bluuebunny/crossref_metadata_2025_split huggingface dataset:
Expression of gp 185HER‐2 in human cutaneous melanoma: Implications for experimental immunotherapeutics
Authors: Natali Pier Giorgio , Nicotra Maria Rita , Digiesi Giovanna , Cavaliere Renato , Bigotti Aldo , Trizio Domenico , Segatto Oreste 
Published: February 2007

AbstractOver‐expression of the HER‐2 oncogene correlates with poor prognosis in breast and ovarian carcinomas. Using a sensitive immunohistochemical assay, we have detected low levels of gp 185 HER‐2 in intradermal nevi (78%) and in primary (75%) and metastatic melanomas (58%). The HER‐2 gene product expressed by cultured melanoma cells had the expected molecular weight, but no levels of tyrosine phosphorylation could be detected. Consistently, we were unable to inhibit in vitro growth of melanoma cells with an anti‐gp 185HER‐2 MAb, in conditions in which the growth of SKBr‐3 breast‐carcinoma cells was severely impaired. However, immunotoxins to gp 185HER‐2 were able to kill gp 185Her‐2‐positive melanoma cells. These data indicate that low levels of gp 185HER‐2 are expressed by the melanocyte lineage, with no correlation with transformation or tumor progression. Nevertheless, gp 185HBR‐2 appears a suitable target for immunotherapy of cutaneous melanoma.
Risk factors for non‐melanomatous skin cancer in Alexandria, Egypt
Authors: El Khwsky Fayek , Bedwani Ramez , D'Avanzo Barbara , Assaad Sameir , Ali Adel El Shafei , Mokhtar Samiha , La Vecchia Carlo 
Published: February 2007

AbstractThe role of constitutional and environmental factors on the risk of non‐melanomatous skin cancer was evaluated in a case‐control study conducted in 1992 in Alexandria, Egypt, on 136 incident historically confirmed (99 basal‐cell and 37 squamous‐cell) cases of non‐melanomatous skin cancer (NMSC) and 145 controls in hospital for a broad spectrum of acute non‐sun‐related dermatological conditions. In relation to skin colour, compared with brown‐skinned subjects, the multivariate relative risks (RR) were 2.3 for olive‐skinned subjects and 3.8 for fair/medium‐skinned subjects. Three cases and 29 controls were black (RR = 0.2). The trend in risk with skin colour was significant. Likewise, compared with subjects with brown or hazel eyes, those with green or blue eyes had a RR of 3.1. In relation to acute sun reaction, compared with subjects reporting easy tanning, the RRs were 2.5 for subjects reporting moderate tanning and 4.7 for those reporting easy burning. The risk of NMSC was higher for subjects reporting an outdoor occupation than for those reporting an indoor occupation (RR = 7.7). A significant trend in risk was observed with degree of sun exposure: compared with subjects reporting light sun exposure, the RR was 3.0 for those reporting moderate exposure, and 6.1 for those reporting heavy sun exposure. There was an indication of a relationship between clothing pattern and skin‐cancer risk: compared with subjects reporting frequent use of traditional Egyptian clothes, the RR for dressing in short clothes was 1.8. The presence of signs of photo damage was also associated with NMSC (RR = 3.7). Exposure to arsenic was reported by 10 cases and 1 control (RR = 9.5). A positive interaction between sun exposure and skin colour was observed, and the RR rose to 14.2 for medium‐or fair‐skinned subjects with heavy exposure compared with brown‐or black‐skinned subjects with light or moderate sun exposure. In this Egyptian population, over 60% of NMSC could be attributed to sun exposure and approximately 45% to skin colour.
Body iron stores and risk of cancer
Authors: Knekt Paul , Reunanen Antti , Takkunen Heikki , Aromaa Arpo , Heliövaara Markku , Hakuunen Timo 
Published: February 2007

AbstractA high level of available tissue iron may increase the risk of cancer through its contribution to the production of free oxygen radicals. Serum iron, total iron‐binding capacity (TIBC) and transfer‐fin saturation levels were studied for their prediction of different cancers in a cohort of 41,276 men and women aged 20–74 years and initially free from cancer. During a mean follow‐up of 14 years, 2,469 primary cancer cases were diagnosed. Excess risks of colorectal and lung cancers were found in subjects with transferrin saturation level exceeding 60%. The relative risks, adjusted for age, sex and smoking, were 3.04 for colorectal cancer and 1.51 for lung cancer, in comparison with subjects having lower levels. The risk of lung cancer was inversely related to serum TIBC, with a relative risk between the highest and lowest quartiles of 0.69 for men and 0.19 for women. For the risk of stomach cancer, we detected inverse relationships with serum iron and with transferring saturation and a positive relationship with TIBC, but these associations weakened when the cancer cases occurring during the 5 first years of follow‐up were excluded. High iron stores may increase th risk of colorectal cancer, whereas low iron stores may be an early sign of occult stomach cancer.
Detection of increased amounts of the extracellular domain of the c‐erbB‐2 oncoprotein in serum during pulmonary carcinogenesis in humans
Authors: Brandt‐Rauf Paul W. , Luo Jiin‐Chyuan , Carney Walter P. , Smith Steven , Devivo Immaculata , Milling Cassandra , Hemminki Kari , Koskinen Heikki , Vainio Harri , Neugut Alfred I. 
Published: February 2007

AbstractOver‐expression of the c‐erbB‐2 oncogene‐encoded p185 protein product has been implicated in the pathogenesis of a wide variety of human malignancies, including lung cancer. Over‐expression of p185 can be detected immunologically by quantification of the extracellular domain of p185 (c‐erbB‐2 oncopeptide) in extracellular fluid in vitro and in serum in vivo. An enzyme‐linked immunosorbent assay (ELISA) for the c‐erbB‐2 oncopeptide was used to examine banked serum samples of 11 pneumoconiosis patients who subsequently developed lung cancer and serum samples from 11 hospital controls matched for age, sex, ethnic group and smoking as well as 55 unmatched general population controls. The mean serum level for the c‐erbB‐2 oncopeptide in human neu units/ml in the lung cancer cases (1,756 ± 549 HNU/ml) was statistically significantly elevated (p < 0.001) in comparison to the mean level in the matched controls (976 ± 488 HNU/ml) or the general population controls (888 ± 655 HNU/ml). Defining a positive elevation of the serum c‐erbB‐2 oncopeptide as any value more than 2 standard deviations above the mean of the matched controls, 64% (7 of 11) of the lung cancer cases were positive compared to 0% (0 of 11) matched controls and 5% (3 of 55) of the unmatched controls. In addition, 4 of the 7 c‐erbB‐2 oncopeptide‐positive cancer cases had positive serum samples prior to the time of disease diagnosis (average = 35 months). These results suggest that serum c‐erbB‐2 oncopeptide may be elevated at an early stage of pulmonary carcinogenesis and that further prospective study of the utility of this biomarker is warranted.
Angiostatic activities of medroxyprogesterone acetate and its analogues
Authors: Yamamoto Takashi , Terada Nobuyuki , Nishizawa Yasuko , Petrow Vladimir 
Published: February 2007

AbstractThe effects of medroxyprogesterone acetate (MPA) (1) and related compounds (II‐VI) upon angiogenesis induced by basic fibroblast growth factor (bFGF) or transforming growth factor‐α (TGF‐α) were investigated using a rabbit cornea system for assay of angiogenesis. Dexamethasone (Dex) was used as a positive control. The MPA analogues tested were 6,6′‐dehydro MPA (II), megestrol acetate (III), l‐dehydromegestrol acetate (IV), melengestrol acetate (V), and l‐dehydromelengestrol acetate (VI). The inhibitory activities of these steroids using bFGF were in the order: Dex = MPA = (VI) = (V) > (IV) > (III). Steroid (II) was inactive. 5α‐dihydrotestosterone was weakly active, while estradiol‐17β and progesterone were inactive. The angiostatic activity of MPA was completely abolished by mefipristone (RU 486) which showed no anti‐angiogenic activity in this assay. With TGF‐α, the order of angiostatic activities was Dex = (VI) > (IV) > (III) > (V). Steroid (II) was again inactive. Dex, MPA, and all the MPA analogues except steroid (II) markedly inhibited the activity of plasminogen activator secreted by cultured calf pulmonary artery endothelial cells, but did not inhibit growth of these cells. The binding affinities of MPA and its analogues to glucocorticoid, progesterone and androgen receptors were determined, but were found not to be correlated with their angiostatic activities.
Susceptibility of lactating rat mammary glands to gamma‐ray‐irradiation‐induced tumorigenesis
Authors: Suzuki Keiko , Ishi‐Ohba Hiroko , Yamanouchi Hiroshi , Wakabayashi Katsumi , Takahashi Masakazu , Inano Hiroshi 
Published: February 2007

AbstractLactating rats of the Wistar‐MS strain were irradiated with 260 cGy of gamma rays 21 days after parturition (day 21). Diethylstilbestrol (DES) pellets were implanted one month after termination of nursing and were allowed to remain for one year. A significantly higher incidence (96.4%) of mammary tumors was observed in these rats irradiated during late lactation than in virgin irradiated animals (30.4%). A control group of lactating animals irradiated during late lactation but not treated with DES was also observed for one year; the final incidence of mammary tumors in this group was 35.3%. The latency period was shortest in the DES‐treated group irradiated during late lactation. Histological examination showed that the mammary glands of lactating rats were highly developed, with alveoli filled with milk. Five days after weaning, there was degeneration of alveolar tissue, concomitant with a marked decrease in the concentration of estrogen and prolactin receptors. A considerable amount of epithelial tissue remained in the mammary glands during the process of atrophy. When the rats were irradiated 5 days after weaning, and then were treated with DES for one year, the incidence of mammary tumors was 73.3%, significantly higher than that in virgin irradiated rats. However, this incidence was not significantly different from that in animals irradiated during late lactation. These results suggested that the induction of mammary tumors by gamma irradiation before or after weaning was more dependent upon the stage of differentiation in mammary glands than upon the proliferative activity of epithelial cells, and that DES is essential as a promoter for radiation‐induced mammary tumorigenesis.
Karyotypic characterization of human T‐cell lines immortalized by Herpesvirus saimiri
Authors: Troidl B. , Simmer B. , Fickenscher H. , Müjller‐Fleckenstein I. , Emmrich F. , Fleckenstein B. , Gebhart E. 
Published: February 2007

AbstractMerpesvirus saimiri subgroup‐C strains transform non‐neoplastic human T lymphocytes in vrtro to antigen‐independent continuous growth. The karyotypes of 8 of these T‐cell lines, derived from peripheral blood or bone marrow, are analyzed here, In general, these lines showed a normal diploid karyotype, although one of them had acquired a clonal chromosomal rearrangement after 21 months in culture. Chromosomally aberrant cell clones were found more frequently in cell lines derived from blood lymphocytes of leukemia patients than in cultures from healthy donors: However, the observed aberrations, some of which were defined in detail using chromosome in situ suppression hybridization (CISS) with chromosome‐specific recombinant ONA libraries, did not show any relation between the various cell lines nor to the respective types of leukemia.
Inhibition of human B‐cell chronic lymphocytic leukemia by a monoclonal antibody in xenograft models
Authors: Zhu Zhenping , Ghose Tarunendu , Hoskin David , Lee Christine L. Y. , Fernandez Louis A. , Rowden Geoffrey , Lee Spencer H. S. 
Published: February 2007

AbstractTo establish xenograft models of human B‐cell chronic lymphocytic leukemia (CLL), we inoculated S × 106 D10‐1 cells, a subline of Epstein‐Barr virus (EBV)‐transformed human B‐cell CLL with a marker chromosomal anomaly, into SCID or irradiated nude mice by the intravenous (i.v.) or intraperitoneal (i.p.) route. All i.p. tumor‐inoculated mice developed rapidly progressive, lethal ascites tumor, and 100% of i.v. tumor‐inoculated mice developed disseminated CLL. All mice died of tumor within 8 weeks of tumor inoculation. Tumor‐inoculated SCID mice died earlier with wider tumor dissemination than the tumor‐inoculated nude mice. All the tumor‐inoculated mice had histologically confirmed metastases in lymph nodes, and most of them also had metastases in one or more internal organs. Cytogenetic analysis confirmed the origin of these tumors from the xenografted D10‐1 cells. The D10‐1 cells harvested from the xenografts did not differ from the parent D10‐1 cells as regards (i) reactivity with 2 monoclonal antibodies (MAbs) directed against CLL‐associated cell‐surface antigens; (ii) rate of proliferation in vitro; and (Hi) sensitivity to the 2 chemotherapeutic agents, methotrexate and adriamycin. Administration of 50 μg/mouse of Dal B02, an IgG1 (K) MAb directed against surface‐associated antigens of human B‐cell CLL, significantly prolonged the survival of D10‐1‐inoculated nude and SCID mice. The MAb was more effective in D10‐1‐inoculated nude mice than in SCID mice. In all the D10‐1 xenograft models, the effectiveness of Dal B02 decreased with higher tumor load but increased with the amount of MAb injected. Dal B02 F(ab)'2 fragment failed to demonstrate any anti‐tumor activity in D10‐1‐inoculated nude mice. In vttro assays revealed that Dal B02 had no direct inhibitory effect on D10‐1 cells, but could be cytotoxic towards D10‐1 cells in the presence of splenic cells or peritoneal macrophages from nude and SCID mice, or together with rabbit complement.
p53 genetic abnormalities and myc activation in human lung carcinoma
Authors: Gazzeri Sylvie , Brambilla Elisabeth , De Fromentel Claude Caron , Gouyer Valérie , Moro Denis , Perron Pascal , Berger François , Brambilla Christian 
Published: February 2007

Abstractp53 mutations and myc gene amplification and expression were studied in 119 lung carcinomas of all histological types. A mutant p53 immunophenotype was previously found in 47% of these tumors by immunohistochemical analysis. Seven cases exhibited p53 genomic rearrangements on Southern blots. Elevated levels of p53 transcript were found in 12 carcinomas (10%) and decreased levels in 27 carcinomas (23%) on Northern blots. In most of the cases, low levels of transcript were associated with negative immunostaining, whereas elevated levels of mRNA were related to positive immunostaining (mutant immunophenotype). p53 RT/PCR analysis in 10 tumors with absence of transcript on Northern blots revealed only weak or absent expression of normal and/or altered size transcripts. These abnormal transcripts showed deletions, insertions or splicing abnormalities. Taken together, p53 abnormalities were found in 66% of lung carcinomas [52% of neuroendo‐crine (NE) carcinomas and 75% of NSCLC]. c‐myc was found to be activated in 24% (10/42) of these NE and in 48% (33/69) of these NSCLC carcinomas using Southern‐ and Northern‐blot techniques. In addition, L‐ and N‐myc genes were also activated in 26% (10/42) of NE carcinomas. No correlation was found between p53 mutations and myc activation in SCLC or in NSCLC, but their association was significantly more frequent in NSCLC than in SCLC. These results indicate that the p53‐positive immunophenotype uncovers the occurrence of p53 point mutations in lung cancer and that p53 and c‐myc gene alterations are important but represent independent occurrences in the development of lung tumors.
Epstein‐barr virus (EBV)‐related lymphoproliferative disorder with subsequent EBV‐negative T‐cell lymphoma
Authors: Tao Qian , Srivastava Gopesh , Loke Shee Loong , Liang Raymond H. S. , Liu Yan Tat , Ho Faith C. S. 
Published: February 2007

AbstractA 58‐year‐old Chinese man presented initially with generalized lymphadenopathy, and lymph‐node biopsy showed disturbed architecture with preponderance of large B‐blasts mixed with numerous CD8+ T lymphocytes, consistent with an acute Epstein‐Barr virus(EBV) infection. Immunohistological and gene rearrangement studies confirmed the absence of clonal T or B cells. Polyclonal EBV with lytic infection was detected by Southern blot hybridization (SoBH). Expression of EBV proteins (EBNA2, LMP and ZEBRA) was detected in a proportion of cells by immunostaining. EBV‐lytic proteins EA‐D, VCA, MA were also detected in rare scattered cells. Double immunostaining showed that the LMP‐positive cells were of B and of T phenotype: 73% CD19+, 26% CD2+ 23% CD3+ 8% CD4+ 17% CD8+. After biopsy, there was spontaneous regression of lymph‐node enlargement, but lymphadenopathy recurred 8 months later, and the second lymph‐node biopsy showed T‐cell lymphoma, confirmed by detection of clonally rearranged T‐cell‐receptor beta‐chain gene. However, EBV genome could not be detected in the second biopsy by SoBH, in situ hybridization for EBV‐encoded EBER RNA, and immunostaining for EBNA2, LMP and ZEBRA was also negative. This case is of special interest because an EBV‐negative T‐cell lymphoma developed shortly after an acute episode of EBV‐related lymphoproliferation, even though many EBV‐positive T cells were detected during the acute episode. EBV was apparently not a direct cause of the lymphoma, but the close temporal association of the 2 lesions supports the hypothesis that EBV can act as a co‐factor in lymphomagenesis. © 1994 Wiley‐Liss, Inc.
Time trends in the incidence of renal carcinoma: Analysis of connecticut tumor registry data, 1935‐1989
Authors: Katz David L. , Zheng Tongzhang , Holford Theodore R. , Flannery John 
Published: February 2007

AbstractRecent trends in the incidence of renal cancer, stratified by histology, have not been reported. This study utilized data from the Connecticut Tumor Registry (CTR), the oldest population‐based cancer registry in the United States, to establish time trends in the incidence of adenocarcinoma and transitional cell carcinoma of the kidney and urinary tract. All 10, 209 incident cases of renal cancer reported to the CTR between 1935 and 1989 were analyzed. Regression modelling was employed to determine the effects of age, period, and birth cohort on incidence rates, and to project future trends. The incidence rate of adenocarcinoma increased in females from 0.7/100,000 in 1935‐39, to 4.2/100.000 in 1905‐89; and in males, from 1.6 J. 100,000 in 1935‐39, to 9.6/100,000 in 1985‐89. The reported incidence of transitional cell carcinoma increased in males from 0.5/100,000 in 1950‐54 to 2.8/100,000 in 1985‐89, and in females from 0.2/100,000 to 1.1/100,000 over the same period. Regression modelling revealed that both net and recent drift, the sum of period and cohort slopes, were positive for adenocarcinoma in both sexes, largely due to a positive cohort effect. While the net drift for transitional cell carcinoma was positive, recent drift was negative in both sexes due primarily to a negative cohort effect. Incidence rates of adenocarcinoma are likely to rise in the immediate future, with the rate of rise in females possibly exceeding that in males. Incidence rates of transitional cell carcinoma will stabilize. © 1994 Wiley‐Liss, Inc.
Pre‐Treatment of human osteosarcoma cells with N‐methylformamide enhances P‐glycoprotein expression and resistance to doxorubicin
Authors: Scotlandi Katia , Serra Massimo , Manara Maria Cristina , Lollini Pier‐Luigi , Maurici Daniela , Bufalo Donatella Del , Baldini Nicola 
Published: February 2007

AbstractN‐methylformamide (NMF), 3 powerful differentiating agent, has been extensively used in experimental and preclinical cancer chemotherapy studies, alone or in association with conventional anti‐cancer drugs. To evaluate the use of this molecule in the treatment of osteosarcoms (OS), we have analyzed the effects of NMF and doxorubicin (DXR) or DXR‐sensitive and ‐resistant human OS cell lines. Our study shows that NMF exerts remarkable effects on cell proliferation and, in Saos‐2 and SARG cells, also induces differentiation, as shown by increasing alkaline phosphatase activity. Moreover, NMF increases the cytotoxic activity of DXR when administered after the drug, In both DXR‐sensitive and ‐resistant cells. However, when this agent is given before DXR, it enhances P‐glycoprotein expression in U‐2 OS cell lines. This over‐expression is associated with reduced DXR accumulation within cells and with significant enhancement of resistance to DXR. © 1994 Wiley‐Liss, Inc.
A novel strategy of C‐myc oncogene in NK activity regulation not related to the W6/32 MHC class‐I epitope
Authors: La Cava Antonio , Carbone Ennio , Moscarella Anna , Barcová Mária , Salzano Salvatore , Zappacosta Serafino , Fontana Silvia 
Published: February 2007

AbstractThe C‐myc gene encodes a nuclear protein whose precise function is still not folly understood. Introduction of a c‐myc gene into a number of cell lines leads to an increase in their susceptibility to NK‐cell lysis. It was reported earlier that c‐myc can induce a decrease in the membrane expression of the MHC class‐1 molecules and this may be one of the factors that render target cells relatively more susceptible to NK lysis. In this contribution, we show, in a human LCL line transfected with a constitutively active c‐myc gene, an increased sensitivity to NK lysis, which correlates with an augmented effector‐target binding ability of c‐myc‐transfected LCLs and with a high 1CAM‐1 expression rather than with down‐regulation of MHC class‐l W6/32 epitope expression. © 1994 Wiley‐Liss, Inc.
Involvement of protein kinase C and an elastase‐like enzyme in the processing of transforming growth factor‐α in human colon carcinoma cell lines
Authors: Levine Alan E. 
Published: February 2007

AbstractHuman colon carcinoma cell lines secrete transforming growth factor‐α (TGF‐α). Previous work indicated that the apparent m.w. of the TGF‐o secreted by these cells ranged between 5 and 25 kDa. The more differentiated GEO cell line secreted a higher percentage of high m.w. TGF‐or than did the poorly differentiated HCT 116 cell line. In addition, the HCT 116 cells secreted 5‐fold more TGF‐a. Treatment of HCT 116 and GEO cells with a phorbol ester (TPA) resulted in a 4‐fold increase in TGF‐α in the conditioned media of both cell types. The TPA‐induced release of TGF‐a was blocked by an inhibitor of elastase‐like enzymes. This suggested a role for protein kinase C (PKC) in TGF‐α processing in colon carcinoma cells. Direct measurement of PKC activity indicated that the HCT 116 cells (which secrete more fully processed TGF‐α) had 10‐fold more PKC activity than GEO cells. The presence of an elastase‐like activity in detergent extracts and the ability of an elastase inhibitor to block the TPA‐induced secretion of TGF‐a suggests that PKC and an elastase‐like enzyme are involved in the processing and secretion of TGF‐a by human colon carcinoma cell lines. © 1994 Wiley‐Liss, Inc.