bluuebunny/crossref_metadata_2025_split huggingface dataset:
Humoral modulation of lymphokine‐activated killer (LAK)‐cell induction in humans: IgG‐related and non‐IgG inhibitors in sera from cancer patients
Authors: Riley Lee B. , Pellis Neal R. , Schantz Stimson P. , Freedman Ralph S. , Balch Charles M. , Itoh Kyogo 
Published: February 2007

AbstractSoluble inhibitors of lymphokine‐activated killer (LAK) cell induction were characterized and purified from serous fluids from healthy donors or from patients with advanced cancer. Inhibitory activity in sera from cancer patients was partially absorbed with protein A agarose or anti‐human IgG agarose. Following absorption, residual inhibition varied with individ ual sera, suggesting the presence of IgG‐related and non‐IgG inhibitory factors, and the proportions varied in the patient population. IgG, purified by affinity chromatography from ascitic fluids, from plasma of cancer patients, and from plasma of healthy donors, significantly inhibited IL‐2 induction of LAK cells in a dose‐dependent manner. Irrespective of the sources, inhibitory activity resided in the high‐molecular‐weight IgG fraction composed of IgG aggregates and immune complexes, but not monomeric IgG Commercially prepared human IgG in aggregated form, but not in monomeric form, inhibited LAK cell induction in a dose‐dependent manner. In contrast, neither bovine IgG nor human albumin affected LAK cell induction, even at higher concentrations. Aggregated human IgG inhibited LAK cell induction in unfractionated peripheral blood mononuclear cells (PBMC) but not in monocytedepleted peripheral blood lymphocytes (PBL). Despite exten sive (>99%) depletion of IgG by protein‐G affinity chromatography, the serous fluid from cancer patients displayed significant inhibitory activity. Fractionation of the IgG‐depleted inhibitory materials by Sephacryl S‐300, high‐pressure ionexchange column (HPIEC) or gel‐permeation chromatography (HPGPC) demonstrated a 65‐kDa inhibitor, distinct from IgG. Affigel‐blue affinity chromatography of the 65‐kDa fraction depleted albumin but did not remove the inhibitory activity, suggesting that the 65‐kDa inhibitor is not serum albu min nor an albumin‐bound component. These results suggest that serous fluids from patients with advanced‐stage cancer contain 2 distinct regulators for LAK cell induction: (I) aggregated IgG and (2) a 65‐kDa inhibitor, distinct from albumin.
Age at menarche, age at menopause, height and obesity as risk factors for breast cancer: Associations and interactions in an international case‐control study
Authors: Hsieh Chung‐Cheng , Trichopoulos Dimitrios , Katsouyanni Klea , Yuasa Shu 
Published: February 2007

AbstractThe importance of age at menarche, age at menopause, height, and obesity as risk factors for breast cancer, and the possible interactions among these factors in breast cancer causation were investigated in a data set collected in the late 1960's, in an international multicenter case‐control study. Multiple logistic regression procedures were used to model data from 3,993 breast cancer cases and 11,783 controls from 7 study centers representing the range of international variation of breast cancer incidence. Height and obesity (measured through the weight/height2 index) were independent risk factors for breast cancer among post‐menopausal but not pre‐menopausal women; post‐menopausal women taller by 10 cm had a 12% higher risk of breast cancer (95% confidence interval, Cl, 3‐21%) and post‐menopausal women of average height (say 158 cm) had an 11% higher risk of breast cancer (Cl 7‐16%) when they were heavier by 10 kg (and, therefore, more obese by 4 kg/m2). Age at menarche was a risk factor among both pre‐menopausal and post‐menopausal women, a delay of 2 years corresponding to a 10% reduction in breast cancer risk (Cl 6‐15%). Age at menopause was also a breast cancer risk factor, women with menopause at each 5 year age difference having a 17% higher risk of breast cancer (Cl 11‐22%). There is evidence of an interaction (deviation from the logistic regression‐postulated multiplicativity) between obesity and age at menarche, implying that the protective effect of late menarche may not apply to overweight women or that late menarche may become detrimental in obese women. The estimated relative risk coefficients, when applied to average risk factor levels observed among control women, can explain only a small fraction of the difference in breast cancer incidence between Boston and Tokyo.
Expression of HLA‐A, B, C, β2‐microglobulin (β2m), HLA‐DR, ‐DP, ‐DQ and of HLA‐D‐associated invariant chain (Ii) in soft‐tissue tumors
Authors: Mechtersheimer Gunhild , Staudter Martina , Majdic Otto , Dörken Bernd , Moldenhauer Gerhard , Möller Peter 
Published: February 2007

AbstractNon‐neoplastic mesenchymal cells, along with 33 benign and 87 malignant soft‐tissue tumors (STT) were examined for expression of HLA‐A, B, C, β2‐microglobulin (β2m), HLA‐DR, ‐DP, and ‐DQ molecules and the HLA‐D associated invariant chain (Ii). Serial frozen sections were immunostained using monoclonal antibodies (MAbs) to monomorphic framework determinants of HLA sublocus products, β2m and li, and to CD53, a recently defined broadly distributed pan‐leucocyte molecule. Compared with the normal state, an induction/neo‐expression of HLA‐A, B, C/β2m was found in a considerable number of tumors of muscle, peripheral nerve, cartilageforming, adipose, and vascular tissues. Conversely, some tumors of fibrous origin and of autonomic ganglia showed an abnormal abrogation/loss of HLA‐A, B, C/β2m with respect to their cells of origin. Small, round tumor cells present in various types of STT exhibited a heterogenous pattern of expression of these molecules with a preponderance of HLA‐A, B, C/β2m‐negativity. HLA‐D/Ii determinants were rarely detectable in STT. Besides their expression in some fibrohistiocytic tumors, they were only occasionally found in tumors of smooth‐muscle, peripheral‐nerve and vascular origin as well as in one clear‐cell sarcoma. In all tumors but one, there was no microtopographic association between HLA‐D/Ii‐positive tumor cells and inflammatory cells. CD53 allowed discrimination between dendritic interstitial cells (DIC) and neoplastic cells and additionally revealed that, in contrast to other solid tumors, STT are generally characterized by an extreme scarcity of lymphohistiocytic infiltrates. Our data indicate that, aside from very rare exceptions, aberrant induction or abrogation of MHC molecules in STT occurs in the absence of lymphohistiocytic stromal infiltrates, suggesting that these alterations might not be a consequence of local cytokine effects.
Diet, body mass and colorectal cancer: A case‐referent study in Stockholm
Authors: De Verdier Maria Gerhardsson , Hagman Ulla , Steineck Gunnar , Rieger ÅKe , Norell Staffan E. 
Published: February 2007

AbstractA population‐based case‐referent study on diet (total energy, protein, fat, dietary fiber), body mass and colorectal cancer was performed in Stockholm in 1986–1988. The study included 1,081 subjects. The relative risks (RR, with a 95% confidence interval, highest versus lowest quintile) for colon cancer were as follows: total energy (1.7, 1. 0–3.0), protein (2.4, 1.5–4.0), total fat (2.2, 1.3–3.6), dietary fiber for men (0.5, 0.2–1.1), dietary fiber for women (1.2, 0.7–2.3) and body mass (2.0, 1.3–3.1). The relative risks for rectal cancer were: total energy (2.4, 1.2–4.7), protein (3.6, 2.0–6.4), total fat (2.5, 1.4 4.6), dietary fiber (0.5, 0.3–0.9), body mass for men (1.7, 0.7–4.0), and body mass for women (1.0, 0.5–1.9). Adjustment for physical activity, body mass (in the diet analysis), the abovementioned dietary factors (in the body mass analysis), and browned meat surface had little or no influence on the results.
Detection of colonic growth factors using a human colonic carcinoma cell line (LIM 1215)
Authors: Whitehead R. H. , Nice E. C. , Lloyd C. J. , James R. , Burgess A. W. 
Published: February 2007

AbstractAlthough the colonic mucosa is one of the most rapidly proliferating epithelial tissues in the body, little is known about the factors that direct this proliferation. In this report we have studied the parameters of both a mitogenic and a clonogenic assay for detecting potential colonic growth factors (CGF). Using a colon carcinoma cell line (LIM 1215), which has retained a number of the properties of normal colonic mucosa, we have assayed a range of mitogenic factors for CGF activity. 3H‐thymidine incorporation by the LIM 1215 cell line was stimulated by low concentrations of epidermal growth factor and basic fibroblast growth factor and, to a lesser extent, by higher concentrations of interleukin‐I and insulin‐like growth factor I. The cells did not respond to a range of other mitogens and lymphokines. Optimal clonogenic response in a soft‐agar assay was obtained using a primary pituitary extract.
Epidermal growth factor receptors and EGF‐responsiveness of the human breast‐carcinoma cell line PMC42
Authors: Monaghan Paul , Ormerod Michael G. , O'hare Michael J. 
Published: February 2007

AbstractPMC42 is an early‐passage, well‐differentiated, pleiomorphic human breast‐cancer cell line. It expresses an average of 2.4 × 105 EGF receptor (EGFR) sites per cell when cultures are assayed using a radioreceptor assay. This is a relatively high figure for breast‐carcinoma cell lines. Its responses to epidermal growth factor (EGF) were analyzed morphologically and by flow cytometry and immunocytochemistry. PMC42 responded in vitro to EGF with morphological changes, inhibition of “doming” and an increase in DNA synthesis in serum‐containing medium in confluent or near confluent cultures. When EGF receptor sites were localized immunocytochemically in PMC42, they were found to be variably expressed on the membrane of cells grown in the absence of EGF, with discrete areas of strong and weak cells of different morphological appearances; flow cytometry indicated a 10‐fold range in EGFR levels between individual cells. Cultures maintained in the presence of EGF were less heterogeneous in their morphology and had a predominantly cytoplasmic, relatively uniform localization of EGFR with downregulation of membrane EGFR levels. EGF‐stimulated cultures were stained simultaneously for the presence of EGFR and the proliferation‐related antigen Ki‐67 and analyzed by both flow cytometry and immunocytochemistry. No correlation was observed between Ki‐67 positivity and level of EGFR expression by individual cells. Electron microscopic localization of receptor sites demonstrated that the receptors were concentrated predominantly on the lateral and basal membranes. These results show that the PMC42 line reflects a number of the properties of heterogeneous breast tumours in situ. It may also continue to express growth‐factor receptors in a manner that reflects their topographical distribution on normal luminal breast epithelial cells.
Biliary‐tract cancer in Chile
Authors: Serra Ivan , Calvo Alfonso , Maturana Mauricio , Sharp Allan 
Published: February 2007

AbstractThis epidemiological study in Chile shows a marked increase in biliary‐tract cancer based on mortality data, from an age‐adjusted rate (1970 world population) of 5.1 per 100,000 in 1970 to 12.0 per 100,000 in 1988. There is an increased risk of this cancer in all age groups but especially in young adults (15‐44 years). The female ratio of 3:1 persists. The increase in biliary‐tract cancer in 1970‐1985 was particularly important for young women but occurred in all female age groups whereas in men it was mostly in the elderly (65 years and more) and less in the middle‐aged (45‐64 years); no changes were observed in young men. Regional differences have begun to be appreciated. One of the factors which may account for this impressive and unexpected increase is the remarkable decrease in cholecystectomy rates. Less than 20% of the 154% increase in biliary‐tract cancer mortality in the period 1970‐1985 could be attributed to population aging. Improvements in diagnostic methods did not appear to be an important contributing factor. Other factors that could affect this increase in the incidence to epidemic levels include: an increase in the prevalence of cholelithiasis, an increase in the number of typhoid carriers and possible environmental carcinogens.
Reproductive factors and breast cancer risk in Iceland. A second cohort study
Authors: Tulinius Hrafn , Sigvaldason Helgi , Hrafnkelsson Jón , Ólafsdóttir Guðriður , Tryggvadóttir Laufey , Sigurðsson Kristján 
Published: February 2007

AbstractIn a previous prospective study we showed elevated risks for breast cancer in nulliparous women compared to parous women, in those having their first pregnancy at a higher age, and those with few children. This was based on 216 women diagnosed with breast cancer during 1965 to 1975 among 34,525 women having attended the cervix cancer detection clinic in Iceland by the end of 1974, and born between 1906 and 1945. The present investigation on 848 cases, diagnosed among 6 1,040 women attending the cervix cancer detection clinic during 1964 to 1984 and born between 1901 and 1960, shows the same risk factors to be significant. The relative risks are, however, smaller. The reasons for the difference in relative risks are discussed, We find that the effect of age at first birth is significant for women up to the age of 65 and not for older women. In both cohorts, women older than 55 are underrepresented and more so in the earlier report. In addition, the small number of cases in the reference group with age at first birth below 20 appears to have made the figures of our earlier report unreliable.
Monoclonal antibody against a tumor‐associated sialoglycoprotein of superficial papillary bladder tumors and cervical condylomas
Authors: Fradet Yves , Larue Hélène , Parent‐Vaugeois Carmen , Bergeron Alain , Dufour Colette , Boucher Lucie , Bernier Léonard 
Published: February 2007

AbstractA mouse IgG1 monoclonal antibody (MAb), 19A211, defining a tumor‐associated cell‐surface antigen of superficial papillary bladder tumors, was generated by immunizing with fresh bladder tumor cells mice neonatally injected with normal human urothelial cells. The reactivity of the antibody with cell lines was examined by indirect immunofluorescence staining and was restricted to 3/14 bladder cancer lines and 3/31 cancer cell lines of non‐bladder origin, including HeLa cervical cancer. No normal fibroblast, kidney cells, EBV‐lymphocytes, erythrocytes or leukocytes expressed the antigen. Reactivity of MAb 19A211 was well preserved on tissue paraffin sections. Immunoperoxidase staining of normal adult or fetal tissues showed no reactivity except for a patchy or uniform staining of umbrella cells in 6/23 adult and 1/4 fetal urothelium samples. Positive and often heterogeneous staining was observed on 24/38 papillary superficial tumors (Ta) and 4/5 carcinoma in situ bladder lesions but on only 4/20 infiltrating tumors. It was also observed on 5/6 cervical condylomas and one bladder condyloma, but none of 6 penile or vulvar condylomas. All other tumors tested were negative. The antigenic determinant is present on a heterogeneous group of proteins with molecular weights ranging from 90 to 200 kDa. It is sensitive to periodate treatment and to neuraminidase but only partially sensitive to proteases. MAb 19A211 is different from other reported MAbs with similar reactivity to superficial bladder tumors and umbrella cells of normal urothelium. When tested in competition assays, several of these MAbs, but not 19A211, were found to react with Lewis X blood group determinant. Our results suggest that 19A211 may be useful for detection and stratification of bladder tumors.
Expression of intercellular adhesion molecule‐1 (ICAM‐1) on renal‐cell cancer: Possible significance in host immune responses
Authors: Tomita Yoshihiko , Nishiyama Tsutomu , Watanabe Hisami , Fujiwara Michio , Sato Shotaro 
Published: February 2007

AbstractIn this study we examined the expression of intercellular adhesion molecule‐1 (ICAM‐I) in 28 cases of renal‐cell cancer (RCC). We also examined ICAM‐I expression on RCC cell lines in response to cytokines. Immunohistochemistry revealed frequent expression (23 positive cases among the 28 RCCs) of ICAM‐I in RCC. The molecule was not detected on renal tubular cells as far as could be determined. Furthermore, the number of ICAM‐I‐positive cells in RCC was significantly correlated with the degree of mononuclear cell infiltration, involving mainly T lymphocytes and a smaller number of macrophages bearing the LFA‐I molecule. Expression of ICAM‐I on RCC cell lines was augmented by in vitro treatment with interferon (IFN)‐γ, tumor necrosis factor (TNF)‐α and interleukin‐I (IL‐I)β. These results suggest that the expression of ICAM‐I on RCC might be modified by cytokines produced by tumor‐infiltrating mononuclear cells, and that ICAM‐I expression on RCC might augment the host immune reaction.
Loss of MHC class‐I expression in cervical carcinomas
Authors: Connor Mary E. , Stern Peter L. 
Published: February 2007

AbstractThe expression of MHC class‐I antigens was analysed in 67 cervical carcinoma biopsies; 16% of the biopsies showed complete or heterogeneous loss of HLA expression as judged by reactivity with antibodies recognizing monomorphic determi nants of the class‐I heavy chain bound to β2 microglobulin (β2m). In addition, other biopsies showed a loss in expression of particular allelic products: 23% for HLA‐A2; 17% for HLA‐A3; 23% for HLA‐Bw4 and 19% for HLA‐Bw6. Three biopsies showed changes at 2 alleles, 2 of which were at both HLA‐A and ‐B loci. Down‐regulation of class‐I expression may be virally mediated and HPV DNA is frequently found in cervical carcinomas. However, there appeared to be no direct correlation between the detection of HPV 16 or 18 DNA in these tumours and changes in HLA expression. There was also no correlation with the expression of the oncofoetal antigen 5T4. Our results show that a significant proportion (at least 30%) of the cervical carcinomas showed some alteration in MHC class‐I expression. Such changes may allow tumours to evade immune surveillance with more rapid progression. There was, however, no correlation with tumour type, degree of differentiation or stage of disease at presentation.
Participation of CD11a‐c/CD18, CD2 and ROD‐binding receptors in endogenous and interleukin‐2‐stimulated NK activity of CDS‐negative large granular lymphocytes
Authors: Timonen Tuomo , Gahmberg Carl G. , Patarroyo Manuel 
Published: February 2007

AbstractThe effect of RGD‐sequence‐containing pentapeptides and monoclonal antibodies (MAbs) against the adhesion molecules CD) la‐c/CDIB, ICAM‐1 (CD54) and CD2 on the binding and cytotoxicity of endogenous (freshly purified) and IL‐2‐stimulated CD3‐negative NK cells has been studied. Antibody to CD 18 exerted the most significant inhibition of adhesion and cytotoxicity of endogenous NK cells to MOLT‐4 lymphoma cells, followed by antibodies to CD2 and CD54. Antibodies to either CD 11 a, CD 11 b or CD 11c did not inhibit adhesion when used separately, whereas as a mixture their inhibitory capacity was as strong as that of anti‐CD 18. Antibodies against CD 18, CD54 and CD2 exerted an additive effect on the inhibition of adhesion. Their combination eradicated the binding of endogenous NK cells. The RGD‐containing peptide did not inhibit the binding or cytotoxicity of freshly purified NK cells to MOLT‐4, whereas some inhibition was detected against the adenocarcinoma cell line COLO‐205. According to FACS analysis, IL‐2 increases the expression of CD2 and CD54 on NK cells. However, the relative contribution of the adhesion molecules to the NK cell binding did not change as a result of the stimulation with IL‐2. The RGD‐peptide substantially in hibited the binding of IL‐2‐stimulated killer cells to COLO, and the combination of this peptide with MAbs to CD 18, CD54 and CD2 practically blocked the adhesion. Our results indicate that both CD 11a‐c/CD18‐ (involving the 3 heterodimers) and CD2‐dependent adhesion pathways are used by LGL in endogenous and IL‐2 stimulated natural killing. In addition, RGD‐binding receptors are involved in adhesion to some target cells.
Potentiation of tnf‐mediated cell killing by VP‐16: Relationship to DNA single‐strand break formation
Authors: Branellec Didier , Markovits Judith , Chouaib Salem 
Published: February 2007

AbstractInteraction between tumor necrosis factor (TNF) and the DNA topoisomerase II inhibitor, etoposide VP‐16, in cell killing has been studied. To accurately investigate the nature of DNA damage during the cell killing process, experiments were assessed using the highly TNF‐sensitive WEH1164.13 murine fibrosarcoma clone and DNA filter elution methodology. Concomitant treatment of cells with combination of TNF/VP‐16 resulted in marked enhancement of cell lysis. Using the alkaline elution technique, we show that TNF fails to induce DNA single‐strand breaks as compared to those generated by VP‐16. In addition, the potentiating effect of VP‐16 on TNF‐mediated WEH1164.13 cell killing was not associated with an increase in its intrinsic activity with respect to DNA single‐strand break formation. While the 2 phospholipase A2 inhibitors, quinacrine and dexamethasone, were efficient in inhibiting TNF‐mediated cell lysis, only quinacrine was efficient in selectively abrogating the TNF/VP‐16 cell killing pathway. The inhibitory effect of quinacrine on VP‐16/TNF‐mediated cell lysis was accompanied by a marked decrease in VP‐16‐mediated DNA single‐strand break generation. Taken together, our findings suggest that TNF and TNF/VP‐16 treatments may involve different events during cell killing and support the hypothesis that 2 signals are required for optimal induction of cell lysis by the combination of VP‐16/TNF: one signal provided by VP‐16 resulting in topoisomerase II inhibition and subsequent DNA single‐strand break generation, and a second signal involving TNF.
Effect of retinoic acid on tumor‐mediated immunologic alterations in mice bearing a variant of the ß16 melanoma
Authors: Jiang Cheng Gan , Taylor Douglas D. , Black Paul H. 
Published: February 2007

AbstractThis investigation examined the effect of retinoic acid on tumor progression and immunological status of mice bearing the B16‐F10 melanoma (previously selected for high lungcolonizing capacity). Tumor cells were implanted s. c. in syngeneic C57BL/6 mice, half of which were treated with β‐all trans retinoic acid (RA). Although RA failed to exhibit direct toxicity on this variant at the concentration used, the immunologic aberrations induced by the tumors were diminished by i. p. RA administration (at45μ twice/week for 3 weeks). In mice bearing B16‐F10 tumors, tumor burdens were decreased from 2.9% of body weight to 1.6%. The mitogenic responses of splenic lymphocytes to concanavalin A (ConA) were increased in tumor‐bearing mice following this RA treatment. The presence of these tumor cells decreased the absolute number of CD4‐ and CD8‐positive splenic lymphocytes. Following RA treatment, the CD8‐positive population was increased in tumor‐bearing mice, while the CD+ population was not significantly altered. Since previous studies indicated that plasma membrane fragments (or vesicles) could alter lymphocyte distributions and proliferative capacities, the in vitro shedding of membrane fragments from B16‐F10 tumor cells was assayed and observed to be decreased after continuous treatment of cultures with 10−6M RA for 21 days. Membrane shedding from B16‐F10 cells was inhibited by 48.5% following RA treatment. Based on these in vivo and in vitro results, we suggest that RA treatment may diminish tumor growth by decreasing tumor‐induced immunosuppressive events.