bluuebunny/crossref_metadata_2025_split huggingface dataset:
Growth control of human colon‐adenocarcinoma‐derived Caco‐2 cells by vitamin‐D compounds and extracellular calcium in vitro: relation to c‐myc‐oncogene and vitamin‐D‐receptor expression
Authors: Hulla Wolfgang , Kállay Enikö , Krugluger Walter , Peterlik Meinrad , Cross Heide S. 
Published: February 2007

AbstractThe human colon‐cancer cell line Caco‐2, though of malignant origin, is still able to express the c‐myc proto‐oncogene in a regulable fashion. Transition from the logarithmic growth phase into the quiescent, i.e., confluent state, is accompanied by a significant increase in the number of cells in the G0/G1 phase of the cell cycle and a concomitant reduction of c‐myc mRNA and of nuclear association of c‐myc protein. Conversely, growth stimulation by lowering extracellular [Ca++]0 to 0.25 mM results in up‐regulation of c‐myc expression levels and consequently inhibition of re‐entry of Caco‐2 cells into the G0/G1 phase. In contrast, regulation of c‐myc in Caco‐2 cells is completely resistant to vitamin‐D sterols, since the anti‐mitogenic action of 1α,25‐dihdroxyvitamin D3 (1α,25(OH)2D3) and of 2 synthetic analogs, 1α,25(OH)2–16‐ene‐23‐yne‐D3 and 1α,25(OH)2–26,27‐F6–16‐ene‐23‐yne‐D3, occured independently of any change in c‐myc mRNA and nuclear protein levels. Although the anti‐proliferative effect of the vitamin‐D sterols requires high‐affinity binding to the cytoplasmic vitamin‐D receptor (VDR), vitamin‐D sterols have no effect on VDR mRNA levels in Caco‐2 cells. However, VDR mRNA expression changed in an anti‐parallel fashion to c‐myc regulation upon transition between different growth states. This suggests that VDR mRNA abundance could nevertheless be important for vitamin‐D‐related c‐myc‐independent growth control in Caco‐2 cells. © 1995 Wiley‐Liss, Inc.
DNA‐binding properties of novel cis‐ and trans platinum‐based anticancer agents in 2 human ovarian carcinoma cell lines
Authors: Mellish Kirste J. , Barnard Christopher F. J. , Murrer Barry A. , Kelland Lloyd R. 
Published: February 2007

AbstractWe have investigated the comparative initial DNA binding properties of 7 platinum‐based anticancer drugs: 5 cis‐oriented compounds, cisplatin, tetraplatin (Ormaplatin), JM118 [cis ammine dichloro (cyclohexylamine) platinum (II)], JM216 [bis‐acetato cis ammine dichloro (cyclohexylamine) platinum (IV)] and JM149 [cis ammine dichloro (cyclohexylamine) trans dihydroxo platinum (IV)], and 2 trans‐oriented compounds, transplatin and JM335 [trans ammine dichloro (cyclohexylamine) dihydroxo platinum (IV)] in SKOV‐3 and CH1 human ovarian carcinoma cells. Unlike transplatin, the trans complex JM335 was comparably cytotoxic to its cis isomer JM149 and cisplatin. No significant correlation was observed between levels of total platinum bound to DNA after exposure to the 7 drugs and cytotoxicity in either cell line. Using a competitive enzyme‐linked immunoabsorbent assay, DNA extracted from CM1 cells exposed to the 5 cis platinum drugs was recognized by the monoclonal antibody ICR4 (raised against DNA platinated by cisplatin) in the order JM118 > cisplatin > JM216 > tetraplatin > JM149; a strong positive correlation which just attained statistical significance was observed between recognition by ICR4 and cytotoxicity. In contrast, DNA extracted from CH1 cells exposed to the trans platinum drugs transplatin and JM335 was no more immunoreactive than control DNA. Using alkaline elution, interstrand cross‐link levels after exposure to drug did not correlate with cytotoxicity in either cell line. The 5 cis drugs formed interstrand cross‐links in both cell lines, whereas transplatin formed very low levels in SKOV‐3 and undetectable levels in CH1. JM335 was efficient at forming interstrand cross‐links in SKOV‐3 but, notably, none were observed in CH1. In contrast, in the CH1 cells, single‐strand breaks were observed with JM335 (but not with any other drug). The novel trans complex JM335 was unique, among the platinum drugs studied, in its ability to form both DNA interstrand cross‐links and single strand breaks (DNA lesion formation being cell line dependent), a property which may account for its cytotoxicity. © 1995 Wiley‐Liss, Inc.
Elevation of aldose reductase gene expression in rat primary hepatoma and hepatoma cell lines: Implication in detoxification of cytotoxic aldehydes
Authors: Takahashi Motoko , Funjii Junichi , Miyoshi Eiji , Hoshi Ayumu , Taniguchi Naoyuki 
Published: February 2007

AbstractAldose reductase and aldehyde reductase are members of the aldo‐keto reductase super‐family, and participate in the reduction of a wide range of carbonyl compounds. We have purified aldose reductase from rat lens and raised antiserum against it in rabbits. Immunoblot analyses using this antibody showed that a significant amount of aldose reductase was expressed in cell lines derived from hepatomas while it was negligible in normal hepatocytes. Elevated expression of aldose reductase was also observed in cancerous lesions of 3′‐methyl‐4‐dimethyl‐aminoazobenzene (3′‐Me‐DAB)‐induced hepatocarcinomas. Expression of aldose reductase mRNA was confirmed in these cells by Northern‐blot analysis, suggesting that the induction occurred at the stage of gene transcription. The level of aldehyde reductase, however, did not change in cancerous tissue or in the cell lines. The viability of hepatoma cells in the presence of 3‐deoxyglucosone and glyceraldehyde was decreased by an aldose reductase inhibitor, ONO‐2235 (5‐[(1Z,2E)‐2‐methyl‐3‐phenylpropenylidene]‐4‐oxo‐2‐thioxo‐3‐thiazolidin‐eacetic acid). Taken together, induction of aldose reductase gene expression during hepatocarcinogenesis may render cancer cells resistant to various toxic carbonyl compounds produced during metabolism or administered as anti‐cancer drugs. © 1995 Wiley‐Liss, Inc.
Migratory patterns of lac‐z transfected human glioma cells in the rat brain
Authors: Pedersen Paal‐Henning , Eovardsen Klaus , Garcia‐Cabrera Inmaculada , Mahesparan Rupavathana , Thorsen Jon , Mathisen Berit , Rosenblum Mark L. , Bjerkvig Rolf 
Published: February 2007

AbstractMalignant brain tumors are characterized by extensive tumor‐cell infiltration into the normal brain tissue. The present work describes the migratory behavior of human glioma cells transplanted into the adult rat brain with the aim of exploiting the extent of active cell migration and passive cell displacement within the central nervous system. To detect every transplanted tumor cell, a stably bacterial β‐galactosidase (loc‐z) transfected human glioma cell line was used. To distinguish between an active cell migration process and passive cell displacement, rat brains were also implanted with inert fluorescent polystyrene microspheres and the distribution of tumor cells and micro‐ spheres was studied 1 hr and 3 days after implantation. One hour after implantation the tumor cells were strictly localized at the implantation site. However, 3 days after implantation, both tumor cells and microspheres showed an extensive distribution within the brain. Confirming earlier neuropathological and experimental studies, it is shown that the loc‐z‐transfected glioma cells had the capacity to move within the Virchow‐Robin and subarachnoid spaces. However, since fluorescent micro‐spheres were also found in these areas, this spread of tumor cells may be primarily mediated by the extensive cerebrospinal fluid flow that exists within the brain. Three days after implantation, the glioma cells also showed an active migration over the corpus callosum. In comparison, the fluorescent microspheres showed only limited spread along the callosal body. It is concluded that the bacterial lac‐z gene can be stably transfected into human glioma cells and, since every tumor cell can be visualized within the brain, this model provides a tool for studying the mechanisms behind tumor‐cell invasion of the brain. © 1995 Wiley‐Liss, Inc.
Bladder tumours following chemotherapy and radiotherapy for ovarian cancer: A case—control study
Authors: Kaldor John M. , Day Nicholas E. , Kittelmann Berndt , Pettersson Folke , Langmark Froydis , Pedersen Dorthe , Prior Patricia , Neal Frank , Karjalainen Sakari , Bell Janine , Choi Won , Koch Maria , Band Pierre , Pompe‐Kirn Vera , Garton Catherine , Staneczek Wolfhardt , Zarén Birgitta , Stovall Marilyn , Boffetta Paolo 
Published: February 2007

AbstractA collaborative group of cancer registries and hospitals carried out a case—control study of tumours of the bladder in women who had previously been treated for ovarian cancer. A total of 63 cases of bladder tumours were identified, and 188 controls were selected matching for age, year of ovarian cancer diagnosis and survival time. Full details of the treatment for ovarian cancer were sought both for cases and for controls. The risk of bladder tumours was increased for patients who had been treated by radiotherapy alone (1.9; 95% confidence interval, 0.77–4.9), by chemotherapy alone (3.2; 0.97–10), and by chemotherapy and radiotherapy (5.2; 1.6–16), when comparison was made with patients treated only by surgery. Patients treated by chemotherapy were separated into 2 groups according to whether they had received cyclophosphamide. Among those who had, there was a clear increase in risk (approximately 4‐fold) regardless of whether or not they had also received radiotherapy. For those who received only other drugs, risk was increased substantially among patients who had also been treated by radiation, as compared with patients treated by surgery alone, and those who had received radiotherapy only. Both melphalan and thiotepa were implicated as potential bladder carcinogens on the basis of these results. The estimated risk of bladder tumours due to cyclophosphamide was more than twice the risk following radiation to the bladder, and it appeared substantially earlier. For both agents, the risk continued to increase more than 10 years after treatment began.
An ecological study of diet and lung cancer in the South Pacific
Authors: Le Marchand Loïc , Hankin Jean H. , Bach François , Kolonel Laurence N. , Wilkens Lynne R. , Stacewicz‐Sapuntzakis Maria , Bowen Phyllis E. , Beecher Gary R. , Laudon François , Baqué Pierre , Daniel Roro , Seruvatu Laijia , Henderson Brian E. 
Published: February 2007

AbstractIncidence rates of lung cancer have been markedly lower for Fiji than for other South Pacific countries, despite similar rates of smoking. We conducted population‐based surveys in several island nations of the South Pacific (Cook Islands, Fiji, Tahiti and New Caledonia) and used data from Caucasian, Japanese, Hawaiian, Filipino and Chinese controls in a case‐control study of lung cancer in Hawaii to investigate the role of diet in explaining differences in lung cancer incidence among 20 ethnic‐sex groups. In a stepwise linear regression of lung cancer rates on smoking, diet and other variables, smoking, as expected, explained the majority (61%) of the variability in incidence. However, several dietary components also explained significant portions of the variance. Lutein intake explained 14% and vitamin E intake, cholesterol intake and height explained 5–7% each of the remaining variance in incidence. Associations with lutein and vitamin E were inverse, whereas those with cholesterol and height were direct. Dietary β‐carotene intake was not associated with lung cancer incidence. These ecological data provide evidence for a protective effect of lutein against lung cancer. A protective effect of dietary vitamin E and a risk‐enhancing effect of dietary cholesterol are also suggested.
Effectiveness of screening for breast cancer in women under 50 years at entry: The Kotka pilot project in Finland
Authors: Hakama Matti , Pukkala Eero , Kallio Mervi , Godenhjelm Kari , Svinhufvud Ulla 
Published: February 2007

AbstractIt is still uncertain whether mammography is beneficial to women under 50 years of age. We report a follow‐up of 4 I ‐year birth cohorts in 13 Finnish municipalities subjected to service screening. The women in these cohorts were born in even calendar years and they were 40–47 years old at the time of first screening, which was repeated every other year. At the beginning, 4, 163 women were invited and 86% attended. Women were screened with mammography, physical breast examination and information on detection and early diagnosis of breast cancer by breast self‐examination (BSE) was given. Incident cases of breast cancer and breast‐cancer deaths were recorded. The expected numbers of incident breast‐cancer cases and deaths from breast cancer were derived from control women who were residents of the same municipalities but who were born in adjacent calendar years (odd years) to those screened. In the screened cohorts 13 cancers were screen‐detected, 32 cancers were interval cases and 8 cases were diagnosed among the non‐attenders, while in the controls 85 cancers were detected during a 9‐year follow‐up from 1982 to 1990. One death from breast cancer occurred in the screened cohorts among cases diagnosed between 1982 and 1990, against 10 expected breast‐cancer deaths during a 10‐year follow‐up from 1982 to 1991 of women initially free of breast cancer. Breast‐cancer mortality in the screened cohorts was significantly lower than in the controls (Rate Ratio 0.11), but it is not clear how much of the reduction in mortality could be accounted for by the mammography itself and how much to other activities included in the screening programme (especially training in BSE) or to chance variation. It is unlikely that a programme sensitivity of 25% (13/53) would have resulted in 89% (100‐11) effectiveness or reduction in the risk of death from breast cancer.
Clonal heterogeneity in breast cancer: Karyotypic comparisons of multiple intra—and extra—tumorous samples from 3 patients
Authors: Teixeira Manuel R. , Pandis Nikos , Bardi Georgia , Andersen Johan A. , Mitelman Felix , Heim Sverre 
Published: February 2007

AbstractIntratumor phenotypic heterogeneity is one of the characteristics of breast carcinomas, and genetic mechanisms are likely to contribute to it. We have studied breast cancer clonal heterogeneity by cytogenetic analysis of multiple tumor samples (one from each tumor quadrant) as well as samples of macroscopi‐cally normal surrounding breast tissue from 3 patients with this disease. Clonal chromosome aberrations were found in all 8 successfully analyzed samples from the carcinomas. Two to 6 cytogenetically unrelated clones were detected in each case, unevenly distributed among the tumor quadrants. Karyotypic abnormalities were also found in 4 out of 9 macroscopically tumor‐free samples from the surrounding tissue; in 2 of these samples, a ductal carcinoma in situ was detected histologically, and the cytogenetic evidence suggests that the remaining 2 samples also contained neoplastic cells. Quantitative analysis of the findings revealed a statistically significant higher frequency of karyotypically abnormal cells in samples with a histologic diagnosis of carcinoma vs. samples without any detected malignancy. That cells bearing cytogenetic evidence that they belong to the tumor parenchyma are left behind during breast‐conserving surgery for carcinoma of the breast may account for the relatively high long‐term local relapse rates seen in this disease.
Effect of gastrointestinal hormones and synthetic analogues on the growth of pancreatic cancer
Authors: Robertson John F. R. , Watson Susan A. , Hardcastle Jack D. 
Published: February 2007

AbstractThe effects of hormones and synthetic analogues have been examined on the growth of 2 human pancreatic cancer cell lines, MiaPaCa2 a well‐established cell line and PAN I which was derived in our own laboratories from a tumour specimen. The hormones/growth factors included gastrin (G‐17), epidermal growth factor (EGF) and bombesin, while the synthetic analogues used were a gastrin receptor antagonist (CR 1718), a somatostatin analogue (RC‐160) and a bombesin receptor antagonist (ICI 216, 140). Cell proliferation was assessed by the [75Se]selenomethionine uptake method which has been shown to correlate with cell counts. The effect of each hormone or growth factor on growth was expressed as a percentage of the untreated control. There were 5 replicates in each experiment, and each one was repeated at least 3 times. In vitro growth of both cell lines was unaffected by gastrin, bombesin or the respective antagonists (CR 1718 and ICI 216140). The somatostatin analogue RC‐160 also had no effect on basal growth. Significant growth stimulation of both MiaPaCa2 and PANI was seen with epidermal growth factor. We tested the hypothesis that somatostatin analogues may inhibit EGF‐stimulated growth on both MiaPaCa2, a somatostatin receptor positive cell line, and on PANI which is negative for somatostatin receptors. RC‐160 did not inhibit EGF‐stimulated growth of either Mia‐PaCA2 or PANI. Both cell lines were established in vivo as xenografts in nude mice. The effect of RC‐160 on tumour growth was measured. RC‐160 inhibited the growth of Mia‐PaCa2, the somatostatin receptor‐positive cell line, but not of PANI.
Human chromosome 11 suppresses the tumorigenicity of adenovirus transformed baby rat kidney cells: Involvement of the wilms' tumor 1 gene
Authors: Menke A. L. , Van Ham R. C. A. , Sonneveld E. , Shvarts A. , Stanbridge E. J. , Miyagawa K. , Van Der Eb A. J. , Jochemsen A. G. 
Published: February 2007

AbstractHuman chromosome 11 was introduced into adenovirus‐transformed baby rat kidney (BRK) cells by microcell‐mediated chromosome transfer. The resulting microcell hybrids (MCHs) showed a reduced ability to form tumors upon s.c. injection into athymic mice. Further analysis, with the use of defined deletion chromosomes of lip, indicated that the presence of region 11 p 13‐p 12 is necessary for the suppression of tumorigenicity. In contrast, the presence of region lip 15–14.1 appeared to increase the rate of tumor growth. Expression studies on the human Wilms' tumor I (WTI) and the insulin‐like growth factor II (IGF‐II) genes, which lie in regions 11 p 13 and 11 p 15, respectively, suggested the involvement of both genes in determining the degree of suppression of tumorigenicity. Finally, stable expression of a murine WTI protein in the adenovirus‐transformed cells resulted in almost complete suppression of tumorigenicity, establishing the WTI protein as a tumor suppressor in this cell system.
Loss of cell‐contact regulation and altered responses to autocrine motility factor correlate with increased malignancy in prostate cancer cells
Authors: Silletti Steve , Yao Ji Ping , Pienta Kenneth J. , Raz Avraham 
Published: February 2007

AbstractTumor cell migration and proliferation in new organ environments are critical steps in cancer progression and can be modulated by tumor‐ and host‐secreted molecules. Autocrine motility factor (AMF) is a tumor‐secreted cytokine which regulates growth and motility by a receptor‐mediated pathway. The AMF receptor, a 78‐kDa cell surface glycoprotein (gp78), is regulated by cell contact in normal fibroblastic and bladder cells; however, this mechanism is disrupted during tumor progression. A prostatic carcinoma cell line which is low‐ to non‐metastatic in nude mice (PC‐3) and a derived metastatic variant (PC‐3M) were examined to determine if gp78 cell density regulation is involved in prostate cancer progression. Both cell lines expressed gp78 and, although the basal migration of the parental PC‐3 cells was higher than that of the metastatic variant, only the PC‐3M cells were capable of responding to tumor‐derived AMF with increased motility. Furthermore, these cells exhibited differential patterns of wound closure in an experimental system whereby the low‐metastatic PC‐3 cells migrated primarily along the wound edge while individual high‐metastatic PC‐3M cells entered the cell‐free wound area directly. Cell surface gp78 distribution distinguished the cell populations with a markedly concentrated display of gp78 in polarized capped regions on the surface of the metastatic cells. Cell‐cell contact down‐regulated gp78 expression in the parental, but not the metastatic, cells, and mitogenic responses to exogenous AMF differed between these cell lines as well. In this model, metastasis appears to be associated with aberrant regulation of gp78 expression and distribution, coupled with enhanced exploitation of AMF's locomotory and prolifera‐tive effects.
Ultraviolet‐B‐light‐induced mutagenesis of C‐H‐ras codons 11 and 12 in human skin fibroblasts
Authors: Amstad Paul A. , Cerutti Peter A. 
Published: February 2007

AbstractMutations in the ras oncogene are detected with a high frequency in non‐melanoma skin cancer. Approximately half of the squamous‐cell carcinomas (SCC) and one third of the basal‐cell carcinomas (BCC) carry mutations at the second position of Ha‐ras codon 12 (GGC to GTC), whereas mutations in Ki‐ras codon 12 occur less frequently. Since the mutations in the Ha‐ras and Ki‐ras oncogenes are located opposite potential pyrimidine dimer sites (C‐C), it is likely that the mutations are induced by ultraviolet radiation present in sunlight. We studied the capacity of ultraviolet B (UVB) light to induce base‐pair changes in Ha‐ras codons 11 and 12 in human skin fibroblasts. UVB induced mostly C to T and G to A transitions and C to A and G to T transversions. The base‐pair change with the highest relative abundance was C to T in the middle position of codon 11 followed by (in diminishing relative abundance) C to A in the middle position of codon 11, G to A and G to T in the middle position of codon 12. The C to T and G to A transitions are compatible with pyrimidine photodimers as pre‐mutagenic lesions, whereas the C to A and G to T transversions could be generated due to the formation of 8‐hydroxyguanine, which is the major oxidation product of guanine. The relative abundance of mutations induced by UVB in Ha‐ras codons 11 and 12 does not correlate with mutations observed in the DNA from non‐melanoma skin cancer, where the G to T transversion in the middle position of codon 12 is selected.
Malignant transformation of human fibroblast strain MSU‐1.1 by v‐fes requires an additional genetic change
Authors: Lin Chiencheng , Maher Veronica M. , McCormick J. Justin 
Published: February 2007

AbstractTo determine whether the v‐fes oncogenc can malignantly transform human fibroblasts that have acquired an infinite life span and are partially growth‐factor‐independent, we trans‐fected cell strain MSU‐1.1 with a plasmid containing the v‐fes oncogene and a bacterial histidinol dehydrogenase gene. Of the 60 independent histidinol‐resistant clones isolated and assayed for v‐fes expression using a fes‐specific monoclonal antibody, 6 were found to express the v‐fes protein at a detectable level. When progeny cells from these 6 clones were further characterized, 3 of the 6 clonal populations exhibited a significant increase in the ability to form medium‐sized colonies in agarose, but none were tumorigenic in athymic mice. However, when the 6 populations were propagated for many generations, the same 3 populations acquired the ability to form very large colonies in agarose (± 100 μm in diameter) at a frequency of 2% to 17%, and formed malignant tumors in athymic mice. This suggests that an additional genetic change required for malignant transformation had been spontaneously acquired in 3 of the v‐fes ‐transformed cell strains. To determine whether the change or changes were the equivalent of an activated sis or ras proto‐oncogene, we transfected the v‐fes oncogene into derivative strains of MSU‐1.1 that express a transfected v‐sis, c‐H‐ras or c‐N‐ras oncogene, but that do not form tumors, and assayed the v‐fes‐expressing transfectants for tumorlgenicity. The results showed that when complemented either by a ras oncogene expressed at a somewhat enhanced level or by the v‐sis oncogene, v‐fes can supply the additional change required for malignant transformation.