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  • Li, Li, et al. (författare)
  • Induction of apoptosis or necrosis in human endometrial cancer cells by 2-Methoxyestradiol
  • 2004
  • Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 24:6, s. 3983-3990
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND:We investigated the effects of 2methoxyestradiol (2-ME), an endogenous estrogenic metabolite, on human endometrial cancer HEC-1-A and RL-95-2 cell lines.MATERIALS AND METHODS:After exposure of HEC-1-A and RL-95-2 cells to 2-ME, the morphological changes were evaluated by acridine orange staining and transmission electron microscopy. Cell cycle progress, apoptosis and necrosis were assessed by flow cytometry, DNA fragmentation and Western blot.RESULTS:2-ME inhibited cell growth by blocking the S- and G2/M-phase in both cell lines, by inducing apoptosis in HEC-1-A cells and by causing necrosis in RL-95-2 cells. Apoptosis, on HEC-1-A cells, was accompanied by an increased expression of iNOS and STAT1. This apoptotic effect was prevented by the iNOS inhibitor 1400W and eliminated by the caspase inhibitor Z-VAD-FMK. Necrosis, on RL-95-2 cells, was due to a severe disruption of the mitochondrial membrane potential. 2-ME had no significant effect on normal human endometrial cells.CONCLUSION:The data suggest that 2-ME has an antitumor effect on human endometrial carcinoma cells (HEC-1-A and RL-95-2) and may contribute as a new therapeutic agent for endometrial cancer patients.
  • Lindahl, Bengt, et al. (författare)
  • Adjuvant tamoxifen in breast cancer patients affects the endometrium by time, an effect remaining years after end of treatment and results in an increased frequency of endometrial carcinoma
  • 2008
  • Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 28:2B, s. 1259-1262
  • Tidskriftsartikel (refereegranskat)abstract
    • Tamoxifen is the most used adjuvant drug in breast cancer treatment. Its main action is as an anti-oestrogen, but in the endometrium of some patients it acts as an oestrogen. Some investigators have even reported an increased risk of developing endometrial carcinoma. The question of how to follow-up these patients and how to identify patients at risk of developing endometrial premalignant changes was investigated by the noninvasive ultrasound method. The follow-up of 292 patients from before the start of adjuvant treatment with tamoxifen and 94 without tamoxifen treatment was conducted at regular intervals. The changes in endometrial thickness as measured by ultrasound and histopathological changes are reported. A thicker endometrium was found in patients with receptor positive breast cancer even before the treatment with tamoxifen started. Cumulative increasing thickness was found during treatment and this thicker endometrium remained until almost 3 years after the end of treatment. If the endometrium was <3 mm after 3 months of treatment the probability that it would be thin after 5 years was high. An increased risk of developing endometrial carcinoma was found, however due to this regular follow-up the cancer was identified at an early stage.
  • Lindström, Annika K., et al. (författare)
  • Associations between ten biological tumor markers in squamous cell cervical cancer and serum estradiol, serum progesterone and smoking
  • 2007
  • Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 27:3B, s. 1401-1406
  • Tidskriftsartikel (refereegranskat)abstract
    • Background and Aim: To study possible associations between selected tumor markers and co-factors in squamous cell cervical cancer. Materials and Methods: Ten biological tumor markers representing different functions in carcinogenesis were diagnosed in 128 cases of squamous cell cervical cancer. These were p53, c-myc, EGFR, COX-2, CD4+, VEGF, E-cadherin, CD44, Ki-67 (MIB-1), and p27. Smoking habits and previous oral contraceptive use were registered. Serum estradiol and progesterone levels were evaluated in 80 women. Each marker was compared to these four variables. Results: Highly significant associaions were found between strong c-myc staining (≥50%) and increased serum progesterone (p=0.01), a low EGFR staining (<20%) and high serum estradiol (p=0.0007), and an absence of p53 staining and smoking (p=0.008). There was a association between the absence of p53 and high serum progesterone (p=0.046). Conclusion: The study supports a role of progesterone as a promoter of cervical cancer and indicates that smoking is associated with tumor development.
  • Lindström, Annika K., et al. (författare)
  • Predicting the outcome of squamous cell carcinoma of the uterine cervix using combinations of individual tumor marker expressions
  • 2007
  • Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 27:3B, s. 1609-1615
  • Tidskriftsartikel (refereegranskat)abstract
    • Aim: To evaluate if combining the individual expression patterns of biomarkers targeting different molecular alterations in tumor development will improve prognosis prediction in invasive squamous cell carcinoma of the uterine cervix. Patients and Methods: Ten-year follow-up results in 128 women with cervical cancer were compared to the expression of 10 relevant tumor markers, assessed with immunohistochemistry. The markers were selected to represent cell proliferation, tumor suppression, cell-cell adhesion, angiogenesis, apoptosis, inflammation and immune response. All analyses were adjusted for stage. Results: p53 expression, and low expression of c-myc and COX-2 correlated significantly with survival. In addition CD4+ expression was included in the analyses of combinations. When these four tumor markers were combined, two-by-two, ten combinations correlated significantly with 10-year survival. The overall 10-year survival rate with a low COX-2 and a high CD4+ expression was 76% versus 53% in the remaining women (odds ratio 3.73, 95% CI 1.42-11.0). The survival rate with absent p53 and high COX-2 expression in the tumors was 42% versus 71% (odds ratio 0.25, 95% CI 0.10-0.37), while the corresponding figures for the combination of high COX-2 intensity and expression of c-myc were 27% versus 62% (odds ratio 0.13, 95% CI 0.02-0.52). None of the single markers correlated significantly with outcome in the final Cox regression analyses, while five combinations did. Conclusion: Combinations of selected, biologically plausible tumor markers might be more useful for predicting the outcome than using single markers.
  • Lopez-Egido, Juan R., et al. (författare)
  • Differentially regulated genes in MEN1-transfected BON cells using RT-differential display and oligonucleotide microarrays
  • 2009
  • Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 29:6, s. 1859-1866
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND:Apart from inactivation of the MEN1 gene, the molecular mechanisms involved in tumorigenesis of the endocrine organs and MEN1-associated non-endocrine lesions remain unknown.MATERIALS AND METHODS:In order to learn more about down-stream effects upon MEN1 gene inactivation BON1 cells were transfected with a MEN1 gene construct (BON/M1C), and both RT-differential display and oligonucleotide microarrays were performed.RESULTS:Three genes (SMARCC1, OVCA2 and SRp55) found to be differentially regulated on differential display were corroborated by northern blots on cell line RNA when comparing MEN1 transfected cells with control (empty vector transfection). When comparing two different passages of BON/M1C with two passages of vector control using oligonucleotide microarrays, 25 up-regulated genes and 64 down-regulated genes could be found using a cut-off of >or=1.6 times.CONCLUSION:These findings might contribute to the understanding of the molecular pathways involved in MEN1 tumorigenesis, and may also provide knowledge of genes involved in sporadic endocrine tumorigenesis.
  • Lunde, Mai Lill Suhr, et al. (författare)
  • Gene expression analysis by cDNA microarray in oral cancers from two Western populations
  • 2010
  • Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 30:4, s. 1083-1091
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: In this work, gene expression profile was examined in 19 cases of oral cancer (OC) obtained from patients from Sweden (n=8) and UK (n=11) and the findings were tested for correlation to patient's clinicopathological data. MATERIALS AND METHODS: Following total RNA extraction, cDNA synthesis, labeling with fluorescent dyes and hybridization to the 21 k human oligonucleotide microarrays, slides were scanned and images were subjected to Genepix and J-Express analysis. Results for selected genes were validated by quantitative reverse transcriptase polymerase chain reaction (Q-RT-PCR). RESULTS: 42 genes were identified as being differentially expressed. These included 39 genes of known functions (such as fatty acid synthase (FASN), 5' nucleotidase, ecto (NT5E), high mobility group AT-hook (HMGA1), and v-fos FBJ murine osteosarcoma viral oncogene homolog (FOS)) and 3 novel genes; 26 (67%) of the 39 genes with known functions were previously reported in oral/head and neck tumors examined from other populations. Hierarchical clustering of the samples using the 42 genes demonstrated that samples mainly clustered in the same population. CONCLUSION: These results illustrate that microarrays can be used to identify distinct patterns of gene expression in different populations, but with no direct association to clinicopathological parameters. The fact that 67% of the 39 genes with known functions found in this work were previously reported in oral/head and neck tumors from other populations provides clear evidence that development of these tumors follows the same biological pathways irrespective of the source of the samples used.
  • Mahteme, H, et al. (författare)
  • 5-FU uptake in liver metastases after intravenous and intraperitoneal administration : an autoradiographic study in the rat
  • 1998
  • Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 18:2A, s. 943-949
  • Tidskriftsartikel (refereegranskat)abstract
    • AIM:To analyse 5-fluorouracil (5-FU) uptake in hepatic metastases and normal tissues after intravenous (i.v.), intraperitoneal (i.p.e.) and intraportal (IPO) administration.METHODS AND RESULTS:A total of 18 inbred rats with hepatic metastases were injected with 14C-labelled 5-FU either through the i.v. (n = 7), i.p.e (n = 7) or IPO (n = 4) route. Radioactivity was visualised autoradiographically and quantified by computer-based image analysis. After 20 minutes, 10 i.v. injected tumours showed a higher amount of radioactivity (mean +/- SD) 23.8 +/- 7.8 than 6 i.p.e. injected (16.5 +/- 5.1, P = 0.06). At 2 hours, 9 i.v. injected metastases contained more radioactivity (49.6 +/- 9.2) than 19 i.p.e. injected tumours (28.2 + 11.3, P = 0.00003). After 24 hours, 2 i.p.e. injected tumours had higher radioactivity (mean 25.2) compared with 7 i.v. injected (7.6 +/- 4.1). IPO administration did not confer higher radioactivity at any time point. When the calculations were based on average metastatic radioactivity of individual rats, the difference between i.v. and i.p.e. injected rats was still present at 2 hours.CONCLUSION:These results indicate that early tumour 5-FU uptake after intraperitoneal and intraportal administration may be inferior to that after intravenous injection. Deposition of the drug in the peritoneal cavity may, however, act as a slow release preparation giving continuous drug exposure for prolonged periods of time. These results suggest a role for combined intravenous and intraperitoneal adjuvant therapy.
  • Mahteme, Haile, et al. (författare)
  • 5-FU uptake in peritoneal metastases after pretreatment with radioimmunotherapy or vasoconstriction : an autoradiographic study in the rat
  • 2005
  • Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 25:2A, s. 917-922
  • Tidskriftsartikel (refereegranskat)abstract
    • This study was conducted to test if tumour drug uptake could be increased in experimental colorectal cancer peritoneal metastases, by using pretreatment with peritoneal vasoconstriction or radioimmunotherapy. A total of 29 nude rats with peritoneal metastases were injected intraperitoneally (i.p.) with 14C-labelled 5-FU. The animals were randomly allocated to 5 groups. Six days prior to 5-FU, group I (control) received i.p. NaCl, group II was subjected to i.p. radioimmunotherapy (RIT) 131I-labelled anti-CEA monoclonal antibody (150 MBq) and group III received i.p. Norbormide 10 minutes before 5-FU. Two days prior to 5-FU group IV and V received i.p. NaCl (control) and RIT, respectively. 5-FU uptake was visualised with autoradiography and quantified by computer-based image analysis. Tumours in group III showed a higher uptake (mean+/-SD, 21.4+/-17) than in group I (11.8+/-10, p=0.04). This was also true when the analysis was restricted to larger tumours (> or = median 627 pixels) group III (23.2+/-19) vs. group I (11.8+/-7, p=0.002). Peritoneal tumours in group II were of smaller size (median area 308 pixels) than in group I (619 pixels), in group III (901 pixels), in group IV (769 pixels) and in group V (808 pixels). RIT decreased the tumour size whereas it did not affect 5-FU uptake. The uptake of 5-FU was potentiated by pretreating the animals with Norbormide. These results demonstrate that 5-FU uptake in experimental peritoneal metastases is increased when the peritoneal absorption of the drug is blocked using pretreatment with a vasoconstrictive agent. This principle may also be relevant when treating patients with colorectal cancer peritoneal metastases.
  • Mahteme, Haile, et al. (författare)
  • Adjuvant 131I-anti-CEA-antibody radioimmunotherapy inhibits the development of experimental colonic carcinoma liver metastases
  • 1998
  • Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 18:2A, s. 843-848
  • Tidskriftsartikel (refereegranskat)abstract
    • Adjuvant radioimmunotherapy (RIT) for human colonic cancer was performed in a nude rat model of experimental liver metastases. Thirty-three rats were injected intraportally through a mesenteric vein with 5 x 10(6) cells from the human colonic cancer cell line LS174T. Within half an hour, 20 MBq (n = 2), 75 MBq (n = 5), or 150 MBq (n = 10) of the 131I-labelled anti- carcinoembryonic antigen (CEA) monoclonal antibody (MAb) 38S1 was administered intravenously (i.v.), whereas control groups received either i.v. saline injections (n = 12) or 150 MBq of the irrelevant 131I-labelled MAb 79C (n = 4). Decay corrected whole-body data showed that more than 80% of the initially MAb-bound radioiodine was excreted during the first 2 weeks. Whole- body clearance and blood clearance of 131I-38S1 and 131I-79C were essentially similar. At sacrifice 5-7 weeks after administration, neither 20 MBq nor 75MBq 131I-38S1 significantly prevented the development of liver metastases. By contrast, with 150 MBq, no metastases formed in the animals treated with MAb 131I-38S1 or 131I-79C. A radiation induced effect on the haematopoietic system was found in the 150MBq dosage groups. It is concluded that the inhibition of tumour induction was not strictly dependent on a radiation dose delivered by a tumour-specific MAb. Since a non-tumour-specific 131I-MAb, in a smaller group of animals, proved equally efficacious in preventing tumour growth, the total body 131I dose was probably the major contributing factor.
  • Marikkannu, Rajeshwari, et al. (författare)
  • Whole-genome Linkage Analysis and Sequence Analysis of Candidate Loci in Familial Breast Cancer
  • 2015
  • Ingår i: Anticancer Research. - 0250-7005 .- 1791-7530. ; 35:6, s. 3155-3165
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Known breast cancer-predisposing genes account for fewer than 25% of all familial breast cancer cases and further studies are required to find the remaining high-and moderate-risk genes. We set-out to couple linkage analysis using microsatellite marker data and sequence analysis of linked regions in 13 non-BRCA1/2 families in order to find novel susceptibility loci and high-penetrant genes. Materials and Methods: Genotyping with 540 fluorescently-labeled microsatellite markers located on the 23 chromosomes at 7.25 cM resolution was used for primary linkage analysis and an additional 40 markers were used for fine-mapping of loci with a logarithm of odds (LOD) or heterogeneity LOD (HLOD) score greater than one. Whole-exome sequencing data of 28 members from all 13 families were used for the bioinformatics sequence analysis on the linked regions of these families. Results: Linkage analysis identified three loci on chromosome 18q as a putative region of interest (overall LOD=1, HLOD=1.2). Sequencing analysis of the three linked regions on 18q and mutation prediction algorithms did reveal three probable damaging variants. Conclusion: Overall, our study identified three weakly linked loci on 18q and three probable damaging variants of interest in the 13 families with breast cancer.
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