bluuebunny/crossref_metadata_2025_split huggingface dataset:
Risk of cutaneous melanoma associated with a family history of the disease
Authors: Ford Deborah , Bliss Judith M. , Swerdlow Anthony J. , Armstrong Bruce K. , Franceschi Silvia , Green Adèle , Holly Elizabeth A. , Mack Thomas , Mackie Rona M. , Østerlind Anne , Walter Stephen D. , Peto Julian , Easton Douglas F. 
Published: February 2007

AbstractIn a combined analysis of 2952 melanoma patients and 3618 controls from 8 case‐control studies in white populations the risk of cutaneous melanoma was 2.24‐fold higher (95% Cl, 1.76–2.86) in subjects who reported at least one affected first‐degree relative than in subjects who did not. There was no evidence for heterogeneity in the relative risk between the studies, which were from a wide range of latitudes and hence degrees of sun exposure. The effect of family history on melanoma risk was independent of age, naevus count, hair and eye colour, and freckling. There was no evidence for a relationship between family history and primary site of melanoma but there was some suggestion that the familial patients were more likely to have superficial spreading melanoma or lentigo maligna melanoma than acral lentiginous melanoma or nodular melanoma. © 1995 Wiley‐Liss, Inc.
Effects of 1,25‐dihydroxyvitamin D3 on transformed C3H/10T1/2 fibroblasts grown as multicellular spheroids
Authors: Brackman Damien 
Published: February 2007

AbstractWe have previously shown that 1,25‐dihydroxyvitamin D3(1,25‐(OH)2D3) is able to modulate proliferation of C3H/10T1/2 fibroblasts grown in monolayer cell culture. The aim of this study was to investigate the effects of the hormone in a 3‐dimensional culture system, which is considered to better reflect the cellular environment that is found in vivo. Two transformed cell lines of C3H/10T1/2 fibroblasts (C116 and TPA 482) were grown as multicellular spheroids, whereas the non‐tumorigenic C3H/10T1/2 C18 cells failed to form spheroids. The hormone had no effect on spheroids made of TPA 482 cells but had a biphasic effect on C116 spheroid growth with stimulation at low and inhibition at higher concentrations. In C116 spheroids, 10–8M 1,2S‐(OH)2D3 induced complete arrest of spheroid growth. Light and electron microscopic studies and immunocy‐tochemistry showed that 10–8M 1,25‐(OH)2D3 induced morphological changes in C116 spheroids, with a marked reduction in expression of fibronectin, laminin and the gap junction protein connexin 43. These effects were followed by a loosening of the spheroid structure, detachment of viable cells, and finally disaggregation of the spheroids. The results of this study, together with the data previously obtained in monolayer cell cultures, indicate that the effects of 1,25‐(OH)2D3 may be conditioned by the cellular environment. Therefore, the spheroid model is an interesting tool for investigation of the anti‐neoplastic effect of the hormone. © 1995 Wiley‐Liss, Inc.
Comparison of solutol HS 15, cremophor EL and novel ethoxylated fatty acid surfactants as multidrug resistance modification agents
Authors: Buckingham Lela E. , Balasubramanian M. , Emanuele R. Martin , Clodfelter Kathleen E. , Coon John S. 
Published: February 2007

AbstractSome well‐known fatty acid ester surfactants, e.g., Cremophor EL and Solutol HS 15, are modulators of multidrug resistance in vitro and in vivo. Because they are pelydisperse, and their active component(s) have not been identified, the therapeutic potential of such surfactants is unclear. To better define the active components of Solutol HS 15 and to make more potent surfactant multidrug resistance modulators, highly purified C‐18 fatty acids were esterified with ethylene oxide at 5–200 molar ratios. Unexpectedly, ethylene oxide esters of pure 12‐hydroxy stearic acid, the major components of Solutol HS 15, displayed negligible resistance modification activity compared with Solutol HS 15 itself or to stearic and oleic acid esters synthesized under identical conditions. Since oleic acid esters appeared to have good activity, a series of these compounds was prepared to determine the optimal ethylene oxide J. fatty acid ratio. The optimal ratio was found to be 20 mole ethylene oxide: I mole fatty acid, with a steep decline in activity for products made with ratios above and below the optimum. The most active oleic acid ester, designated CRL 1337, was 8.4‐fold as potent as Solutol HS 15 and over 19‐fold as potent as Cremophor EL in promoting rhodamine 123 accumulation in multidrug‐resistant KB 8–5–11 cells in vitro. Our results show that the structure of the hydrophobic domain (fatty acid) of surfactants as well as its hydrophile‐lipophile balance are critical in determining the potency of surfactants as reversing agents. © 1995 Wiley‐Liss, Inc.
RB and A novel E2F‐1 binding protein in MHC class II deficient B‐cell lines and normal IFN‐γ induction of the class II transactivator ciita in class II non‐inducible RB‐defective tumor lines
Authors: Tschickardt Michael E. , Lu Yanmei , Jacim Mark , de Wayne Ussery G. , Steimle Viktor , Mach Bernard , Blanck George 
Published: February 2007

AbstractThe major histocompatibility (MHC) class II genes encode cell surface proteins that bind antigenic peptide for presentation to T‐cells. The class II proteins are expressed constitutively on B‐cells and EBV‐transformed B‐cells, and are inducible by IFN‐γ on a wide variety of cell types. Retinoblastoma protein (RB) is a tumor suppressor and functions as a transcriptional represser by binding and inactivating the transactivator E2F‐1. RB‐ defective tumor lines are non‐inducible for MHC class II by IFN‐γ, or very weakly inducible, but transfection of 2 different lines with RB expression vectors re‐establishes or substantially enhances class II inducibility. Therefore, we examined the RB status of a series of B‐cell mutants that are defective in class II expression, generated either in vitro or derived from Bare Lymphocyte Syndrome (BLS) patients. Nuclear matrix‐bound RB was detectable in all cases, indicating that loss of RB is not responsible for decreased class II expression in these lines. A second E2F‐1 binding protein, most likely DP‐1, was also apparantly normal in both class II‐positive and ‐negative B‐cell lines. We also examined the IFN‐γ induction of CIITA in RB‐defective lines. CIITA is a class II gene transactivator known to be defective in one form of BLS and to be required for the induction of MHC class II by IFN‐γ. CIITA mRNA is normally inducible by IFN‐γ in class II non‐inducible, RB‐defective lines, and in one line, re‐expression of RB has no effect on CIITA mRNA induction levels. Thus, the block in MHC class II inducibility in RB‐defective cells is not due to a block in CIITA inducibility. © 1995 Wiley‐Liss, Inc.
Risk of lung cancer in pre‐ and post‐menopausal women with ano‐genital malignancies
Authors: Frisch Morten , Melbye Mads 
Published: February 2007

AbstractWomen diagnosed during the period 1943–1990 and reported to the Danish Cancer Registry with invasive squamous‐cell carcinomas of the uterine cervix, vulva, vagina or anus, together with those having pre‐cancerous lesions (CIN III or carcinoma in situ) of the uterine cervix diagnosed in the period 1958–1990, were followed for the occurrence of subsequent lung cancer over 762,000 person‐years. Overall, these patients developed 2 to 2° times more lung cancers than women in the general Danish population. Women in whom cervical cancer was diagnosed recently, and before the age of 45 years, had a 4.6 times elevated risk of developing lung cancer, while young women with vulvar or vaginal cancer were at a 4.0‐fold elevated risk. Similarly, women in whom anal cancer was diagnosed before the age of 60 years were at a 3.5‐fold increased risk of developing lung cancer. The present study supports the hypothesis that smoking is involved in the aetiology of ano‐genital malignancies. The particularly high risk of developing subsequent lung cancers seen in women who were pre‐menopausal (<45 years) at the time of the ano‐genital cancer diagnosis suggests that the effect of smoking in ano‐genital carcinogenesis might be partly mediated through alterations in oestrogen metabolism. Alternatively, patients who developed their initial ano‐genital cancer at a young age might harbour some genetic susceptibility which could explain their excess lung‐cancer risk. © 1995 Wiley‐Liss, Inc.
Non‐Hodgkin's lymphoma and skin malignancies‐shared etiology?
Authors: Hall Per , Rosendahl Ingvar , Mattsson Anders , Einhorn Stefan 
Published: February 2007

AbstractThe Stockholm‐Gotland Cancer Register was used to evaluate the clinical observation that patients with non‐Hodgkin's lymphoma (NHL) had an increased risk of malignant melanoma or squamous‐cell carcinoma of the skin (SCCS) and vice verso. During 1958–1992, NHL was diagnosed in a total of 6,176 patients. Of these patients, 504 developed a second primary cancer of any type except NHL, compared to 301.9 expected, giving a standardized incidence ratio (SIR) of 1.7 [95% confidence interval (Cl) 1.5–1.8]. The risk of SCCS and malignant melanoma in patients with NHL was 4.8 (95% Cl 3.6–6.2; n = 54) and 1.7 (95% Cl 0.8–3.1; n = 10), respectively. The hazard risk for a second malignancy was relatively constant over time, whereas the skin malignancies revealed the highest risks 3–10 years after initial diagnosis. Similarly, the risk of a secondary NHL was studied in patients with malignant melanoma and SCCS during the same period and found to be 1.3 (95% Cl 0.8‐2.1; n = 17) and 1.8 (95% Cl 1.2–2.5; n = 34), respectively. The highest risk for NHL following malignant melanoma was seen 3–10 years after first diagnosis, while the highest risk following SCCS was observed 0‐2 years after initial diagnosis. One of several possible explanations for the development of NHL and a skin malignancy in the same patient is an immunological defect caused by sun exposure. © 1995 Wiley‐Liss, Inc.
Methyl‐p‐Hydroxyphenyllactate‐esterase activity and type‐II estrogen‐binding sites in ovarian cancer: Correlation with biological and clinico‐pathological parameters
Authors: Ranelletti Franco O. , Scambia Giovanni , Panici Pierluigi Benedetti , Piantelu Mauro , Ferrandina Gabriella , D'agostino Giuseppe , De Vincenzo Rosa , Rinelli Alessandro , Isola Giulio , Mancuso Salvatore 
Published: February 2007

AbstractWe examined the levels of activity of methyl‐p‐hydroxyphenyl‐lactate esterase (MeHPLA‐ase) and cytosolic Type‐II‐estrogen‐binding sites (Type‐II EBS) in 61 and 71 cases, respectively, of primary ovarian cancer. MeHPLA‐ase activity and Type‐II EBS were seen to by asymmetrically distributed, in that levels were skewed towards the lower values. A statistically significant direct correlation was found between MeHPLA‐ase activity and Type‐II EBS. MeHPLA‐ase activity and Type‐II EBS were inversely correlated with ER and PR levels and showed a trend towards inverse correlation with the percentage of cells in S‐phase of the cell cycle. MeHPLA‐ase activity and Type‐II EBS did not correlate with clinico‐pathological parameters. The median MeHPLA‐ase activity tended to be higher in responders than in unresponsive patients, but statistical significance was not reached. Higher Type‐II‐EBS levels were found in cases showing complete and partial response to chemotherapy than in cases which did not respond. A statistically significant relationship was found between high MeHPLA‐ase activity and longer overall survival. © 1995 Wiley‐Liss, Inc.
Human peri‐tumoral and lung fibroblasts produce paracrine motility factors for recently established human sarcoma cell strains
Authors: Hu Mei , Pollock Raphael E. , Nakamura Toshikazu , Nicqlson Garth L. 
Published: February 2007

AbstractParacrine motogenic cytokines secreted by normal cells can stimulate metastatic cell invasion. For example, human fibroblasts secrete hepatocyte growth factor/scatter factor (HGF/ SF), which stimulates paracrine migration of epithelial and certain carcinoma cells, and migration‐stimulating factor (MSF), which stimulates autocrine migration of fibroblasts from certain breast carcinomas. We found that human peri‐tumoral and lung fibroblasts secrete motility‐stimulating activity for several recently established human sarcoma cell strains. Motility of lung metastasis‐derived SYN‐I sarcoma cells was preferentially stimulated by human lung and peri‐tumoral fibroblast motility‐stimulating factors (FMSFs). FMSFs were non‐dialyzable, susceptible to trypsin and sensitive to dIthiothreitol. Cycloheximide inhibited accumulation of FMSF activity in conditioned medium; however, addition of cycloheximide to the migration assay did not significantly affect motility‐stimulating activity. Purified HGF/SF, rabbit anti‐hHGF and RT‐PCR analysis of peri‐tumoral and lung fibroblast HGF/SF mRNA expression indicated that FMSF activity was unrelated to HGF/SF. Partial purification of FMSF by gel exclusion chromatography revealed several peaks of activity, suggesting multiple FMSF molecules or complexes. Since human soft tissue sarcomas have a distinctive hematogenous metastatic pattern (predominantly lung), FMSF may play a role in this process independent of HGF/SF. © 1995 Wiley‐Liss, Inc.
Characterization of a 95 kilodalton membrane glycoprotein associated with multi‐drug resistance
Authors: Doyle L. Austin , Gao Yongming , Yang Weidong , Ross Douglas D. 
Published: February 2007

AbstractOver‐expression of a 95‐kDa membrane protein (P‐95) has been reported previously in the multi‐drug‐resistant (MDR) breast cancer cell line MCF‐7/AdrVp and the MDR small cell lung cancer line NC1‐H1688. We have now developed anti‐sera against gel‐purified P‐95 protein from each of these cell lines. Western blotting with each serum demonstrates a broad band at 95‐kDa with detergent‐solubilized membrane proteins from MCF‐7/AdrVp and NC1‐H1688 cells, which is barely detectable in membrane proteins from drug‐sensitive parental MCF‐7 cells. Each anti‐serum cross‐reacts with a 190‐kDa membrane protein (P‐190) in NC1‐H1688 but not MCF‐7/AdrVp cells. Immunoblotting and silver staining of NC1‐H 1688 membrane proteins separated by two‐dimensional gel electrophoresis demonstrates that P‐95 and P‐190 run as broad streaks with low iso‐electric points. Incubation of NC1‐H 1686 cells with tunicamycin or cleavage of carbohydrate residues of NCI‐H 1688 or MCF‐7/AdrVp membrane proteins with PNGase F leads to the appearance of a sharp 35‐kDa band reactive with anti‐P‐95 antisera. This 35‐kDa protein has been isolated by two‐dimensional gel electrophoresis. Neuraminidase digestion converts P‐95 to a broad 65‐kDa immunoreactive band, indicating the presence of terminal sialic acid residues. In conclusion, P‐95 is an N‐linked sialoglycoprotein with a 35‐kDa polypeptide core. © 1995 Wiley‐Liss, Inc.
Local delivery of the topoisomerase I inhibitor camptothecin sodium prolongs survival in the rat intracranial 9L gliosarcoma model
Authors: Weingart Jon D. , Thompson Reid C. , Tyler Betty , Colvin O. Michael , Brem Henry 
Published: February 2007

AbstractCamptothecin, a naturally occurring inhibitor of the DNA‐replicating enzyme topoisomerase I, demonstrated promising anti‐tumor activity in pre‐clinical testing; however, because of unexpected toxicity and low anti‐tumor effects in the initial clinical trials, further testing was discontinued. We hypothesized that local controlled delivery of camptothecin sodium would achieve effective concentrations in brain tumors without the observed systemic side effects, thereby allowing this novel drug to be used to treat patients with malignant gliomas. To test this hypothesis, we evaluated the sensitivity of rat glioma lines and established human glioma lines to camptothecin in vitro. We found that the LD90 for the established rat and human lines was 0.3 to 1.4 μM after a 1 hr exposure and decreased to less than O.1 μM after continuous exposure for 7 days. We loaded camptothecin into a controlled‐release polymer (ethylene‐vinyl acetate co‐polymer; EVAc) and showed by high‐pressure liquid chromatography that controlled release occurred over at least 21 days. We then tested camptothecin against 9L gliosarcoma, implanted into the brain of Fischer 344 rats. Five days after tumor implantation, animals were treated with camptothecin delivered either systemically or locally by release from EVAc. Local controlled delivery by the polymer significantly extended survival: 59% of the treated animals were long‐term survivors (> 120 days) compared to 0% of controls. Systemic administration did not extend survival compared to controls. We compared the efficacy of camptothecin delivered locally with a polymer to camptothecin injected directly into the tumor. Camptothecin increased survival only when delivered locally by polymer. © 1995 Wiley‐Liss, Inc.
Suppression of human melanoma cell growth and metastasis by the melanoma‐associated antigen CD63 (ME491)
Authors: Radford Kristen J. , Mallesch Julia , Mersey Peter 
Published: February 2007

AbstractCD63 has been identified in human melanoma cells by a number of different monoclonal antibodies (MAbs). Studies with MAbs have shown that expression is most marked in naevi and early forms of cutaneous melanoma and reduced in vertical growth phase and metastatic lesions. To investigate further the role of CD63 in progression of melanoma, genomic CD63 was transfected into a CD63‐negative human melanoma cell line using an episomal vector. The stable transfected melanoma cells had similar growth rates to control transfected melanoma cells in vitro but much lower growth rates when injected intradermally into athymic nude mice. The CD63‐transfected cells also had a reduced number of metastases in the peritoneal cavity and subcutaneous sites when injected intravenously. MAb against CD63 did not influence the growth of CO63‐transfected melanoma cells in vitro. Our results confirm previous studies using H‐ros‐transformed NIH3T3 fibroblasts and suggest that CD63 may have a role as a tumor suppressor gene in human melanoma that acts to limit invasion and progression of melanoma. © 1995 Wiley‐Liss, Inc.
Role of a small molecular weight phosphoprotein in the mechanism of action of CI‐994 (N‐acetyldinaline)
Authors: Rummel Sue A. , Kraker Alan J. , Steinkampf Randall W. , Hook Kenneth E. , Klohs Wayne D. 
Published: February 2007

AbstractThe mechanism of action of the novel anti‐cancer compound CI‐994 was studied in C26 murine colon tumor and HCT‐8 human colon adenocarcinoma cells. Treatment of either cell line resulted in the specific loss of a 16‐kDa phosphoprotein in a time‐ and concentration‐dependent manner. Treatment with salicylanilide, C1–940, mimosine, aphidicolin, quercetin or ciclo‐ pirolxalamine, which, like C1–994, block cells in the G,‐S phase of the cell cycle, did not affect the production of this protein. Loss of the 16‐kDa protein preceded the block in cell proliferation induced by C1–994 treatment, and recovery of this protein was evident prior to the resumption of cell growth. Cellular fractionation studies demonstrated that the 16 kDa phosphoprotein is confined to the nuclear compartment. Our data indicate that loss the 16‐kDa nuclear phosphoprotein appears to be a direct effect of C1–994 treatment and that the inhibition of this phosphoprotein may play a critical role in the mechanism of action of C1–994. © 1995 Wiley‐Liss, Inc.
Epidermal growth factor expression in human colon and colon carcinomas: Anti‐sense epidermal growth factor receptor rna down‐regulates the proliferation of human colon cancer cells
Authors: Rajagopal Sriram , Huang Shuang , Moskal Thomas L. , Lee Bang‐Ning , El‐Naggar Adel K. , Chakrabarty Subhas 
Published: February 2007

AbstractHuman colon cancer cell lines express epidermal growth factor (EGF) mRNA, secrete EGF and may respond to it via the cell‐surface EGF receptor (EGFR). Expression of these molecules in human colon and colon tumor, however, is not clear. Reverse transcription‐polymerase chain reaction (RT‐PCR) analyses of RNA prepared from paired normal human colon and colon tumor samples from 12 individuals followed by Southern blotting analyses of the RT‐PCR products revealed a major fragment of 527 bp and a minor fragment of 404 bp that hybridized to a human EGF cDNA probe under stringent conditions. Identical results were obtained from 8 human colon cancer cell lines. Cloning and sequencing of PCR products confirmed that both fragments were from the human EGF gene; the 527‐bp fragment corresponded exactly to nucleotides 2,891 to 3,417 of the human EGF mRNA reported by others. A deletion of 123 nucleotides (nucleotides 3,172 to 3,294) was found in the 404‐bp fragment. Immunohistochemical studies using cryostat sections of human colon specimens showed that EGF was expressed in the human colon and that expression was restricted to the epithelial colonic crypt cells and epithelium‐ derived cancer cells. Since EGF and EGF‐related molecules are potent mitogens that mediated their effect through the EGFR, we also determined the efficacy of anti‐sense EGFR RNA in circumventing the EGFR‐related pathway of proliferation. Expression of anti‐sense EGFR RNA, by transfection with an inducible anti‐sense EGFR expression vector, down‐regulated cell‐surface EGFR expression and proliferation of these cells and their ability to grow in soft agar. Anti‐sense EGFR RNA was found to be an anti‐proliferative agent in both relatively non‐ aggressive and highly aggressive human colon cancer cells. © 1995 Wiley‐Liss, Inc.
Characterization of a prostate carcinoma mucin‐like antigen (PMA)
Authors: Beckett Mary Lou , Wright George L. 
Published: February 2007

AbstractA recently identified, high m.w. human tumor antigen, reactive with monoclonal antibody (MAb) PD41 and designated prostate mucin antigen (PMA), was found to have expression highly restricted to prostate carcinomas. Both biochemical and immunological characteristics of this antigen and its relationship to other tumor‐associated mucins and various species of submaxillary mucins were evaluated. Immunohistochemical examination of submaxillary tissues revealed differential expression of this antigen and other human tumor‐associated mucins, with MAb PD41 expression found only in bovine submaxillary gland serous cells. Neuraminidase treatment enhanced antibody binding by 50%, suggesting partial masking of the PD41 epitope by sialic acid. Antigenicity was reduced by treatment with alkaline‐borohydride, sodium metaperiodate, β‐galactosidase, O‐glycanase, and various proteolytic enzymes. MAb PD41 antibody binding also could be significantly reduced by selected lectins and sugars suggesting that the immunodominant carbohydrate involved in the epitope was an O‐linked oligosaccharide containing N‐acetyl galactosamine as a major component. This antigen was further distinguished from T, Tn, or Sialyl‐Tn antigens and blood group carbohydrate antigens by radioimmunometric analyses. Cross‐blocking and double determinant RIA experiments also showed a distinction between the PD41 epitope and several well‐characterized tumor‐associated mucin antigens such as MUCI, CEA, M344, OCI25, and AR3 as well as bovine submaxillary core protein. Our results indicate that the PD41‐reactive epitope is a non‐acidic O‐linked carbohydrate or glycopeptide epitope with restricted expression in prostate carcinomas and bovine submaxillary glands. This expression is distinct from other mucin‐like tumor‐associated antigens identified in human prostate carcinomas. © 1995 Wiley‐Liss, Inc.