bluuebunny/crossref_metadata_2025_split huggingface dataset:
A prospective study of esophageal cytological atypia in linxian county
Authors: Lu Jian‐Bang , Yang Wen‐Xian , Dong Wen‐Zhou , Sang Jiu‐Yuan 
Published: September 2008

AbstractBetween I9TS and 1975, in Linxian county (LX), a prospective study of esophageal cytologrcal hyperplasia and atypia was conducted on 3 groups of subjects: 294 with marked atypia, 328 with mild hyperplasia and 336 normal controls; all were diagnosed by cytology. Results showed that no significant difference in incidence of esophageal cancer (EC) appeared between subjects with mild hyperplasia and controls, while the incidence of EC in subjects with marked atypia was 1,178.92/100,000 which was 2.39 (after age‐adjustment 2.90) times higher than that found in the control group and was of statistical significance (x2 = 8.92, p < 0.01). In all groups, the relatively high risk of contracting EC was closely associated with drinking ground water, smoking and a low standard of living. These results suggest that early treatment should be given to subjects with marked atypia, accompanied by preventive measures against carcinoma of the esophagus, such as hygienic drinking water, abstention from smoking and better living conditions.
Spatial relationship of chromosomes 9 and 22 at metaphase in patients with chronic myelogenous leukemia (CML)
Authors: Verma Ram S. , Thomas Samuel , Coleman Morton , Silver Richard T. 
Published: September 2008

AbstractOne hundred patients with Ph1‐chromosome‐positive chronic myelogenous leukemia (CML) with t(9;22) are included in the present investigation. The position of the Ph1 chromosome in relation to the normal as well as the abnormal chromosomes 9 was localized at metaphase in 1,000 bonemarrow cells. Our study suggests that the rearranged chromosomes, i.e., Ph1 and t(9;22), are closer together than their normal homologues. This impression is based on extensive statistical analysis. The intimate relationship may be due to the fact that they carry reciprocal genetic material responsible for a power of attraction between them. Alternatively, it is tempting to hypothesize that there may be a DNA sequence homology in the bands of chromosomes 9q and 22q involved in the reciprocal translocation perpetuating this relationship in subsequently generating cells during mitotic cell divisions. Furthermore, c‐abl and bcr genes might play some role in maintaining the spatial relationship.
Hormonal changes following tumor transplantation: Factors increasing corticosterone and the relationship of corticosterone to tumor‐induced anti‐inflammation
Authors: Normann S. , Besedovsky H. , Schardt M. , Del Rey A. 
Published: September 2008

AbstractEL‐4 lymphoma cells transplanted to syngeneic C57BL/6J mice induced a biphasic decrease in inflammation and a biphasic increase in serum levels of corticosterone. In addition, this tumor altered serum levels of 3 other hormones, resulting in a biphasic decrease in insulin, an early decrease in protactin, and a terminal severe deficiency in thyroxine. Early changes occurred 16 to 48 hr after tumor transplantation and were of variable duration, while late‐phase defects developed during the last few days of life. Soluble factors associated with tumor growth may mediate certain hormonal changes since serum levels of corticosterone increased and insulin decreased following injection of tumorous ascites into normal mice. Further, injection of cell‐free tumor culture supernatants increased corticosterone levels. Hormonal changes following injection of soluble factors occurred after a delay of 16 hr indicating that the factors acted indirectly. Surgical adrenalectomy blocked the corticosterone increase induced by tumor transplantation or ascites injection and eliminated the anti‐inflammatory effect of tumor transplantation while significantly decreasing the effect associated with injection of tumorous ascites. Thus, the physiologically induced increase in serum levels of corticosterone reached anti‐inflammatory levels. Further, elevated levels of corticosterone are a major contributing factor to anti‐inflammation induced by tumorous ascites injection and constitute the principal mechanism of anti‐inflammation following tumor transplantation.
Differential effects on expression of IL‐2 receptors (p55 and p70) by the HTLV‐I pX DNA
Authors: Sabe Hisataka , Tanaka Atsushi , Siomi Haruhiko , Koyasu Shigeo , Yonehara Shin , Yahara Ichiro , Tagaya Yutaka , Sugie Katsuji , Teshigawara Keisuke , Yodoi Junji , Hatanaka Masakazu 
Published: September 2008

AbstractAbnormal expression of the low‐affinity receptor for inter‐leukin‐2 (IL‐2R) is a characteristic of the HTLV‐I (+) leukemic T cells in adult T‐cell leukemia (ATL). Despite the expression of IL‐2R bearing Tac antigen (IL‐2R/pSS), leukemic cells of the majority of ATL patients do not proliferate in response to IL‐2. In the human NK cell line, YT, as well as in ATL‐derived T cells, the co‐expression of IL‐2R/p55 and the second IL‐2R without the Tac epitope (IL‐2R/p70) is required to produce high‐affinity IL‐2R. To study the effect of HTLV‐I on both of the IL‐2Rs, we transferred a fragment of HTLV‐I containing the p40X gene into YT cells. One of the 2 transfected YT clones (YT/pX‐5.1) had an increased level of expression of IL‐2R/p55. In contrast, expression of (L‐2R/p70 was unaffected, as determined by Scatchard analysis and the cross‐linking study using 125‐IL‐2. Our results show that the T‐cell phenotype is not required for induction of IL‐2R/p55 by p40X. We suggest that HTLV‐I infection induces a disproportionate induction of IL‐2R/pSS without significant enhancement of IL‐2R/p70 expression, resulting in the predominant expression of low‐affintty IL‐2R in ATL. IL‐2R/p70 may be a critical parameter determining the IL‐2 reactivity of HTLV‐I‐infected T cells as well as of normal lymphocytes.
Direct outgrowth of in vivo epstein‐barr virus (EBV)‐infected chronic lymphocytic leukemia (CLL) cells into permanent lines
Authors: Lewin Nongnit , Åman Pierre , Mellstedi Håkan , Zech Lore , Klein George 
Published: September 2008

AbstractIn the course of our efforts to characterize the EBV‐carrying cells that are responsible for direct growth or the 2‐step mechanism, based on virus release from the explanted cells and subsequent transformation of previously uninfected cells, we have encountered an unusual CLL patient who carried a small subpopulation of in vivo EBV‐infected leukemia cells. These were predominantly present in the low‐density fraction and grew into EBV‐carrying lines upon explantation after a relatively short latency period, 3‐4 weeks. Cytogenetic examination conclusively proved the leukemic origin of the established CLL lines. They carry a ring chromosome 15 and are trisomic for chromosome 12. The same changes are also found in the majority of the peripheral blood lymphocyte population. Taken together, our results suggest that the EBV‐genome and the cytogenetic changes may have contributed to the immortalization of the CLL cells in a complementary or synergistic fashion.
Frequent loss of heterozygosity at telomeric loci on 22q in sporadic colorectal cancers
Authors: Yana Ikuo , Kurahashi Hiroki , Nakamori Shoji , Kameyama Masao , Nakamura Tsutomu , Takami Motohisa , Mori Takesada , Takai Shinichiro , Nishisho Isamu 
Published: September 2008

AbstractTo date, several tumor‐suppressor genes responsible for the tumorigenesis of colorectal cancer have been identified. However, studies of loss of heterozygosity (LOH) have suggested several chromosomal regions which may contain additional tumor‐suppressor genes for colorectal cancer. To determine the extent and variation of allelic loss on 22q, on which LOH has been frequently observed, a total of 68 sporadic colorectal cancers was examined for LOH on the chromosome arm by means of 16 polymorphic DNA markers. LOH was observed in 28 tumors (41 %), of which 9 showed LOH at all informative loci. The remaining 19 tumors showed variable patterns of partial loss on 22q, delimiting the smallest region of overlap (SRO) between D22S90 and D22S94. Moreover, LOH within the SRO correlated with a progression in terms of Dukes' stages. These results suggest that an additional tumor‐suppressor gene for colorectal cancer may exist on 22q distally to the NF2 locus and that inactivation of the gene may possibly play a role in the progression or metastasis of colorectal cancers. © 1995 Wiley‐Liss, Inc.
Deletion mapping of the long arm of chromosome 22 in human meningiomas
Authors: Akagi Kenzo , Kurahashi Hiroki , Arita Norio , Hayakawa Toru , Monden Morito , Mori Takesada , Takai Shinichiro , Nishisho Isamu 
Published: September 2008

AbstractCytogenetic and molecular genetic analyses have shown that a tumor‐suppressor gene for human meningioma is located on the long arm of chromosome 22. Recently, somatic mutations of the NF2 gene have been identified in sporadic meningiomas. However, tumorigenesis of certain cases of meningioma cannot be fully explained by inactivation of the NF2 gene alone. Thus, to obtain some indication as to the existence of another tumorsuppressor gene, it seemed important to re‐examine the loss of heterozygosity (LOH) on 22q in sporadic meningioma. A total of 46 sporadic meningiomas was examined for LOH at 20 loci on 22q. LOH was observed in 29 tumors (63%), of which 13 (28%) showed different patterns of a partial loss of 22q. However, the NF2 locus was retained in one tumor that lost a more distal part of 22q. Moreover, 27 of the 28 tumors which showed LOH at the NF2 locus also lost alleles at more telomeric loci. These results raise the possibility that another tumor‐suppressor gene for meningioma may exist on 22q and that its localization may be distal to the D22S102 locus. © 1995 Wiley‐Liss, Inc.
Cancer risk after renal transplantation in the nordic countries, 1964–1986
Authors: Birkeland Sven A. , Storm Hans H. , Lamm Lars U. , Barlow Lotti , Blohmé Ingemar , Forsberg Bjorn , Eklund Bjorn , Fjeldborg Ole , Friedberg Michael , Frödin Lars , Glattre Eystein , Halvorsen Stein , Holm Niels V. , Jakobsen Amt , Jorgensen Hans E. , Ladefoged Jorgen , Lindholm Tore , Lundgren Goran , Pukkala Eero 
Published: September 2008

AbstractThe theory that cancer may arise under conditions of reduced immune capacity is supported by observations of humans with immune deficiencies such as occur following organ transplants. However, no study on humans has been done in which the reference population was the same as that in which the cancer cases arose and in which there was a sufficiently long period of follow‐up. Information on 5,692 Nordic recipients of renal transplants in 1964–1982 was linked with the national cancer registries (1964‐1986) and population registries. Person‐years at risk were calculated from the date of first transplantation until death or the end of the study period and were multiplied by the appropriate age‐ and calender‐specific incidence rates to obtain the expected numbers of cancers. Standardized incidence ratios (SIR) were calculated after stratification by a number of recorded variables. Altogether, 32,392 person‐years were accrued, and 471 cancers occurred, yielding overall SIR of 4.6 (95% CI, 4.0 to 5.2) for males and 4.5 (95% CI, 4.0 to 5.2) for females. Significant overall 2‐ to 5‐fold excess risks in both sexes were seen for cancers of the colon, larynx, lung and bladder, and in men also for cancers of the prostate and testis. Notably high risks, 10‐fold to 30‐fold above expectation, were associated with cancers of the lip, skin (non‐melanoma), kidney and endocrine glands, also with non‐Hodgkin's lymphoma, and in women also with cancers of the cervix and vulva‐vagina. Among a number of donor and recipient variables studied, including tissue types and compatibility (ABO, HLA, DR), age below 45 years at the time of transplantation was the most important determinant for increased risk at most sites. Kidney transplantation increases the risk of cancer in the short and in the long term, consistent with the theory that an impaired immune system allows carcinogenic factors to act. The tumor risk is small in comparison with the benefits of transplants, but patients should be followed up for signs of cancer. © 1995 Wiley‐Liss. Inc.
Mitoxantrone treatment of murine myeloid leukaemia sublines
Authors: Abubakar Aminu A. , Riches Andrew C. 
Published: September 2008

AbstractThe low‐cell‐dose (LD) and the high‐cell‐dose (HD) transplant variants of the SA7 murine myeloid leukaemia cell line have different growth characteristics and clinical presentations. In addition, the low‐cell‐dose transplant subline (SA7LD) was more responsive than the high‐cell‐dose variant (SA7HD) to mitoxantrone treatment in vivo. Bone‐marrow cells of mice cured of SA7LD leukaemia, as well as bone‐marrow cells of normal mice treated with priming doses of mitoxantrone in vivo became significantly (p = 0.012) less sensitive to subsequent treatment with mitoxantrone in vitro. This effect was detected by both the colony assay and the tritiated thymidine uptake assay. There appears to be a correlation between the ability of normal bone‐marrow cells present in leukaemic mice to develop this protective effect and their ability to survive chemotherapy with mitoxantrone. The protective effect was “lost” by bone‐marrow cells of mice dying while in remission. Doses of mitoxantrone that resulted in the loss of protective effect by bone‐marrow cells of normal mice were found to be fatal to SA7HD leukaemia‐bearing mice. However, these doses were not toxic to normal mice. © 1995 Wiley‐Liss, Inc.
Relationship between stages of mammary development and sensitivity to gamma‐ray irradiation in mammary tumorigenesis in rats
Authors: Yamanouchi Hiroshi , Ishii‐Ohba Hiroko , Suzuki Keiko , Onoda Makoto , Wakabayashi Katsumi , Inano Hiroshi 
Published: September 2008

AbstractMature Wistar‐MS rats were ovariectomized and treated with estradiol benzoate and/or progesterone. Control animals were treated with olive oil. The rats were then exposed to γ‐rays and implanted with a pellet of diethylstilbestrol. The incidence of mammary tumors in rats treated with estradiol benzoate or with progesterone was significantly higher than in rats in the non‐treated control group, whereas, in rats treated with both estradiol benzoate and progesterone, the incidence was not significantly different from that in the controls. Histological examination of the mammary tumors showed 2 types of neoplasm: adenocarcinoma and fibroadenoma. Interestingly, over half of all the tumors in the rats treated with estradiol benzoate were adenocarcinomas, while fibroadenomas were mainly induced in the rats treated with progesterone or with both estradiol benzoate and progesterone. The expression of estrogen and progesterone receptors in the tumor tissues showed some differences according to whether the groups were treated with estradiol benzoate or with progesterone. Morphologically, mammary glands at irradiation showed well‐developed lobuloalveoli in both the estradiol‐benzoate‐treated rats and in those rats treated with both estradiol benzoate and progesterone. This was consistent with the higher incorporation of [3H]thymidine into the DNA in the mammary glands of rats in both of these groups. Our findings suggest that a more advanced developmental stage of the mammary glands, dependent upon ovarian hormones, is related to a higher incidence of mammary tumors induced by irradiation. © 1995 Wiley‐Liss, Inc.
Reduction of tumour intracellular pH and enhancement of melphalan cytotoxicity by the ionophore nigericin
Authors: Wood P. J. , Sansom J. M. , Nhweli K. , Tannock F. F. , Stratford I. J. 
Published: September 2008

AbstractNigericin is an ionophore which permits the influx of H+ ions into cells down a concentration gradient, thus reducing intracellular pH (pHi) when extracellular pH is low. The effects of nigericin on the pHi of solid murine tumours in vivo were examined using31P magnetic resonance spectroscopy. Nigericin at 2.5 mg/kg i.p. reduced pHi by 0.2–0.3 pH unit in the KHT and RIF‐1 tumours but had no effect on pHi in the SCCVII/Ha tumour. In vitro studies have shown that reduced pH can increase the toxicity of melphalan. Therefore, the anti‐tumour effect of combining nigericin with melphalan was also examined. Nigericin at 2.5 mg/kg i.p. given before various doses of melphalan resulted in substantial delay in growth of the RIF‐1 tumour over that induced by melphalan alone. This observation was confirmed by an in vivo/in vitro excision assay, where nigericin given before melphalan produced a 30‐fold increase in cell killing. By contrast, no enhancement of melphalan‐induced cell killing by nigericin was observed in the KHT and SCCVII/Ha tumours, using growth delay and in vivo/in vitro excision assays, respectively. © 1995 Wiley‐Liss, Inc.
Down‐regulation of collagen XII in transformed mesenchymal cells
Authors: Kopp Martin U. , Croci Luigi P. , Trueb Beat 
Published: September 2008

AbstractCollagen XII is a complex multidomain protein associated with the surface of interstitial collagen fibrils. This protein is produced in large amounts by fibroblasts cultivated in vitro. However, it is completely absent from cells transformed by the oncogene v‐myc or v‐src and from cells derived from a methyl‐cholanthrene‐induced fibrosarcoma. Since all these cells lack any mRNA for collagen XII, it seems likely that the synthesis is blocked at the transcriptional level. Experiments with a temperature‐sensitive mutant of Rous sarcoma virus demonstrated that a single oncogene product is sufficient to inhibit the synthesis. A reduction in the expression of collagen XII might have profound effects on the stability of the extracellular matrix of transformed cells. © 1995 Wiley‐Liss, Inc.
Experimental local therapy of human melanoma with lytic magainin peptides
Authors: Sloballe Peter W. , Lee Maloy W. , Myrga Michelle L. , Jacob Leonard S. , Herlyn Meenhard 
Published: September 2008

AbstractMagainin peptides and model amphipathic peptides exhibit antibiotic activity and are also cytolytic for transformed human cells. Here we demonstrate in vitro that MSI‐511 (an all‐D amino‐acid model magainin peptide) and MSI‐130 (a magainin analogue) were more lytic for 17 human melanomas than for normal melanocytes. Melanomas established s.c. in athymic nude mice and then injected once with the peptide MSI‐511 completely disappeared in 6 out of 9 animals, whereas a control peptide had no effect. Murine skin at the tumor injection site was initially affected, but healed within 2 weeks with minimal scarring. Similarly, accelerated healing was seen in human skin grafted to SCID mice and injected with MSI‐511. Our results indicate that lytic magainin peptides can be used for local tumor therapy with minimal long‐term damage to normal tissues. © 1995 Wiley‐Liss, Inc.
Epstein‐barr virus is localized in the tumour cells of nasal lymphomas of NK, T or B cell type
Authors: Tao Qian , Ho Faith C. S. , Loke Shee Loong , Srivastava Gopesh 
Published: September 2008

AbstractSeven cases of nasal lymphoma were studied to identify the lineage of Epstein‐Barr virus (EBV)+ cells using dual‐labelling methods. Five cases were phenotypically and genotypically of natural killer cell (NK) type with germ‐line configuration of T‐cell receptor (TcR) β‐chain gene and immunoglobulin heavy‐chain joining region (lg/H) gene, with one case each of T‐ and B‐cell type showing rearranged TcRβ or lg/H and Λ‐light chain genes respectively. EBV genome was clonal in all these cases except in the B‐cell case where its clonality was undeterminable. Using in situ hybridization (ISH) for EBV‐encoded small nuclear RNA 1 and 2 (EBER), signal was detected in 45% to 88% of nucleated cells in the tumours. Immunostaining for EBV latent membrane protein‐1 (LMP) also revealed numerous LMP+ cells in 3/5 NK‐type cases and the T‐ and B‐cell cases. Using ISH for EBER combined with immunostaining for CD markers and double immunohistochemistry for LMP and CD markers, the predominant lineage of the EBV+ cells was identified as: CD2+CD3−CD19−CD20‐ CD45R0+CD56+CD68‐ in the NK‐type cases, CD2+CD3+CD19−CD20− CD45R0+CD56−CD68− in the T‐cell case and CD20+CD45R0−CD68‐ in the B‐cell case, in agreement with the genotype and phenotype of each tumour. These results show that, in EBV+ nasal lymphomas of NK, T‐ or B‐cell lineage, EBV was consistently associated with the tumour‐cell population and support the view that EBV serves a promoting role in the pathogenesis of different types of EBV+ nasal lymphoma. © 1995 Wiley‐Liss, Inc.
Reproductive factors and the risk of renal cell cancer among women
Authors: Chow Wong‐Ho , McLaughlin Joseph K. , Mandel Jack S. , Blot William J. , Niwa Shelley , Fraumeni Joseph F. 
Published: September 2008

AbstractIn etiologic studies of renal cell carcinoma the role of reproductive variables and the use of exogenous hormones have not been well examined. In a population‐based case‐control study including 165 female cases and 227 controls, we assessed the risk of renal cell cancer associated with reproductive factors and use of oral contraceptives and menopausal hormones. Odds ratios were computed using logistic regression analyses. Risk was positively associated with number of births and inversely associated with age at first birth, with the largest increases in risk (more than 2‐fold) among women with 5 or more births after age 25. After adjustment for age, smoking status, body mass index and age at first birth, women with 5 or more births had a 2‐fold risk (OR = 2.2, 95% CI = 1.2‐4.0) relative to those with 1 or 2 births. Age at first birth, however, was no longer a risk factor when the number of births was adjusted for. The association with parity was considerably stronger among women with a history of hypertension or above‐median body mass index than among those without these conditions. In addition, risk was reduced among long‐term oral contraceptive users but elevated among women who had had a hysterectomy or used menopausal hormones. Our findings suggest that reproductive factors, particularly the number of births, may play an etiologic role in renal cell cancer among women and deserve further study. © 1995 Wiley‐Liss, Inc.
Cancer in patients with ulcerative colitis
Authors: Mellemkjaer Lene , Olsen Jsorgen H. , Frisch Morten , Johansen Christoffer , Gridley Gloria , McLaughlin Joseph K. 
Published: September 2008

AbstractA cohort of 5,546 ulcerative colitis patients was identified from the Danish Hospital Discharge Register for 1977–1989. Patients not included in the cohort comprised those with proctitis, those treated in outpatient clinics and those for whom follow‐up was less than 1 year. The cohort was linked to the Danish Cancer Registry in order to assess the risks for colorectal and other cancers. The linkage revealed a significant increase in the number of colorectal cancers over that in the general population (RR = 1.8; n = 42; 95% CI = 1.3–2.4) with consistent relative risks during early and late follow‐up. The relative risk was considerably higher among younger (20–39 years: RR = 22; n = 8; 95% CI = 9.7–44) than older patients (≥60 years: RR = 1.3; n = 25; 95% CI = 0.8–1.9), but the risk difference between patients and the general population was approximately constant across all ages. In addition, we observed a significant increase in the relative risk of hepatobiliary cancers (RR = 2.3; n = 9; 95% = 1.0–4.3) and a slight but significant increase in the relative risk of non‐melanoma skin cancer (RR = 1.4; n = 37; 95% CI = 1.0–1.9). In summary, our population‐based study confirms the increased risk of colorectal cancer among patients with ulcerative colitis and provides new leads suggesting that hepatobiliary cancer and non‐melanoma skin cancer should be considered as possible sites for future patient monitoring. © 1995 Wiley‐Liss, Inc.