bluuebunny/crossref_metadata_2025_split huggingface dataset:
Correlation of L‐myc RFLP with metastasis, prognosis and multiple cancer in lung‐cancer patients
Authors: Kawashima Kazuko , Nomura Sachio , Hirai Hiroyuki , Fukushi Shuetsu , Karube Tsuyoshi , Takeuchi Kumiko , Naruke Tsuguo , Nishimura Susumu 
Published: February 2007

AbstractFor further study of the correlation of L‐myc restriction‐fragment‐length polymorphism (RFLP) and metastasis of lung cancer to lymph nodes or other organs at the time of surgery, L‐myc RFLP was analyzed in 252 Japanese lung‐cancer patients. A close correlation between L‐myc RFLP and metastasis was confirmed in this large number of patients (p = 0.01). The correlation was particularly pronounced in cases of adenocarcinoma and squamous‐cell carcinoma. Poor prognosis (additional metastases after surgery) was observed in lung‐cancer patients with L‐S (identified as long and short bands produced with EcoRI) and S‐S type L‐myc RFLP. In addition, the death rate of lung‐cancer patients with the L‐S and S‐S types was greater than that of those with the L‐L type. Lung‐cancer patients of the L‐S and S‐S types had almost 4 times higher incidence of multiple cancer in the lung, pharynx and other organs than those with the L‐L type. Our results indicate that, in patients with lung cancer, genetic disposition with respect to the L‐myc gene influences the extent of metastasis, the incidence of multiple cancers and prognosis.
Distribution of individual components of basement membrane in human colon polyps and adenocarcinomas as revealed by monoclonal antibodies
Authors: Ljubimov A. V. , Barter J. , Couchman J. R. , Kapuller L. L. , Veselov V. V. , Kovarik J. , Perevoshchikov A. G. , Krutovskikh V. A. 
Published: February 2007

AbstractDouble‐label immunofluorescence was used to monitor basement‐membrane composition and integrity in 22 human colon polyps, 36 adenocarcinomas and 2 metastases. Cryostat sections were stained with polyclonal anti‐laminin anti‐serum combined with monoclonal antibodies (MAbs) to all major basement‐membrane components (laminin, entactin/nidogen, collagen type IV and large heparan sulfate proteoglycan), as well as to keratin 8. In all adenocarcinomas, including mucinous, basement membranes were altered more at the invasive front than in the parenchyma. The degree of this alteration was inversely correlated with the level of tumor differentiation. An uncoordinated loss of basement membrane components (dissociation of markers), previously described by us in rat colon adenocarcinomas, was also found in human tumors. In the great majority of adenocarcinomas a pronounced stromal reaction was seen. It was manifested by the presence of fibrillar deposits of basement‐membrane components, mainly of collagen type IV and/or heparan sulfate proteoglycan. This reaction was never observed in polyps and may be derived from myofibroblasts reported to accumulate in colon cancer stroma. The combined use of antibodies to basement‐membrane components and to a specific keratin may constitute an adequate immunohistochemical test for the presence of invasion, and may be useful in the histologic analysis of polyps, especially in dubious cases.
Body mass at different ages and subsequent endometrial cancer risk
Authors: Levi Fabio , La Vecchia Carlo , Neori Eva , Parazzini Fabio , Franceschi Silvia 
Published: February 2007

AbstractThe relationship between body mass index (BMI) at different ages and subsequent endometrial‐cancer risk was investigated in a multicentre case‐control study conducted between 1988 and 1991 in Vaud, Switzerland, and Northern Italy on 272 histologically confirmed incident cases of endometrial cancer and 571 controls admitted to hospital for acute, non‐neoplastic conditions, unrelated to known or potential risk factors for endometrial cancer. The risk of endometrial cancer increased with increasing BMI in the 3rd decade of age (20 to 29 years), in the 5th decade (40 to 49 years) and in the 7th decade (60 to 69 years), although the risk estimates tended to be substantially higher at older ages: compared with women whose BMI (kg m−2) was < 20, the relative risks (RR) were 1.8 for BMI ± 25 at age 20 to 29, 2.7 for BMI ± 30 at age 40 to 49 and 3.8 at age 60 to 69. All the trends in risk were significant, except that for BMI at age 25 after allowance for current BMI. When data were examined in separate strata of current BMI, among women of normal body mass at diagnosis no significant effect of past overweight was observed. In contrast, among subjects overweight at diagnosis, there were significant direct relationships with BMI at ages 20 to 29 and 40 to 49. To reduce endometrial cancer risk, it is therefore important to avoid obesity in later middle and older age, and the benefit can be even greater for women who were overweight at younger age.
Regulation of leukocyte binding to endothelial tissues by tumor‐derived GM‐CSF
Authors: Fu Yang‐Xin , Cai Jian‐Ping , Chin Yee‐Hon , Watson Gordon A. , Lopez Diana M. 
Published: February 2007

AbstractThe adherence of leukocytes to endothelial cells is the first step in the migration of these cells into tumor tissues. Specific binding to the endothelial cells by leukocytes is mediated by the development and maintenance of adhesion molecules on the endothelium; however, the mechanisms of leukocyte traffic into tumors and of their interactions with neoplastic tissue are not clearly understood. The infiltration of leukocytes occurs in most spontaneous and transplanted solid tumors and we have previously reported that not only are murine mammary tumors heavily infiltrated by leukocytes but tumor‐derived factors alter the development and function of leukocytes in tumor‐bearing mice. We now present evidence that a tumor‐derived cytokine, namely granulocyte‐macrophage‐colony‐stimulating factor, appears to be of importance in the regulation of leukocyte binding to endothelial cells. The data suggest that tumor‐derived factors may influence leukocyte trafficking within tumor tissue.
Cell phenotype (CD23)‐dependent variation in EBV genome copy numbers within lymphoblastoid cell lines (LCL)
Authors: Wendel‐Hansen Vidar , Tao Wen , Ericson Mats , Klein George , Rosen Anders 
Published: February 2007

AbstractThree Epstein‐Barr‐virus‐transformed lymphoblastoid cell lines (LCL) were analysed on the basis of their CD23 expression. Levels of EBV‐DNA were compared in the positive and negative subpopulations. Two lines were further analysed with regard to EBNA, cytoplasmic immunoglobulin (clg) and lytic (EA/VCA) protein expression. Both subpopulations had a similar MHC class‐11 transcription, but the CD23− subpopulation had a lower plating efficiency and a lower rate of DNA synthesis. In the B6, NAD50 and 0467.3 cell lines, CD23− cells contained 2 ± 0.2–6.4 ± 3.0 times less EBV DNA than the corresponding CD23+ population. EBNA was expressed in 81 ± 4.2%‐93 ± 3.8% of the CD23+ cells and in 0–46 ± 8.0% of the CD23− cells. No CD23+ cells in B6 or NAD50 contained any EA/VCA, while 19 ± 2.8%‐24 ± 4.2% of the CD23− cells were positive for the lytic‐cycle‐associated antigens. Of the CD23− cells, 70 ± 8.6%‐86 ± 6.0% were positive for cytoplasmic immunoglobulin compared to 14.7 ± 2.7%‐14.9 ± 1.8% in the corresponding CD23+ population. We have previously shown that only 18% of the clg‐positive cells were EBNA‐positive in the B6 line compared to 94% in the clg population. This was open to 2 alternative interpretations: loss of EBV genomes from a fraction of the cells with subsequent differentiation to secretory immunoglobulin production, or down‐regulation of EBNA expression in differentiating, EBV‐genome‐positive cells. Our present findings speak for the first alternative, indicating that a certain proportion of the cells may lose their EBV genomes in both long‐established and freshly transformed LCLs. This is accompanied by a reduced percentage of EBNA‐positive cells, the disappearance of at least one activation marker (CD23) associated with the virally induced blast transformation, and an increased synthesis of clg.
Effects of CPT‐11 in combination with other anti‐cancer agents in culture
Authors: Kano Yasuhiko , Suzuki Kenichi , Akutsu Miyuki , Suda Keiichi , Indue Yoshiharu , Yosnida Minoru , Sakamoto Shinobu , Miura Yasusada 
Published: February 2007

AbstractCPT‐11, 7‐ethyl‐10‐[4‐( 1 ‐piperidino)‐1 ‐piperidino]carbonyloxy camptothecin, is a newly developed water‐soluble camptothecin derivative now undergoing phase‐II evaluation. In an attempt to establish whether the combination of CPT‐11 with other standard anti‐cancer agents would be of any benefit, we studied the effects of CPT‐11 in combination with 11 other anti‐cancer agents on a human T‐cell leukemia cell line, MOLT‐3, in culture. We used both CPT‐11 and SN‐38 (active substance of CPT‐11 in vivo), for our study. Cells were incubated for 3 days in the presence of 2 drugs (CPT‐11 or SN‐38 and another drug) and cytotoxic effects were determined by MTT assay. The effects of drug combinations on ID50 were analyzed, by an improved isobologram method. Supra‐additive and marginal supra‐additive effects (synergism) were observed for CPT‐11 in combination with cisplatin, cytosine arabinoside and mitomycin C. Additive effects were observed for its combination with amsacrine, bleomycin, doxorubicin, etoposide, 5‐fluorouracil, mitoxantrone and vincristine. Alternate sub‐additive and protective effects (antagonism) were observed for CPT‐11 in combination with methotrexate. Similar tendencies were observed for SN‐38 in combination with other agents. These results suggest that CPT‐11 in simultaneous administration with a majority of anti‐cancer agents has an advantage for cytokilling. Of these agents, cisplatin, cytosine arabinoside and mitomycin C are most suitable for simultaneous administration with CPT‐11.
An anti‐doxorubicin monoclonal antibody modulates kinetic and dynamic characteristics of the drug
Authors: Sardini Alessandro , Villa Elena , Morelli Daniele , Ghione Mario , Ménard Sylvie , Colnaghi Maria Ines , Balsari Andrea 
Published: February 2007

AbstractA monoclonal antibody (MAb) directed against doxorubicin (DXR), denominated MAD11, was found to exert an antidotal action by modulating the kinetic and dynamic characteristics of the drug. In vitro, MAD11 has been found to reduce the cytotoxicity of DXR and the drug uptake on spleen lymphocytes more efficiently than on tumor cells (P388 leukemia cells). In vivo, the anti‐DXR MAb modified the drug distribution; the drug uptake was found to be reduced in the intestine and myocardial tissues and increased in the tumor, liver and spleen. In mice treated with DXR, the administration of anti‐DXR MAb exerted an antidotal activity which was proved by the reduction in body‐weight loss and mortality. In contrast, the therapeutic efficacy of the drug in P388‐tumor‐bearing mice was not influenced by the anti‐DXR MAb.
Pre‐treatment of a human T‐lymphoblastoid cell line with L‐asparaginase reduces etoposide‐induced DNA strand breakage and cytotoxicity
Authors: Shimizu Tsunehiro , Kubota Masaru , Adachi Souichi , Sano Hirohiko , Kasai Yasufumi , Hashimoto Hisako , Akiyama Yuichi , Mikawa Haruki 
Published: February 2007

AbstractThe effect of L‐asparaginase (L‐asp) pre‐treatment on etoposide‐induced DNA strand breakage and cytotoxicity was investigated. In a T‐lymphoblastoid cell line, Molt 4, etoposide‐induced DNA strand breaks, DNA‐protein cross‐links and cytotoxicity were reduced by pre‐treatment with L‐asp for 15 hr, but it did not cause these changes in a promyelocytic‐leukemia cell line, HL‐60, which is less sensitive than Molt 4 to L‐asp. However, pre‐treatment of Molt 4 cells with L‐asp did not significantly alter the accumulation of [3H]‐etoposide. Cell‐cycle analyses snowed an increase in G1‐phase cells, a significant decrease in both S‐phase cells and G2/M‐phase cells pre‐treated with L‐asp in Molt 4 cells, but L‐asp exposure did not result in any significant changes in HL‐60 cells. On the other hand, L‐asp pre‐treatment did not affect topoisomerase‐I (Topo‐I) inhibitor, camptothecin (CPT)‐induced DNA strand breaks or toxicity in Molt 4 cells. Our data imply that a decrease in S‐ and G2/M‐ phase cells following L‐asp treatment may explain the reduction of etoposide‐induced DNA lesions and cytotoxicity in Molt 4 cells, since topoisomerase‐II (Topo‐II) content or activity is a function of cellular proliferation status.
in situ expression of the IL‐I‐α and tnf‐α genes by reed‐sternberg cells in Hodgkin's disease
Authors: Xerri L. , Birg F. , Guigou V. , Bouabdallah R. , Poizox‐Martin I. , Hassoun J. 
Published: February 2007

AbstractThe histopathologic pattern of tissues involved by Hodgkin's disease (HD) suggests excessive activation of environmental cells by cytokines released by Hodgkin‐Reed‐Sternberg (HRS) cells, which are considered as the neoplastic component of HD lesions. This hypothesis has been supported by many studies performed in vitro using HD cell lines. In this study, we have tried to demonstrate the cytokine‐producing cells in an environment as close as possible to the in vivo conditions, using in situ hybridization onto frozen sections of HD samples. [35S]‐labelled single‐stranded RNA probes were prepared by transcribing human cDNA fragments of the TNF‐α and IL‐1 α genes sub‐cloned into appropriate vectors. A total of 19 specimens of HD lesions, including 7 cases of nodular sclerosing (NS) type and 12 cases of mixed cellularity (MC), were tested with both types of probes. Clinical stages included stage I (6 cases), stage II (4 cases), stage III (6 cases) and stage IV (3 cases). TNF‐α and/or IL‐I α expression was observed in 12 among 19 HD cases. However, neither the histological type nor the clinical status of the patients was correlated with the profile of cytokine secretion. Most of the cytokine‐producing cells could be identified as HRS cells due to their morphological appearance. In 3 cases, simultaneous analysis by immunohistochemistry and in situ hybridization showed that IL‐1 α/TNF‐α mRNA‐producing cells simultaneously expressed the CD30 antigen, thereby confirming the HRS nature of these cells.
Prevalence of human papillomavirus types 16 and 18 in squamous‐cell carcinoma of the penis: A retrospective analysis of primary and metastatic lesions by differential polymerase chain reaction
Authors: Wiener John S. , Effert Peter J. , Humphrey Peter A. , Yu Li , Liu Edison T. , Walther Philip J. 
Published: February 2007

AbstractHuman papillomaviruses (HPV), particularly types 16 and 18, may be carcinogenic effectors in a variety of human lower‐genital‐tract malignancies. Using the highly sensitive technique of differential polymerase chain reaction (D‐PCR) with amplimers from the E6 open reading frames of HPV types 16 and 18, a retrospective analysis of a 20‐year institutional experience with squamous‐cell carcinoma of the penis (SCCP) was performed to determine the prevalence of these HPV types in this malignancy. Paraffin‐embedded surgical specimens of primary (N = 27), locally recurrent (N = 5), and metastatic deposits (N = 26) from 29 patients with invasive SCCP were analyzed, as well as primary (N = 3) and recurrent (N = 2) specimens from 2 patients with penile carcinomain situ(CIS) (Bowen's disease). Nine of the 29 (31%) patients had invasive SCCP containing HPV 16 or 18 DNA, with HPV 16 found in 8 (28%) and HPV 18 in I (3%); no patient had both. In 7 patients in which only tissue from metastatic sites was available, 2 had HPV 16 detected in 2 separate metastatic sites each. Specimens from both primary and metastatic sites were available in an additional 6 patients, and HPV 16 was defected in specimens from 3 of these 6 patients. HPV was detected in comparable copy number at both sites in each patient, indicating that HPV DNA may be a stable component within cancer cells during disease progression. Of patients with CIS only, I of 2 was positive for HPV 16, and upon multifocal recurrence, showed persistence of the virus at 2 separate sites. Southern blotting was performed to confirm the presence of type‐specific HPV DNA and showed complete concordance with D‐PCR, but discordant hybridization intensities for HPV 18 were noted between the control and positive patient specimens; sequence analysis of the patient specimen revealed 4 point mutations in the HPV‐18 target segment. Comparison of the HPV‐positive (both HPV 16 and HPV 18) and HPV‐negative groups revealed no statistical differences between groups in patient age or ethnic origin, tumor histologic grade, or incidence of nodal involvement. Kaplan‐Meier analysis of both overall and cause‐specific survival likewise was not different between groups. These data, particularly the presence of HPV in metastatic deposits, provide strong evidence for an etiologic role of HPV type 16 (and possibly 18) in a substantial sub‐set of patients from the southeastern United States who developed SCCP.
Micronucleus formation in peripheral‐blood lymphocytes from smokers and the influence of alcohol‐ and tea‐drinking habits
Authors: Xue Kai‐Xian , Wang Su , Ma Guo‐Jian , Zhou Ping , Wu Pan‐Quan , Zhang Rui‐Feng , Xu Zhen , Chen Wen‐Sheng , Wang You‐Qin 
Published: February 2007

AbstractIn recent years, studies on the genotoxic effects of smoking and its modifying factors have been widely followed with interest. In this report, frequencies of micronuclei (MNF) in peripheral‐blood lymphocytes in 220 healthy smokers have been detected by the micronucleus test by finger‐skin puncture, which needs only 1 to 2 drops of peripheral blood. On the basis of analysis of matched‐pair data, the modifying effects of alcohol and tea are discussed. Our results show that (1) smoking significantly increases MNF in lymphocytes as compared with healthy non‐smokers (p < 0.01); (2) alcohol significantly increases MNF in smokers (p < 0.01); (3) tea decreases MNF induced by smoking (p < 0.01). Therefore, the anti‐carcinogenic role of tea merits further study.
Immunohistochemical evaluation of parathyroid hormone‐related protein (PTHrP) in the uterine cervix
Authors: Kitazawa Sohei , Kitazawa Riko , Fukase Masaaki , Fujimori Takahiro , Maeda Sakan 
Published: February 2007

AbstractWe investigated the immunohistochemical localization of parathyroid hormone‐related protein (PTHrP), a major factor responsible for the humoral hypercalcemia of malignancy, in uterine cervical lesions. Formalin‐fixed paraffin‐embedded specimens from 16 cases of normal and reactive conditions, 45 cases of cervical intra‐epithelial neoplasm (CIN) and 63 cases of invasive cancer were studied immunohistochemically by the avidine‐biotin‐peroxidase method, using an anti‐PTHrP monoclonal antibody (MAb), 4B3. In normal and reactive conditions, PTHrP was positive in parabasal cells, squamous metaplasia, and hyperplastic reserve cells. In neoplastic conditions, 96% (43/45) of invasive squamous‐cell carcinomas were positive for PTHrP, regardless of the patients' serum calcium levels. Two cases with hypercalcemia were strongly positive for PTHrP and showed prominent stromal interaction of the scirrhous type. In CIN, including koilocytic atypia, 76% (32/42) of cases were positive for PTHrP. In contrast, 91% (10/11) of adenocarcinomas were negative for PTHrP. In conclusion, we found, first, that in non‐neoplastic conditions, the presence of PTHrP was correlated with the transformation of progenitor cells into squamous epithelia and with the maturation of keratinocytes and, second, that in squamous‐cell carcinoma, the degree of keratinization and stromal interaction was higher in direct proportion to the apparent incidence of detectable PTHrP.
Nitrate and N‐nitrosoproline excretion in two italian regions with contrasting rates of gastric cancer: The role of nitrate and other factors in endogenous nitrosation
Authors: Knight T. , Pirastu R. , Palli D. , Cocco P. , Leach S. , Packer P. , Iannarilli R. , Manca P. , Møller H. , Forman D. 
Published: February 2007

AbstractExposure to nitrate and propensity for endogenous nitrosation were examined in 80 healthy males, aged 25–40 years, residing in areas of Italy with long‐standing high (Florence) and low (Cagliari) rates of gastric cancer. Nitrate exposure was assessed by measurement of urinary nitrate excretion over 12 hr, and endogenous nitrosation was assessed using the N‐nitrosoproline test (NPRO‐test). Our hypothesis was whether the geographic variation in cancer rate correlated with nitrate exposure or nitrosating ability. Exposure to background sources of NPRO was significantly higher in the high‐risk subjects (p = 0.04) whereas no differences were found in exposure to nitrate or in urinary NPRO levels after L‐proline loading (test NPRO levels). The regional difference in test NPRO was almost completely accounted for by background NPRO exposure. Examination of individual rather than grouped data revealed that exposure to nitrate was a major factor in NPRO formation. No other factors studied (age, dietary‐questionnaire‐assessed intake of anti‐oxidant vitamins) had a significant effect. Geographical variation in gastric cancer risk did not, therefore, correlate with either nitrate exposure or propensity for endogenous nitrosation of L‐proline.
Patterns of growth and differentiation in the colon carcinoma cell line lim 1863
Authors: Hayward Ian P. , Whitehead Robert H. 
Published: February 2007

AbstractThe LIM 1863 colon carcinoma cell line grows in the form of morphologically and functionally organized organoids. Cells are arranged around a central lumen with a brush border and nuclei are polarized to the periphery. The organoids contain 3 morphological cell types (columnar, goblet and caveolated cells). By agar cloning it has been possible to isolate 29 subclones of the cell line, all of which display the same phenotype and percentage of morphological cell types as the parent line. Cell‐sorting experiments showed that precursor cells of LIM 1863 cultures could express either mucin (large‐intestinal‐mucus antigen) or a brush‐border enzyme (sucrase‐isomaltase). Proliferating cells were predominantly found near the outer periphery of organoids with cell maturation towards the internal lumen. Dead cells were continuously shed from the organoids but terminal non‐cycling cells were not observed within the organoids. The organoid structure was calcium‐dependent and promoted cell survival. Suspension cultures of disaggregated cells could be grown in medium containing less than 100 μM calcium. No decrease in differentiation antigens was observed in the low‐calcium cultures, although polarization of the cells was lost. The organoid cultures formed by this cell line represent a unique in vitro model for colonic crypt growth and organization.
Reconstituted basement membrane (matrigel) promotes the survival and influences the growth of murine tumors
Authors: Vukičević Slobodan , Somogyi Lehel , Martinović Igor , Žic Rado , Kleinman Hynda K. , Marušić Matko 
Published: February 2007

AbstractThe effects of reconstituted basement membrane (Matrigel) on in vivo survival and growth of several murine tumors were studied. Survival of tumor cells was enhanced in all experiments which resulted in increased incidence and/or in increased tumor mass. While basement membrane enhanced the in vivo growth of B16F6 melanoma cells, survival of these mice was prolonged. Basement membrane increased the incidence but reduced the growth of Ehrlich ascites tumor. Walker‐256 hypercalcemic breast carcinosarcoma growth was enhanced and glandular‐like structures were observed when grown on Matrigel. The results indicate that the enhanced survival of tumor cells in the presence of basement membrane is not unequivocally linked with increased malignancy.