin, a receptor mediating interactions between tumor cells and endothelial cells, and between tumor cells and SEM. Antibodies against αllbβ3 integrin effectively inhibited thrombin‐enhanced tumor‐cell adhesion. Thrombin effects on tumor cells involved the PKC signal transduction pathway as thrombin‐enhanced adhesion was inhibited by pre‐incubation with PKC inhibitors and a transient PKC translocation from cytosol to membrane was observed following thrombin challenge. In vivo, thrombin‐treated tumor cells demonstrated a 2‐fold increase in their lung‐colonizing ability. In contrast to the adhesion results, the metastasis‐enhancing effects of α‐thrombin were mimicked by a thrombin precursor (prothrombin) and thrombin analogs.