bluuebunny/crossref_metadata_2025_split huggingface dataset:
Aberrant RB gene expression in routinely processed, archival tumor tissues determined by three different anti‐RB antibodies
Authors: Geradts Joseph , Hu Shi‐Xue , Lincoln Clinton E. , Benedict William F. , Xu Hong‐Ji 
Published: February 2007

AbstractThe retinoblastoma (RB) susceptibility gene encodes a nuclear phosphoprotein which is likely involved in cell cycle control and cell differentiation. The RB protein is mutated or absent in a variety of human malignancies. Its role as a molecular marker for clinical tumor behavior is under extensive investigation. However, studies on the status of the RB protein in primary or metastatic tumors and their precursor lesions have been slowed by the lack of availability of a sensitive, reliable assay which allows examination of RB expression in selected cell populations within archival tissues. Thus far, meaningful immunohistochemical analysis of RB protein in formalin‐fixed, paraffin‐embedded specimens has been achieved only with the polyclonal antibody RB‐WL‐1. We now describe a method which produces excellent staining results in formalin‐fixed, routinely processed tissues, using commercially available monoclonal antibodies (MAbs) in conjunction with an antigen‐retrieval step. The resulting stains were superior to those on frozen sections and comparable to those obtained with RB‐WL‐1. Twelve of 51 random invasive bladder cancers (24%) had abnormal expression of the RB gene, as determined by immunohistochemistry. Smaller cohorts of breast, prostate and lung carcinomas had incidences of aberrant RB gene expression ranging from 9% to 24%. Since the staining method was widely applicable to essentially all formalin‐fixed, archival tissues, it may expedite studies on the biological and clinical significance of altered RB expression in human neoplasia.
Risk factors for esophageal cancer in Shanghai, China. I. Role of cigarette smoking and alcohol drinking
Authors: Gao Yu‐Tang , McLaughlin Joseph K. , Blot William J. , Ji Bu‐Tian , Benichou Jacques , Dai Qi , Fraumeni Joseph F. 
Published: February 2007

AbstractA population‐based case‐control study of esophageal cancer was conducted in urban Shanghai involving interviews with 902 cases and 1,552 controls. Risk of esophageal cancer was increased among tobacco smokers and alcohol drinkers. Odds ratios (OR) for smoking were 2.1 and 1.6 for men and women, respectively, and increased with number of cigarettes smoked per day, duration of smoking, number of pack‐years and decreasing age at start of smoking. For men who were current alcohol drinkers OR was 1.4, with the excess risk primarily among heavy drinkers. Few women drank alcoholic beverages. The combined effect of heavy smoking and drinking among men was pronounced: OR was 12.0 for those who smoked more than 1 pack per day and drank more than 750 g of ethanol per week. The relation with smoking appeared stronger for cancers of the middle and lower thirds of the esophagus than for the upper third, while patterns of risk for squamous cell carcinoma and adenocarcinoma were similar. Heavy drinking affected all 3 subsites, with increased risks mainly limited to squamous cell carcinoma. Cigarette smoking and alcohol drinking combined accounted for almost 50% of all esophageal cancers among men in Shanghai; among women, 14% of cases were attributed to smoking. Our study confirms that smoking and drinking are important risk factors for esophageal cancer in China, thereby paralleling findings from developed countries.
Biased utilization of immunoglobulin variable region heavy‐ and light‐chain genes by the malignant CD5‐ B lymphocytes from patients with Burkitt's lymphoma
Authors: Moazzeni Mohammad , Mosayyebi Ghasem , Stevenson Freda K. , Abbot Sandra , Mageed Rizgar A. , Shokri Fazel 
Published: February 2007

AbstractTwenty‐six established Burkitt's lymphoma (BL) cell lines from endemic or sporadic groups of patients were examined for the expression of cross‐reactive idiotypes (CRI) associated with VHI, VHIII, VHIV, VHVI, VKIIIa and VKIIIb heavy‐and light‐chain gene products, using a panel of anti‐CRI and anti‐subgroup monoclonal antibodies (MAbs). Membrane, cytoplasmic and secreted immunoglobulins (Ig) were analysed by immunofluorescence, immunoperoxidase and ELISA respectively. While 35% of the lines expressed either of the VHIV‐associated CRI, recognised by the MAbs 9G4 or LCI, none expressed the other VH‐associated CRI included in our study. Of the kappa light chain expressing BL lines 54% and 46% belonged to the VKIII subgroup and VKIIIb sub‐subgroups respectively. None, however, was found to express the VKIIIa or VKIIIb‐associated CRI, recognised by the 6B6.6 and 17‐109 MAbs. A significant association has been observed between the expression of the VHIV‐associated CRI and the VKIII subgroup within the BL lines derived from the sporadic group of patients as compared with their endemic counterparts. Our results suggest that the expressed repertoire of Ig variable region genes within the malignant B lymphocytes of BL is not random and that a highly selective mechanism(s) may operate on this subset of B lymphocytes, as evidenced by the expression of the VH and VK gene products.
Increased UV‐induced SCEs but normal repair of DNA damage in p53‐deficient mouse cells
Authors: Ishizaki Kanji , Ejima Yosuke , Matsunaga Tsukasa , Hara Ryujiro , Sakamoto Ayako , Ikenaga Mituo , Ikawa Yoji , Aizawa Shin‐Ichi 
Published: February 2007

AbstractUV‐induced sister chromatid exchanges (SCEs) in p53‐deficient mouse cells were studied to obtain more evidence regarding the involvement of p53 protein in the DNA repair pathway as a checkpoint protein. After 5 J/m2 UV irradiation, mutant‐type homozygous cells for p53‐deficiency showed the same number of SCEs as the heterozygous and wild‐type homozygous cells. In the heterozygous and wild‐type homozygous cells, no further increase of SCEs was observed after 10 J/m2 UV irradiation. In contrast, in mutant‐type homozygous cells about twice as many SCEs were induced by 10 J/m2 UV as by 5 J/m2 UV. In mutant‐type homozygous cells, fractions of S‐phase cells decreased just after 10 J/m2 UV irradiation, but recovered to higher than control levels within a short time, while in heterozygous and wild‐type homozygous cells, the decrease in S‐phase cells was prolonged by more than 6 hr and no increase above control levels was observed. Although no difference in UV sensitivity and repair of UV‐induced DNA damage was found among the 3 genotypes, which were determined by the relative colony‐forming ability after UV irradiation and removal of thymine dimers and (6‐4) photoproducts from cellular DNA, our data strongly suggest an impaired checkpoint function in p53‐deficient cells when DNA is damaged.
Development of vincristine resistance and increased sensitivity to cyclosporin A and verapamil in the human U‐937 lymphoma cell line without overexpression of the 170‐KDa P‐glycoprotein
Authors: Botling Johan , Liminga Gunnar , Larsson Rolf , Nygren Peter , Nilsson Kenneth 
Published: February 2007

AbstractA vincristine (Vcr)‐resistant subline of the human histiocytic lymphoma cell line U‐937 (U‐937‐vcr) has been established and characterized with respect to its phenotypic features, including growth rate, surface marker expression and ability to respond to differentiation‐inducing agents. The sensitivity of U‐937‐vcr cells to the direct cytotoxicity of cyclosporin A (CsA) and verapamil (Ver), and the capacity of these drugs to modify Vcr resistance, were also examined. The U‐937‐vcr cells exhibited a more than 200‐fold resistance to Vcr, and cross‐resistance to vinorelbin and taxol. Also, there was a slight cross‐resistance to colchin, doxorubicin and VP16. However, the response of U‐937‐vcr to CsA or Ver alone was substantially altered, with a marked decrease in their respective IC50s. The U‐937‐vcr cells did not show increased levels of pgp 170. We conclude that the development of Vcr resistance was not associated with a change in the major phenotyic properties of the U‐937 cell line, and that resistance modifier hypersensitivity was not associated with increase in pgp 170 expression.
Scattered micrometastases visualized at the single‐cell level: Detection and re‐isolation of lacZ‐labeled metastasized lymphoma cells
Authors: Krüger Achim , Schirrmacher Volker , Hoegen Paul Von 
Published: February 2007

AbstractTo study metastasis at the single‐cell level we transduced highly metastatic ESb lymphoma cells with a retroviral expression vector containing the lacZ (bacterial β‐galactosidase) gene. This allowed single ESb‐lacZ tumor cells to be detected in infiltrated target organs by means of X‐Gal staining. Despite expression of the lacZ gene, the tumor cells were still tumorigenic, highly metastatic, unchanged in phenotype and therefore comparable to parental ESb cells. After spontaneous metastasis, whole‐organ staining revealed metastatic foci at the surface of the liver. In histological liver sections, metastatic clusters and single dispersed tumor cells could be detected. In contrast to whole‐organ staining, histological examination revealed scattered distribution of tumor cells throughout the organ, which was not evident with parental ESb cells. In addition, clusters with diffuse or dense (focal) appearance were found, in correlation with the whole‐organ staining. Expression of the foreign lacZ gene allowed the metastatic spread of tumor cells to liver and spleen to be quantified approximately by FACS analysis. Furthermore, it was shown that the newly expressed β‐gal was expressed not only intercellularly but also at the cell surface. There it could be recognized by MAbs and cytotoxic T‐cells (CTL). β‐gal did not affect CTL recognition of the ESb tumor‐associated antigen. In conclusion, lacZ could be used as a genetic marker for a highly metastatic lymphoma, to define scattered metastatic spread in the liver at the single‐cell level and to quantify the tumor load by FACS analysis.
Tumorigenicity of BALB3T3 A31 cells transfected with hamster‐complement‐C1s cDNA
Authors: Sakai Norie , Kusunoki Mayumi , Nishida Munehiro , Toyoguchi Toru , Fukutomi Hisayuki , Sakiyama Hisako 
Published: February 2007

AbstractHamster‐complement‐CIs cDNA was inserted into an expression plasmid BCMGSNeo (BCMGSNeoHACS). BALB/c mouse fibroblast A31 cells, which do not produce CIs, were transfected with BCMGSNeoHACS and the transfectants were selected with G418. Normal CIs production by the transfectants was confirmed by Northern and immunoblot analysis and by an esterase assay. To examine the tumorigenicity of the transfectants, 1 × 106 cells were injected s.c. into 6‐week‐old BALB/c nu/nu mice. Three CIs cDNA transfectants (A3CS9, A3CS12, A3CS13) formed tumors whereas both A31 and A31 transfected with the vector alone (A3BCMI and A3BCM3) did not. The tumors derived from the transfectants showed invasive growth, and many capillaries were observed in the tumors. A tumor derived from A3CS13 was examined immunohistochemically and found to be reactive with an anti‐CIs monoclonal antibody. Tumor cells were cultured in vitro again and CIs secreted into the culture medium was examined by immunoblot analysis. CIs synthesized by the tumor cells derived from A3CS13 maintained its biological functions. Tumor cells derived from A3CS9 and A3CS12 cells, however, produced CIs having abnormal disulfide bonds.
Age‐period‐cohort modelling of large‐bowel‐cancer incidence by anatomic sub‐site and sex in Denmark
Authors: Dubrow Robert , Johansen Christoffer , Skov Torsten , Holford Theodore R. 
Published: February 2007

AbstractIn a previous investigation, statistical modelling was used to examine the relationship between large‐bowel‐cancer incidence and age, time period and birth cohort by anatomic sub‐site and sex, using data from the Connecticut Tumor Registry (CTR) for the period 1950 to 1984. This analysis revealed differences in age‐period‐cohort patterns that suggested etiologic distinctions among sub‐site groupings and between the sexes. To test the generalizability of the Connecticut findings, we have conducted a similar age‐period‐cohort analysis using data from the Danish Cancer Registry (DCR) for the period 1953 to 1987. Cancers of the large bowel were classified into 6 anatomic sub‐sites: cecum, ascending colon, transverse colon, descending colon, sigmoid colon and rectum. Data were fitted to log‐linear age‐period‐cohort models. If we interpret differences in age‐period‐cohort patterns as reflecting etiologic distinctions, the Denmark analysis, in conjunction with the Connecticut findings, was consistent with there being etiologic distinctions between cancers of the colon vs. the rectum in both males and females, between cancers of the cecum and the ascending colon vs. the remainder of the colon in females and between males vs. females for cancers of the sigmoid colon and rectum. Cancers of the cecum and the ascending colon were the most similar between males and females. Due to the ambiguities of age‐period‐cohort modelling, these should be considered only tentative conclusions that can be tested by analytical epidemiologic studies.
A member of the melanoma antigen‐encoding gene (MAGE) family is expressed in human skin during wound healing
Authors: Becker Jürgen C. , Gillitzer Reinhard , Bröcker Eva‐Bettina 
Published: February 2007

AbstractMAGE‐1 has been identified as a human gene, which directs the expression of an antigen being recognized on melanoma cells by autologous cytolytic T cells. MAGE‐1 is expressed in melanomas and some other tumors. It has been proposed that this gene may be linked to the transformation event and therefore might serve as an approach to precisely targeted immunotherapy. Prior to such an approach, extensive testing of normal human tissue is necessary to establish the tumor‐specific nature of MAGE‐1 expression. Similar to events that occur during neoplastic tumor growth and spreading, wound healing involves a complex interrelationship between various cell types which migrate, proliferate and differentiate. Therefore, we investigated the expression of MAGE‐1 in skin during wound repair. We could detect MAGE‐1 mRNA by RT‐PCR followed by specific hybridization as well as by Northern blotting in human skin from the 1st to the 7th day after wounding. Comparison of the expression of MAGE mRNA with that of β‐actin mRNA showed that it is expressed in amounts equal to about and at least one‐fifth that of β‐actin. Our data strongly suggest that MAGE mRNA expression is not necessarily linked to neoplastic transformation, but rather represents the function of a cellular gene which is activated during inflammation or early tissue repair.
A search for unknown blood‐borne oncogenic viruses
Authors: Memon Anjum , Doll Sir Richard 
Published: February 2007

AbstractIn previous decades, infants who received blood transfusions shortly after birth or in utero might have been infected at a particularly vulnerable age by some blood‐borne oncogen it virus. A cohort of such infants has therefore been followed into adult life to see if they suffered any excess of neoplastic disease or of non‐neoplastic mortality.A total of 12,690 infants were identified who were transfused between 1 January 1942 and 31 December 1970, in most cases for the prevention or treatment of haemolytic disease of the newborn. All but 361 (2.8%) were found to have been registered with a National Health Service (NHS) practitioner and were followed in the NHS central records until they died, emigrated, were removed from NHS lists or until 1 January 1992, whichever occurred first. Mortality and cancer incidence were compared with that expected from national rates. No marked disparity was observed and there was no excess of childhood leukaemia. The incidence of non‐Hodgkin's lymphoma at 15 to 49 years of age was about twice that expected, but the excess was not statistically significant.
Endogenous tumor necrosis factor functions as a resistant factor against adriamycin
Authors: Maeda Masahiro , Watanabe Naoki , Okamoto Tetsuro , Yoshiro Niitsu Naoki Tsuji 
Published: February 2007

AbstractOne of the mechanisms of cytotoxicity by tumor necrosis factor (TNF) and heat is the induction of reactive oxygen molecules. Cells producing endogenous tumor necrosis factor (enTNF) show resistance to the cytotoxicity of exogenous TNF and heat by inducing manganous superoxide dismutase (MnSOD) to scavenge the reactive oxygen molecules. Intracellular hydroxyl radical production is also involved in adriamycin‐induced cytotoxicity. In this study, we therefore examined the possibility that enTNF may act as a protective protein against adriamycin‐induced cytotoxicity in a manner similar to that in which it protects against exogenous TNF and heat. Adriamycin‐sensitive L‐M (mouse tumorigenic fibroblast) cells, originally expressing no enTNF, were transfected with an expression vector which directs the synthesis of non‐secretory‐type human TNF (enTNF). The stable transformants became resistant to adriamycin with increased levels of MnSOD. Conversely, when HeLa (human uterine cervical cancer) cells, which originally produce an appreciable amount of enTNF, were transfected with an anti‐sense TNF mRNA expression vector to inhibit enTNF synthesis, their intracellular MnSOD activity was suppressed and adriamycin sensitivity was enhanced. However, no alterations in expression of multidrug‐resistant gene products—P‐170 glycoprotein, glutathione S‐transferase π (GST‐π) and the intracellular concentrations of glutathione (GSH)‐were observed in these transfectants as compared to their parent cells. These results indicate that enTNF exerts its intracellular protective effect against adriamycin‐induced cytotoxicity by the same mechanism as that against exogenous TNF and heat, namely scavenging reactive oxygen with induced MnSOD.
Human recombinant interferons‐beta and ‐gamma decrease gelatinase production and invasion by human KG‐2 renal‐carcinoma cells
Authors: Gohji Kazuo , Fidler Isaiah J. , Tsan Rachel , Radinsky Robert , Von Eschenbach Andrew C. , Tsuruo Takashi , Nakajima Motowo 
Published: February 2007

AbstractWe investigated the effects of human recombinant interferons (r‐IFNs) on gelatinase production and invasion by human renal‐cell carcinoma (HRCC). Incubation of KG‐2 HRCC with human r‐IFN‐β or ‐γ (but not ‐α) suppressed transcription of the 72‐kDa gelatinase gene and, hence, production of gelatinase activity. These inhibitory effects of interferons (IFNs) were independent of their antiproliferative effects. Treatment of KG‐2 cells with r‐IFN‐β or ‐γ significantly inhibited cell invasion through reconstituted basement membrane toward chemoattractants produced by kidney fibroblasts. The inhibitory activity of r‐IFNs was specific to the KG‐2 cells since gelatinase activity by various fibroblasts was unaffected. These findings suggest that r‐IFN‐β or IFN‐γ may be used to inhibit the invasive potential of HRCC.
Hibernomas are characterized by rearrangements of chromosome bands 11q13‐21
Authors: Mertens Fredrik , Rydholm Anders , Brosjö Otte , Willéd Helena , Mitelman Felix , Mandahl Nils 
Published: February 2007

AbstractCytogenetic analysis revealed structural rearrangements of 11q13‐21 in 9 lipogenic tumors—4 hibernomas, 4 typical lipomas and I mixed myxoid and well‐differentiated liposarcoma. Two hibernomas and all lipomas simultaneously showed aberrations attributable to previously recognized cytogenetic subgroups among benign adipose tissue tumors, i.e., supernumerary ring chromosomes or rearrangements of 6p, 12q13‐15, or 13q. The sole anomaly in the liposarcoma was a 4‐way translocation t(9;11;22;12)(q21;q13;q11;q13), an aberration that has not previously been detected in either myxoid or well‐differentiated liposarcomas. Together with our 4 cases, a total of 7 cytogenetically aberrant hibernomas have been reported. Five tumors have shown rearrangements of 11q13 and 2 of 11q21, indicating that this segment of chromosome 11 harbors one or more genes of importance in hibernoma development. Rearrangements of 11q13‐21 also appear to be frequent in typical lipomas; a total of 8 typical lipomas with 11q13‐21 changes have been described, including those in our series. In all but I, however, breakpoints were also found in 6p, 12q13‐15, or 13q.
Widowhood and divorce related to cancer risk in middle‐aged women. A nested case‐control study among norwegian women born between 1935 and 1954
Authors: Kvikstad Anne , Vatten Lars J. , Tretli Steinar , Kvinnsland Stener 
Published: February 2007

AbstractWe have examined whether the risk of cancer among divorced or widowed Norwegian women born between 1935 and 1954 was any different from that of married women. Among a total of approximately 600,000 women, we applied a nested case‐control design. Thus, the study was population‐based and included 17,235 incident cases of cancer with 34,460 agematched controls. For widowed women, there was no overall relation with cancer. For divorced women, 2 strikingly different associations were apparent. A reduced risk was seen for cancers of a number of sites, including thyroid, endometrium, colorectum, and breast, as well as malignant melanoma and hematologic malignancies, with statistically significant estimates of relative risk ranging from 0.64 to 0.84. In contrast, divorced women had a strongly elevated risk of lung and cervical cancer. Moreover, there was a gradual reduction in the relative risk of cancer at some sites with increasing age at divorce, and with duration of marriage prior to divorce. In this study of middleaged women, the risk of cancer among widows was no different from that of married women. Divorced women had an increased risk of cancers which are related to cigarette smoking but, simultaneously, a reduced risk of cancer at a number of other sites. Since the negative associations for some cancers were strongly related to increasing age at divorce and to duration of marriage, the results may indicate that the reduction in risk is related to factors which characterize the marital period preceding divorce.
Association studies of a polymorphism in the Wilms' tumor 1 locus in norwegian patients with testicular cancer
Authors: Heimdal Ketil R. , Lothe Ragnhild A. , Fosså Sophie Dorothea , Børresen Anne‐Lise 
Published: February 2007

AbstractOne strategy for identifying genes involved in genetic predisposition to testicular germ‐cell tumors (TC) is to perform association studies with polymorphic loci at or closely linked to candidate genes. Genes involved in normal fetal genital development, such as the Wilms' tumor 1 gene (WT1) located at 11p13, are among such candidates. The present study compares a TC (n = 442) and a control (n = 384) population for the allele frequencies of 2 polymorphic loci located at chromosome band 11p13. One of the polymorphisms (WT) was located within and the other (D11S325) in close proximity to theWT1gene. No differences in allele frequencies between cancer patients and controls were found. However, the frequency of the A1 allele of the WT polymorphism was significantly increased in one of the cancer subgroups most likely to carry susceptibility genes (patients with bilateral cancer) compared to controls. Furthermore, the frequency of the A1 allele was increased in patients with metastatic disease. Such differences in allele frequencies were not observed for the D11S325 locus. The findings might indicate an involvement of theWT1gene both in susceptibility to TC and in progression of the disease.