bluuebunny/crossref_metadata_2025_split huggingface dataset:
Natural cytotoxicity of human blood monocytes and natural killer cells and their cytotoxic factors: Discriminating effects of actinomycin D
Authors: Uchida Atsushi , Klein Eva 
Published: February 2007

AbstractThe effect of actinomycin D on target susceptibility to human blood natural killer (NK) cells and monocytes was analysed in direct cell‐mediated and their cytotoxic factor‐mediated cytotoxicity assays. Treatment of K562 cells with actinomycin D reduced their susceptibility to lysis by non‐adherent lymphocytes and Percoll‐purified large granular lymphocytes (LGL) in a 4‐hr 51Cr‐release assay, without affecting their sensitivity to monocytes purified by adherence to autologous serum‐coated plastic surfaces. The drug treatment caused no shift in the kinetics of cytotoxicity. In the target binding assay LGL formed fewer conjugates with actinomycin‐D‐treated K562 cells than with untreated ones, while the binding of monocytes to targets was not reduced by the drug treatment of K562 cells. The cold target competition assay revealed that actinomycin‐D‐treated cold K562 cells showed less successful inhibition than untreated cold K562 cells. Lymphocytes and monocytes could be induced to release soluble cytotoxic factors, termed natural killer cytotoxic factors (NKCF) and monocyte cytotoxic factors (MCF), respectively, when co‐cultured with K562 cells. Both cytotoxic factors lysed NK‐sensitive target cells in a 48‐hr assay. Actinomycin‐D‐treated K562 cells reduced or abolished the ability to stimulate the release of NKCF from lymphocytes, whereas they induced MCF secretion from monocytes as effectively as untreated ones. On the other hand, actinomycin D treatment of K562 cells enhanced their susceptibility to NKCF and MCF. This actinomycin‐D‐induced augmentation of target sensitivity to the cytotoxic factors was restricted to NK‐sensitive target cells (K562 and Molt‐4). NK‐resistant target cells (Raji, YAC‐I, EL4 and T blasts) were not lysed by NKCF and MCF even after they were treated with actinomycin D. The capacity of K562 cells to bind NKCF and MCF was not altered by actinomycin D. Treatment of the adherent cell population with OKMI or Leu‐MI plus complement abrogated both cell‐mediated cytotoxicity and MCF production, while Leu‐11b plus complement was ineffective. These results suggest that the effect of actinomycin‐D treatment can be used to distinguish the two distinct types of blood mononuclear cells with natural cytotoxicity, NK cells and monocytes, and that each effector type recognizes different plasma membrane moieties of NK target cells, although the cytotoxic factors released from each effector cell similarly bind to and lyse the target cells.
A tumor‐associated antigen expressed in melanoma cells with lower malignant potential
Authors: Suter L. , Brüggen J. , Bröcker E. B. , Sorg C. 
Published: February 2007

AbstractThe antigen K‐1‐2, detectable by a MAb is found in nevi and melanomas. It is associated with melanoma cells of low invasive and metastatic potential as shown by immunoperoxidase studies with cell lines, biopsies and autopsies: K‐1‐2 occurs in melanoma cell line SK‐Mel 25, but not in cell line A‐375. A‐375 has a higher malignant potential than SK‐Mel 25 because, in contrast to SK‐Mel 25, it produces plasminogen activator and grows in nude mice. K‐1‐2 was frequently strongly expressed (≥ 50% cells positive) in flat (< 1.5 mm) and less frequently in medium and thick primary tumors. In thick primary melanomas K‐1‐2 positive cells were confined to the junctional zone or to marginal, flat areas of the tumor. Only rarely does K‐1‐2 occur in metastases. Strong expression of the K‐1‐2 antigen was found less often in primary melanomas, which develop early metastases, than in tumors that had not metastasized during an observation period of 18 months. In 5 patients with disseminated metastatic disease, metastases strongly expressing K‐1‐2 and those negative for this marker or containing only a minor percentage of K‐1‐2 positive cells were observed simultaneously or at different times. These findings suggest that a change from high malignancy to low malignancy—as observed in animal systems—may also occur in human melanoma.
Isolation and characterization of an activated c‐H‐ras‐1 gene from a squamous‐cell lung carcinoma cell line
Authors: Kagimoto Masaaki , Miyoshi Jun , Tashiro Kosuke , Naito Yasushi , Sakaki Yoshiyuki , Sueishi Katsuo , Tanaka Kenzo , Imamura Takashi 
Published: February 2007

AbstractWe determined a complete nucleotide sequence of an activated form of the c‐H‐ras‐1 proto‐oncogene cloned from the human cell line (QG56), using the DNA transfection technique and NIH3T3 cells as recipients. This cell line was established from a squamous‐cell lung carcinoma of a Japanese patient, and the activated gene had 2 nucleotide substitutions. One substitution of a thymidine for an adenosine was found at position 1069 of the 2898 nucleotide sequence in a restriction endonuclease (Sacl) fragment, which corresponds to the second base of the 61 st codon of the gene encoding P 21 protein. This nucleotide replacement was assumed to be responsible for the transforming activity. Another substitution of a guanosine for an adenosine which was detected at position 746 in the first intron was thought to be a genetic polymorphism unassociated with the transforming activity. Comparison of the various lengths of restricted fragments suggested that the activity was markedly influenced by certain sequences flanking the c‐H‐ras‐1 gene.
Characterization of murine hepatoma BW7756. III. Hematological profile of a tumor‐associated anemia
Authors: Mizejewski G. , Chao E. 
Published: February 2007

AbstractA severe anemia develops in recipient C57L/J mice after syngeneic transplantation of the BW7756 murine hepatoma. The tumor undergoes an exponential growth spurt in the 14–21 days post‐implantation, accompanied by a parallel increase in serum alpha‐feto‐protein levels and a significant decrease of hemoglobin concentration and hematocrit extending to the 28th day. Concomitant with the decreased hematocrit, the blood volume displayed a 10% increase. The blood cell population was generally one of reticulocytosis and leukocytosis. Mild icteric plasma was observed and both “cold” and “warm” antibodies were detected in the sera of tumor‐bearing mice. An elevation of IgM was observed by day 7, followed by a depletion of IgG1 and IgG2 throughout the tumor growth period. When RBCs of tumor‐bearing mice were compared to those of normal mice, the same degree of osmotic fragility was found. However, the lifespan of the transfused RBC was shorter in tumor‐bearing mice than in normal mice (half‐life: 2 days vs. 4 days). The data suggest a type of auto‐immune hemolytic anemia which is analogous to various hematopoietic disturbances described for murine hosts bearing solid tumors distal to hematopoietic sites.
Effect of human serum anti‐htlv antibodies on viral antigen induction in In vitro cultured peripheral lymphocytes from adult T‐CELL leukemia patients and healthy virus carriers
Authors: Tochikura Tadafumi , Iwahashi Masato , Matsumoto Tadashi , Koyanagi Yoshio , Hinuma Yorio , Yamamoto Noaki 
Published: February 2007

AbstractLeukemic cells of adult T‐cell leukemia (ATL) patients contain human T‐cell leukemia virus type I (HTLV‐I) genomes. However, viral antigens (HTLV‐A) are not usually expressed in vivo. It has been shown that HTLV‐I antigens are spontaneously induced after culture of peripheral blood lymphocytes (PBL) from patients with ATL and healthy carriers (HC), who are viral antibody‐positive. In the present communication, we show the suppressive effect of human serum antibodies against HTLV‐I on viral antigen expression in PBL derived from ATL patients and HC. Viral antigen synthesis in various PBL specimens is variable in terms of frequencies and kinetics. (I) Low concentrations (2%) of antibody‐positive but not of antibody‐negative sera efficiently suppressed HTLV antigen induction in lymphocytes from both ATL patients and HC. (2) An inhibitory effect was exerted by HTLV‐I‐specific antibodies which originated from either ATL, HC or even HTLV‐I‐positive monkeys. (3)Sera showed a fairly wide range of suppressive activity in view of their wide range of suppressive activity in view of their concentrations. (4) At the late stage of cultures even continuous presence of antibodies frequently failed to suppress antigen synthesis in lymphocytes. (5) Antibodies were less effective in suppressing the increase of antigens if they were added to cultures which had already HTLV‐A‐positive lymphocytes in antibody‐free media. (6) Pretreatment with protein A completely abolished the activities of the suppressive plasmas. (7) Antibodies did not affect the inhibition of spontaneous or chemical induction of HTLV‐A in 2 HTLV‐I‐positive cell lines. These results suggest that HTLV‐I antigen expression in leukemic cells from patients with ATL in vivo and in vitro is partly regulated by antibodies to HTLV‐I. Furthermore, at least 2 different pathways, one antibody‐sensitive and the other ‐insensitive, might exist to express HTLV‐A.
Descriptive epidemiology of colorectal cancer
Authors: Boyle P. , Zaiudze D. G. , Smans M. 
Published: February 2007

AbstractThe purpose of this report is to present the descriptive epidemiology of colorectal cancer using the most recent data available to highlight two characteristics of the disease. First is the great variation which takes place in the frequency of this disease over geographic areas of all sizes. Colorectal cancer is common in most countries of North America and Europe, is rare in Asia and is particularly uncommon in Africa. Internationally, the variation in colon cancer is 60‐fold, and within Europe there is a 4‐fold difference in the incidence of colon cancer between areas with the highest and lowest rates. For cancer of the rectum, variation internationally is 18‐fold and within Europe it is 3‐fold. Within the United Kingdom, colon cancer is uniformly higher in the 5 Scottish Cancer Registry Regions than in their counterparts in England and Wales. Even within Scotland there is a 4‐fold range of colon cancer incidence rates, with the North and South clearly demarcated by a striking difference in colon cancer incidence in both sexes. Secondly, examination of international mortality rates for colorectal cancer demonstrates remarkable differences in trends over time between countries. In countries where colorectal cancer mortality rates were initially low, rates have increased substantially. In many countries where rates circa 1950 were moderately high, they have increased slightly or become stabilized. However, in countries such as Scotland, Canada, England and Wales and the United States, where rates were initially high, there have been gradual falls in mortality over time.
Seroepidemiologic Studies Of Human T‐cell leukemia/lymphoma virus type I in Jamaica
Authors: Clark Jeffrey , Ensroth Arthur , Blattner William A. , Saxinger Carl , Robert‐Guroff Marjorie , Gallo Robert C. , Gibbs W. Nigel , Lofters Wycliff , Lagranade Lois , Deceulaer Karel 
Published: February 2007

AbstractThe prevalence of HTLV‐I antibodies was evaluated in Jamaica among persons with various malignant, infectious, autoimmune and hematologic disorders and in clinically normal persons. Results document that: (1) the prevalence of HTLV‐I antibodies in this population increases with age; (2) overall, there is no significant difference in the antibody prevalence between males and females; (3) antibody‐positive individuals are born in all major regions of the island and geographical variance in antibody prevalence by place of birth was not prominent; (4) there is further confirmation of the high prevalence of HTLV‐I antibody‐positive lymphomas in Jamaica; and (5) the prevalence of HTLV‐I antibodies in hemophiliacs, patients with chronic lymphocytic leukemia (CLL), myelogenous leukemias, and patients with breast cancer is higher than in the age‐matched population without malignancies, although none of these differences were statistically significant. The increased prevalence in hemophiliacs is most likely related to their frequent transfusion with blood products, but it has not yet been determined whether the prevalence in patients with other diseases is related to their diseases or other as yet undefined factors in common.
Endemic african kaposi's sarcoma is not associated with immunodeficiency
Authors: Kestens Luc , Melbye Mads , Biggar Robert J. , Stevens Wim J. , Piot Peter , De Muynck Aimé , Taelman Henri , De Feyter Marc , Paluku L. , Gigase Paul L. 
Published: February 2007

AbstractTwenty‐seven histologically confirmed Kaposi sarcoma (KS) patients resident in the Kivu Lake area of eastern Zaire were examined for immune competence. Only KS cases of the endemic African type have been observed in this high‐incidence area. The median duration of the symptoms was 6 years and ranged from 1 to 38 years. Forty‐one controls matched for age, sex and tribe and unrelated to the KS patients were selected from the community. Thirteen additional controls were first‐degree relatives of the KS patients. No evidence of immune suppression among KS patients was found and there were no significant differences in the immune status between KS patients and controls. Total lymphocytes, B and T cells, and OKT4 + and OKT8 + cells varied within the normal range. Grouping of the KS patients in categories according to duration and disease extent did not reveal significant differences in their immune status. The number of KS patients reacting positively in a skin test to 5 recall antigens and I mitogen was similar that of controls, except in the case of candidin, to which a higher number of KS patients were negative. The serum levels of immunoglobulins, complement factors and circulating immune complexes were comparable in KS patients and controls. Indicators of inflammatory processes [white blood cells (WBC), complement‐reactive protein (CRP)] were positive in 27% of the KS patients. The prevalence and mean titer of antibody against cytomegalovirus (CMV), Epstein‐Barr virus (EBV), hepatitis B virus (HBV) and syphilis were similar in KS patients and in controls.
Immunohistochemical localization and molecular characteristics of three monoclonal antibody‐defined epitopes detectable on carcinoembryonic antigen (CEA)
Authors: Bosslet K. , Lüben G. , Schwarz A. , Hundt E. , Harthus H. P. , Seiler F. R. , Muhrer C. , Kayser K. , Klöppel G. , Sedlacek H. H. 
Published: February 2007

AbstractThree murine monoclonal antibodies (MAbs) reactive to different epitopes on CEA were selected according to their ability to bind to various human tissue sections. The most selective MAb, BW 431/31, bound to the majority of colon carcinomas but only faintly to normal colon mucosa. In addition to the tissues stained by MAb BW 431/31, MAb BW 250/183 reacted with granulocytes, colon mucosa and faintly with pancreatic ducts. The third MAb, BW 374/14, reacted with granulocytes, colon mucosa, strongly with pancreatic ducts and with alveolar and bronchial epithelium. The antigenic determinants recognized by the 3 MAbs in human tissue sections were resistant to formaldehyde fixation and paraffin embedding as well as to periodic acid oxidation and neuraminidase treatment. The last two treatments suggest that the epitopes are protein in nature. Using MAb affinity chromatography, 3 antigen preparations were isolated from a human colon carcinoma xenograft with an approximate molecular weight of 180 kd. These preparations were shown to bear the epitopes from each of the MAbs and from a polyclonal antiserum specific for purified CEA. Furthermore, the ability of MAb BW 431/31 to localize its antigenic determinant in vivo on a human colon carcinoma xenograft is evaluated and its possible application in the patient is suggested.
Tumor‐derived chemotactic factor(S) from human ovarian carcinoma: Evidence for a role in the regulation of macrophage content of neoplastic tissues
Authors: Bottazzi B. , Ghezzi P. , Taraboletti G. , Salmona M. , Colombo N. , Bonazzi C. , Mangloni C. , Mantovani A. 
Published: February 2007

AbstractSupernatants from freshly disaggregated human ovarian carcinomas maintained in vitro for 24 hr, from primary ovarian carcinoma cultures (4–6 days in culture) and from established ovarian cancer cell lines were examined for chemotactic activity on blood monocytes in blind‐well chemotaxis chambers. Tumor‐cell culture supernatants induced migration of peripheral blood monocytes across polycarbonate filters with considerable heterogeneity among different tumors. Induction of migration occurred only in the presence of a gradient between the lower and upper compartments of the chamber. Chemotactic activity was characterized by means of supernatants from primary ovarian carcinoma cultures. Chemotactic factor(s) was (were) produced in serum‐free conditions and the production was inhibited by emetine but not by mitomycin C. The activity was destroyed by exposure to proteolytic enzymes and by heating at 100°C but was unaffected by RNase, DNase, lipase and exposure to extreme pH values or heating at 56°C. Upon fractionation on Sephadex G 75, the activity eluted as a single peak in the cytochrome C region, corresponding to an apparent molecular weight of about 12 kd. The percentage of macrophages was assessed in 25 freshly disaggregated tumor specimens. Ovarian carcinomas were heterogeneous in their macrophage content with values ranging from 4 to 36%. A significant (r = 0.62; p = 0.00097), though far from absolute, correlation was found between chemotactic activity of culture supernatants and percentage of tumor‐associated macrophages. Tumor‐derived chemotactic factor(s) could be one of the mechanisms involved in the regulation of the macrophage content of human ovarian carcinomas.
Migration and death from malignant melanoma
Authors: Cooke K. R. , Fraser J. 
Published: February 2007

AbstractThe age‐standardized mortality rates for malignant melanoma of the skin in immigrants to New Zealand were compared with those of New Zealand‐born non‐Maoris. Immigrants from European countries had mortality rates that were generally similar to those prevailing in their countries of origin, although, among immigrants from the British Isles, early age at migration was associated with a mortality rate similar to that of New Zealand‐born non‐Maoris. In a community survey, British immigrants were not less likely to have had severe sunburn, but had fewer moles, than New Zealand‐born non‐Maoris. The lower melanoma mortality, and the effect of age at migration, could be mediated by differences in mole frequency.
Prevalence of polyps in an autopsy series from areas with varying incidence of large‐bowel cancer
Authors: Clark John C. , Collan Yrjö , Eide Tor J. , Estève Jacques , Ewen Stanley , Gibbs Norman M. , Jensen Ole M. , Koskela Erkki , MacLennan Robert , Simpson John G. , Stalsberg Helge , Zaridze David G. 
Published: February 2007

AbstractThe results of this multicentre autopsy study emphasize the relationship between the prevalence of adenomas and the incidence of large‐bowel cancer. The highest proportion of autopsies with adenomas was observed in the area with the highest incidence of large‐bowel cancer. The segmental distribution of adenomas within the colon was found to be similar to the site distribution of cancer. However, the lowest proportion of adenomas was found in the rectum, the segment in which cancer is most frequent. The latter finding suggests that either the adenoma‐carcinoma sequence is a less important pathway in the pathogenesis of rectal cancer, or that more rectal than colonic adenomas become malignant. The high proportion of hyperplastic polyps in the rectum, and statistically significant regional differences following the same patterns as the incidence of rectal cancer suggest that there could be at least an indirect relationship between hyperplastic polyps and cancer of the rectum. Adenomas of both colon and rectum were more frequent in men than in women, contrary to findings with colon cancer. However, as for colon cancer, the sex ratio of adenomas changed with age, from slightly below unity in persons under 65, to above unity for those aged 65 and over. A major difficulty that emerged was the histological identification of ‘polyps’ because of the degree of autolysis of epithelial cells in the mucous membrane, and this difficulty largely contributed to the poor consistency of histological reporting. Regular consistency surveys of histological preparations should be recommended in any type of multicentre study in which histological examination is included.
Detection of sialylated lewisX antigen in cancer sera using a sandwich radioimmunoassay
Authors: Kawahara Masaaki , Chia David , Terasaki Paul I. , Roumanas Athan , Sugich Lee , Hermes Mark , Iguro Takashi 
Published: February 2007

AbstractA monoclonal antibody directed against sialylated Lewisx (SLEX) was tested with the serum of 615 cancer patients, 166 patients with non‐malignant diseases, and 136 normal persons. The SLEX antibody reacted with the sera of the cancer patients in the following percentages: 29% lung, 19% breast, 12% ovary, 25% colorectal, 13% head and neck, and 13% miscellaneous. SLEX was positive for 22% of stages III and IV (latestage) cancers as compared with 5% early‐stage tumors. Among 80 patients with adenocarcinoma of the lung in the late stages, 45% were positive for SLEX. However, among 54 patients having squamous‐cell lung cancer in the late stages, 15% were positive. In 25 cases of small‐cell lung cancer, 24% were positive. Among patients who had measurable lung cancer, 4/7 with adenocarcinoma over 3 cm in diameter were positive whereas 0/16 patients with tumors under 3 cm were positive. Four patients who had tumor regression showed a more than 50% decrease in SLEX values whereas in 7 patients with progressive tumors, a more than 50% increase in SLEX levels was found. When tested simultaneously with CEA, SLEX produced positive reactions with the sera of some patients who were negative for CEA. The reaction pattern was distinct, indicating that another antigen was being detected. When used in combination, the percentage of sera that were positive increased. We conclude that the use of SLEX is useful for monitoring of cancer patients.
Hereditary malignant melanoma is not linked to the hla complex on chromosome 6
Authors: Bale Sherri J. , Greene Mark H. , Murray Christine , Goldin Lynn R. , Johnson Armead H. , Mann Dean 
Published: February 2007

AbstractDetailed HLA typing was performed in 11 families with hereditary cutaneous malignant melanoma (CMM) and dysplastic nevi to determine if the melanoma susceptibility locus was genetically linked to the major histocompatibility complex. Previously published data from 19 other families were re‐analyzed in the same manner. When data from all 30 families were pooled and CMM was defined as the disease trait, the hypothesis of linkage was rejected for all values of recombination (θ) less than 40%. Data on family members′ status regarding dysplastic nevi (DN), a well‐characterized precursor of hereditary CMM, were available for our 11 families and 7 previously‐reported families. Linkage analysis between the combined CMM/DN trait and HLA provided strong evidence against this hypothesis. Significant heterogeneity was observed when various sub‐groups of families were compared; these data suggested that preferential reporting of positive linkage findings and misclassification of study subjects′ CMM susceptibility status may have contributed to previous beliefs that the hereditary melanoma gene was linked to HLA. When our data are combined with previously‐published information, we conclude that there is strong evidence against linkage of a CMM/DN gene with the major histocompatibility complex.