bluuebunny/crossref_metadata_2025_split huggingface dataset:
Lectin‐resistant variants of mouse melanoma cells. I. Altered metastasizing capacity and tumorigenicity
Authors: Tao Tien‐Wen , Burger Max M. 
Published: February 2007

AbstractFrom C57BL mouse melanoma B‐16 cells, variant clones were selected in vitro which were resistant to the lectins wheat‐germ agglutinin and ricin. Cells were also selected which survived toxic concentrations of concanavalin A. Four different In vivo assays using intradermal, intravenous, intraperitoneal and intramuscular injections were used to assess the tumorigenidty and metastasizing capacity of these lectin‐resistant variants. It was concluded that to obtain a complete picture of the malignant properties of a given cell line or clone, all four assays have to be carried out. In comparison with the parental cells, the WGA‐resistant cells showed a most dramatic decrease in metastasizing capacity through both lymphatic and vascular channels. Tumorigenidty was also reduced. The ricin‐resistant cells showed a defective development into lung tumors and thus displayed a reduction in metastasis through the hematogenous route. Since this line did not change its capacity to metastasize via the lymphatic route, and the tumorigenidty was not significantly altered, it will be a good model for studies seeking to dissociate these two properties. The Con‐A‐selected cells, when injected intravenously, developed tumor nodules in the liver in addition to those in the kings, while no striking alterations in tumorigenicity or metastasizing capacity could be detected in this line.
Non‐random chromosomal changes involving chromosomes 6 and 7 in spontaneous rat immunocytomas
Authors: Wiener Francis , Babonits Magda , Spira Jack , Klein George , Bazin Herve 
Published: February 2007

AbstractG‐banding analysis of seven Ig‐secreting spontaneous rat immunocytomas showed a consistent translocation of the distal part of the q‐arm of chromosome 7 to the telomerk end of chromosome 6. The breakpoints were assigned to q3.3 on chromosome 7 and q3.2 on chromosome 6. Previously, we found a similar translocation pattern in mouse plasmacytomas induced by different agents. The distal part of die q‐arm of chromosome 15 was translocated to the telomerk end of chromosome 12, known to carry Igh, the immunoglobulin heavy chain cluster. The banding homologies between the chromosomes involved in the translocations in the two species suggest that a similar mechanism is responsible for plasmacytomagenesis in both. We also predict that the rat Ig heavy chain gene cluster will be located to the terminal segment of chromosome 6.
Carcinogenicity of phenacetin: Long‐term feeding study in B6C3F1 mice
Authors: Nakanishi Keisuke , Kurata Yasushi , Oshima Masato , Fukushima Shoji , Ito Nobuyuki 
Published: February 2007

AbstractGroups of 52 B6C3F1 mice of each sex were maintained on a diet containing 1.25 or 0.6% phenacetin for 96 weeks and then fed a basal diet for 8 weeks. Control groups consisted of 50 mice of each sex and were fed a basal diet for 104 weeks. All animals were killed at the end of the experiment and all organs were examined histopathologically. Mice that died during the experiment were also autopsied and those that survived for more than 57 weeks, when the first tumor was observed, were also included in the effective number of mice. Tumors were found in the kidney, liver, lung, skin, hematopoietic system (leukemia or lymphoma) and occasionally in some other organs. The dose‐related induction of renal cell tumors in the male mice fed phenacetin was clearly demonstrated in this experiment. Urinary bladder lesions that developed in the mice of either sex fed 1.25% phenacetin were also considered to be due to the tumorigenicity of phenacetin. Tumors of other organs in either the phenacetin‐treated or the control group were regarded as strain‐related spontaneous tumors of B6C3F1 mice.
Enrichment of cell populations containing terminal deoxynucleotidyl transferase activity by free flow electrophoresis
Authors: Sarin P. S. , Virmani M. , Gallo R. C. 
Published: February 2007

AbstractTerminal deoxynucleotidyl transferase (TdT) is an enzyme that has been utilized as a biochemical marker for following certain leukemia patients during treatment and remission. The potential usefulness of this enzyme in predicting the onset of relapse before any morphological indications has been demonstrated in chronic myelogenous leukemia patients in blast phase of the disease. In order to be able to detect low levels of TdT activity, especially during remission phase, we have used the technique of free flow electrophoresis to enrich cell populations containing TdT. With this technique we have achieved up to 20‐fold enrichment of TdT‐positive cell populations from normal human bone marrow, cells from patients with acute lymphoblastic leukemia and chronic myelogenous leukemia in blast phase of the disease. TdT positive cells were not detected in patients with acute myelogenous leukemia and B cell lines. This technique should prove to be useful in early detection of relapse in patients in remission and for enrichment of cell populations containing other biochemical markers.
A monoclonal antibody (B72.3) defines patterns of distribution of a novel tumor‐associated antigen in human mammary carcinoma cell populations
Authors: Nuti Marianna , Teramoto Yoshio A. , Mariani‐Costantini Renato , Hand Patricia Horan , Colcher David , Schlom Jeffrey 
Published: February 2007

AbstractWe report here both the range and patterns of reactivity of an IgG1, monoclonal antibody, B72.3, prepared against human metastatic mammary carcinoma cells. When the avidin‐biotin complex (ABC) immunoperoxidase technique was used on tissue sections, monoclonal B72.3 reacted with 19 of 41 (46%) primary mammary carcinomas and 13 of 21 (62%) metastatic lesions, either in axillary lymph nodes or at distal sites. Variable concentrations of antigen, recognized by B72.3, were observed among mammary tumors, as well as among different cell populations of a given tumor mass. Several patterns of antigen distribution were observed: membrane, diffuse cytoplasmic, focal, apical and marginal. No reactivity was observed to normal mammary epithelium, stroma, or lymphocytes of the breast, nor to any cell types in a variety of other normal human tissues, melanomas, and sarcomas. Reactivity with all of four colon carcinomas was also observed. Assay of serial sections of mammary carcinomas with B72.3 and a monoclonal antibody directed against carcinoembryonic antigen demonstrated that these antigens were both distinct and non‐coordinately expressed.
Selective depletion of nk cell activity in vivo and its effect on the growth of NK‐sensitive and nk‐resistant tumor cell variants
Authors: Kawase Ichiro , Urdal David L. , Brooks Colin G. , Henney Christopher S. 
Published: February 2007

AbstractIntravenous injection of rabbit anti‐asialo‐GM1 serum, an antiserum previously shown to eliminate splenic natural killer (NK) activity in vitro, profoundly depressed NK activity in CBA, DBA/2 and BALB/c nu/nu mice. The effect on NK activity was selective, as treatment of mice with anti‐asialo‐GM1 serum did not affect the development of other cytotoxic cells including cytotoxic macrophages following injection of poly I:C, or cytotoxic T cells in response to allogeneic cells. The role of NK cells in controlling tumor cell growth was investigated using an NK‐sensitive (cl 27v‐IC2) and an NK‐resistant (cl 27av) subline of the murine lymphoma L5178Y. Initial studies showed that cl 27v‐IC2 cells were at least 100 times less tumorigenic than were cl 27av cells in both syngeneic DBA/2 mice and BALB/c nu/nu mice. In addition, treatment of DBA/2 mice with poly I:C, which boosted NK activity, markedly depressed the growth of cl 27v‐IC2 cells, but not of cl 27av cells. On the other hand, treatment of DBA/2 mice and BALB/c nu/nu mice with antiasialo‐GM11 serum led to a marked increase in tumorigenicity of cl 27v‐IC2 cells, but had no effect on the tumorigenicity of cl 27av cells. In addition, the protection against cl 27v‐IC2 growth afforded by poly‐I:C treatment was abrogated by injection of anti‐asialo‐GM1 serum. The possibility that the effects observed were caused by binding of the injected antibodies to the tumor cells was minimized by: (1) using a clone of tumor cells (cl 27v‐IC2) that lacks chemically detectable asialo‐GM1, and (2) pre treating animals with anti‐asialo‐GM1 rather than administering antiserum and tumor cells concurrently. These studies provided compelling evidence that NK cells could play an active role in controlling tumor growth. Selective depletion of NK activity by injection of antiasialo‐GM1 serum is a method which would be generally applicable to studying the role of NK cells in disease processes.
Separation of high mammary tumor incidence from high hepatoma incidence in backcross mice during segregation of the viable yellow gene
Authors: Smith Gilbert H. , Vlahakis George 
Published: February 2007

AbstractMammary tumorigenesis in strain C3H‐vyfB female mice (approximately 90% incidence) is not due to exogenous mouse mammary tumor virus (MMTV) but to genetic factors transmitted by either parent. Prominent among these genetic factors is the viable yellow (Avy) gene which may increase either the virulence of the endogenous MMTV provirus (Mtv‐l) by promoting expression or the susceptibility of the mammary tissue to tumorigenesis by endogenous MMTV. Crosses were made between the viable yellow strain, C3H‐AvyfB/He(AvyAay) and C3H/Sm (AA) to give heterozygous (AvyA) F1 yellow hybrids from which yellow (Avy) and agouti (AA) back‐cross progeny were produced by mating with C3H/Sm males. AvyA backcross females were expected to have at least twice as many mammary tumors as the AA back‐cross females if the Avy gene were solely responsible for the high incidence of mammary tumors in C3H‐AvyfB since mammary tumor incidence is 90% in AvyfB and 40% in (AA)C3HfB. Alternatively, if the high tumor incidence in C3H‐AvyB were due to a more active endogenous MMTV (Mtv‐l), then a much smaller difference in the mammary tumor incidence of AvyA versus AA backcross females would be expected. The more reactive endogenous MMTV would occur equally between yellow and agouti females, since the C3H Mtv‐l gene is present on a separate chromosome from the Avygene. Unexpectedly, the F1 hybrid females (AvyA) developed mammary tumors at a relatively low rate (28.9%) although hepatoma incidence remained high (89.5%). Both yellow (AvyA) and agouti (AA) backcross females showed an even greater reduction in mammary tumor incidence, 7.9% and 3.8% respectively. In contrast, the high rate of spontaneous hepatoma development segregated with the Avy gene since 86‐5% of the yellow (AvyA) backcross females development hepatomas by 19 months of age, while only 25% of the agouti (AA) backcross females had liver tumors at 24.4 months. The reduction of mammary tumor incidence in (C3H‐AvyfB × C3H/Sm)F1 hybrids was unexpected since earlier studies had shown that reciprocal F1, hybrids between strains BALB/c and C3H‐AvyfB continued to show a 90% mammary tumor incidence. The present result is consistent with the possibility that strain C3H/Sm possesses a heritable factor(s) which attenuates the ability of endogenous MMTV to malignantly transform mammary epithelium.
Geographic pathology of latent prostatic carcinoma
Authors: Yatani Ryuichi , Chigusa Ichiro , Akazaki Kaneyoshi , Stemmermann Grant N. , Welsh Ronald A. , Correa Pelayo 
Published: February 2007

AbstractProstates obtained at autopsy from black and white males in the United States of America, from Colombians, from Japanese migrants in Hawaii, and from Japanese in Japan (all over 50 years old) were serially step‐sectioned and examined microscopically using identical techniques and diagnostic criteria. The age‐adjusted overall prevalence of latent carcinoma was significantly higher in US blacks (36.9%), in US whites (34.6%) and in Colombians (31.5%) than in Japanese in Japan (20.5%). There was no significant difference in prevalence between Japanese migrants in Hawaii (25.6%) and Japanese in Japan. When the carcinomas were subdivided into latent infiltrative type (LIT) and latent non‐infiltrative type (LNT), the LIT component reflected upon the overall prevalence of latent carcinoma. There was an increase in the overall prevalence of latent carcinoma and in the prevalence of LIT tumors with age in Japanese migrants to Hawaii and in Japanese of Japan but only a suggestive increase in blacks and whites in the United States. There was no significant relation between age and prevalence in Colombia. In LNT tumors, there was no consistent trend related to race or age. The size of LIT tumors was significantly greater than that of LNT tumors in all races or in each decade of total material. There were many large LIT tumors in blacks and whites in the United States. These results suggest that the prevalence of LIT tumors shows a race variation similar to the incidence of clinical carcinoma of the prostate, and that LNT tumors probably remain latent during the individual's life span.
A monoclonal antibody with anti‐burkitt lymphoma specificity. I. Analysis of human haematopoietic and lymphoid cell lines
Authors: Wiels J. , Lenoir G. M. , Fellous M. , Lipinski M. , Salomon J. C. , Tetaud C. , Tursz T. 
Published: February 2007

Abstract38‐13 is a hybridoma‐produced monoclonal rat IgM which appears to define a Burkitt's lymphoma‐associated antigen (BLA). In this paper, we describe the reactivity of 38‐13 with a panel of human haematopoietic and lymphoid cell lines. In indirect immunofluorescence (IF) assays, 15 of 26 Burkitt's lymphoma (BL) lines studied were clearly stained with 38‐13 (from 13 to 100% positive cells) by microscope, with varying numbers of heavily labelled cells. In these positive cell lines, fluorescence‐activated cell‐sorter (FACS) analysis demonstrated that BLA was actually present on all the cells. Positive BL included Epstein‐Barr virus (EBV) genome‐carrying lines and EBV‐negative ones; thus, BLA is not related to the presence of EBV. Most of the 15 BL cells that reacted with 38‐13 contained a typical t(8;14) translocation, but had variant translocations such as t(2;8) and t(8;22). The cells were derived from BL patients of different geographical origins and clinical features. Four BL lines were poorly stained and seven were negative with 38‐13 in IF assays. The 32 EBV‐positive lymphoblastoid cell‐lines (LCL) studied were negative. In three line pairs, consisting of a tumor line and an LCL from the same patient, only the BL line was demonstrated to react with 38‐13. A series of non‐BL cells, including haematopoietic, lymphoid and solid tumor lines, all failed to react with 38‐13. Various attempts to modulate the expression of BLA on BL cells were unsuccessful. However, it cannot be ruled out that BLA is actually a transient B‐cell differentiation marker.
SOMATOSTATIN‐REDUCED PROLIFERATION OF MURINE APLASTIC CARCINOMA CONDITIONED TO DIABETES
Authors: Vuk‐Pavlović S. , Božikov V. , Pavelić K. 
Published: February 2007

AbstractMurine mammary aplastic carcinoma, when it is passed from one alloxan‐diabetic animal to another, after several passages becomes conditioned to hypoinsulinemia by secreting its own substances(s) immunologically cross‐reactive with insulin (SICRI). Although not cytotoxic, the total daily dose of 2.5 mg of synthetic linear somatostatin per one kg body mass, administered in three or more portions, retards tumor growth in normoinsulinemic mice and the proliferation of tumors preconditioned by three serial passages in diabetics. After the first passage, somatostatin treatment has no effect on the already slow growth of the unconditioned tumor. Somatostatin‐reduced tumor proliferation is accompanied by the strong suppression of insulin and SICRI levels, respectively; this effect is completely abolished by the administration of modest doses of crystalline insulin. It is concluded that somatostatin retards tumor growth by diminution of plasma levels of insulin and SICRI, respectively.
Possible role of a retrovirus in the expression of tumor‐specific antigens of the meth a sarcoma.
Authors: Deleo Albert B. , Chang Kenneth S. S. , Wivel Nelson A. , Appella Ettore , Old Lloyd J. , Law Lloyd W. 
Published: February 2007

AbstractThe serologically defined tumor‐specific surface antigen (TSSA) of the chemically‐induced BALB/c Meth A sarcoma, highly restricted to one of 20 sarcomas of BALB/c origin, has been detected on a Moloney murine sarcoma virus (Mo‐MuSV)‐transformed BALB/c 3T3 cell line, designated IIA(v). The immunogenicity of the IIA(v) cell in tumor‐rejection assays was specific for the Meth A sarcoma, supporting the evidence for a close relationship between the TSSA and the tumor‐associated transplantation antigen (TATA) of this tumor. Infection of SC‐I cells with retroviruses present in cultured filtrates of IIA(v) cells resulted in Meth A antigen expression. The retroviruses associated with Meth A antigen expression have been tentatively identified as replication and/or transformation‐defective XC‐ MuLV. The possible roles of Mo‐MuSV and cellular genes of the BALB/c strain of mice in the expression of the Meth A antigen are discussed.
Antigens of the basement membrane and the peritumoral stroma in human colonic adenocarcinomas: An immunofluorescence study
Authors: Burtin P. , Chavanel G. , Foidart J. M. , Martin E. 
Published: February 2007

AbstractTwenty colonic adenocarcinomas were studied by immunofluorescence with antisera against components of the basement membrane: type IV collagen, laminin and heparan sulfate‐rich proteoglycan, as well as antisera against antigens of the connective tissue: type‐III collagen, fibronectin and hyaluronectin. Marked alterations of the basement membranes were consistently observed on staining with each one of the first three antisera. In contrast, staining of the normal components of connective tissue was in most cases as intense as in normal colonic mucosa. Hyaluronectin, a marker of peritumoral stroma, was found to be present in 12 out 15 tumors studied.
Histopathological features of rapidly progressing breast carcinoma in Tunisia: A study of 94 cases
Authors: Costa J. , Webber B. L. , Levine P. H. , Muenz L. , O'Conor G. T. , Tabbane F. , Belhassen S. , Kamaraju L. S. , Mourali N. 
Published: February 2007

AbstractThe histological features of 94 cases of carcinoma of the breast seen in Tunisia were recorded and subsequently correlated with the clinical classification of the patients in terms of poussée évolutive (PEV) categories. Histological features analyzed in the breast tissues and skin included tumor type, nuclear grade, number of mitoses, involvement of the dermis, cutaneous inflammatory infiltrate and edema. Twenty‐eight percent of the cases in which the skin was examined showed tumor emboli in the lymphatics of the dermis. The frequency of cutaneous permeation correlated with the PEV categories. The percentage of cases with nuclear grade 3 was higher for the group with rapid progression of the disease (PEV 1,2,3) than for the cases belonging to the PEV‐0 category (90% versus 64.2%). The present study demonstrates that a large proportion of breast carcinoma patients in Tunisia suffer from “inflammatory carcinoma of the breast”.
Hepatitis B virus and primary hepatocellular carcinoma: Family studies in Korea
Authors: Hann Hie‐Won L. , Kim Chung Yong , London W. Thomas , Whitford Pamela , Blumberg Baruch S. 
Published: February 2007

AbstractChronic infection with hepatitis B virus (HBV) is closely associated with the etio‐pathogenesis of primary hepatocellular carcinoma (PHC). It has been proposed that infection with HBV early in life, frequently transmited by an HBV‐carrier mother, leads to persistent infection with HBV, which in turn is associated with the development of chronic active hepatitis (CAH), post‐necrotic cirrhosis and PHC. If this view is correct, then there should be clustering of chronic carriers of HBV in families of patients with chronic liver disease. We tested this hypothesis in Korea by collecting serum from 132 patients with these chronic liver diseases admitted to the Seoul National University Hospital and 664 of their first‐degree relatives. Controls (636) were members of two churches in Seoul and a rural village population; 261 of the controls were between the ages of 30 and 59, the age range that included 95% of the cases of chronic liver disease. Sera were assayed for hepatitis B surface antigen (HBsAg), antibody to HBsAg (anti‐HBs) and antibody to hepatitis B core antigen (anti‐HBc). Almost all cases showed evidence of present or past infection with HBV; 80% were HBsAg(+) and 14% were anti‐HBs(+); 100% of 47 cases of PHC, 100% of 35 cases of cirrhosis, and 94% of 50 cases of CAH were anti‐HBc(+); 6% of males and 4% of females in the control population (30–59 years of age) were HBsAg(+), 71% were anti‐HBc(+), and 51% were anti‐HBs(+), HBsAg(+) patients with chronic liver disease tended to be younger than HBsAg(−) patients with anti‐HBs or anti‐HBc antibodies. Mothers of patients were more frequently HBsAg(+) (9 of 33) than agematched women in the control population (0 of 34) or wives of patients (5 of 68). Five of 23 fathers were also HBsAg(+) compared with 1 of 25 age‐matched controls. As first observed in Africa, there was a deficit of anti‐HBs in the fathers of cases compared with the controls. Siblings of patients were frequently HBsAg(+) (45% of 154), with the highest prevalence in brothers (53%). Family history shows that five fathers, two mothers and five brothers of cases have died of PHC. These data are compatible with the hypothesis tested and lend further support to the view that prevention of infection with HBV will lead to a marked decrease in the incidence of CAH, cirrhosis and PHC in areas where these diseases are endemic. Members of the families of patients with these diseases are at high risk of developing persistent infection with HBV and chronic liver disease. It would be appropriate to focus preventive strategies on infants and children in such families.
Growth responses of rat stomach cancer cells to gastro‐entero‐pancreatic hormones
Authors: Kobori Oichiro , Vuillot Marie‐ThérèSe , Martin François 
Published: February 2007

AbstractVarious hormones and peptides were added to rat stomach cancer cells growing in vitro in a serum‐free medium and the cell number was determined by a spectro‐photometric method. Five gastro‐entero‐pancreatic hormones or related peptides (tetragastrin, glucagon, secretin, cholecystokinin‐pancreozymin and cerulein) significantly increased the number of stomach cancer cells from 150% to 310% of the number of control cells cultivated in a serum‐free, hormone‐free medium. On the other hand, insulin and vasoactive intestinal peptide, and other hormones (thyroxin, epinephrine, hydrocortisone, β‐estradiol, progesterone, testosterone), peptone broth and bovine serum albumin had no significant growth effect. All the active substances belong to the two major families of gastro‐entero‐pancreatic polypeptide hormones, suggesting the existence of hormone receptors at the surface of stomach cancer cells.