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Träfflista för sökning "AMNE:(MEDICAL AND HEALTH SCIENCES Clinical Medicine Cancer and Oncology) ;srt2:(2000-2004)"

Sökning: AMNE:(MEDICAL AND HEALTH SCIENCES Clinical Medicine Cancer and Oncology) > (2000-2004)

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1.
  • Browall, Maria, et al. (författare)
  • Information needs of women with recently diagnosed ovarian cancer - A longitudinal study
  • 2004
  • Ingår i: European Journal of Oncology Nursing. - : Elsevier. - 1462-3889 .- 1532-2122. ; 8:3, s. 200-207
  • Tidskriftsartikel (refereegranskat)abstract
    • The aim of this study was to investigate the information needs among patients with ovarian cancer and whether these information needs change over time. The information needs were evaluated three times, through structured interviews, and were based on the paired comparison approach developed by Degner and colleagues. A consecutive sample of patients (n=82) with recently diagnosed ovarian cancer was asked to participate.Sixty-four patients (78%) chose to participate. The three different measurements of participants' information needs revealed only small changes in these needs. The three most important information needs, in all measurements, were information about the likelihood of cure, information about the stage and spreading of the disease, and information about different treatment options. Information regarding sexual attractiveness was the lowest ranked item in all measurements. Regarding subgroups (age, education) the only significant difference throughout all measurements was that younger patients rated issues of sexual attractiveness higher than older patients (p=0.005).In this longitudinal study patients with ovarian cancer ranked information about the disease and its treatment (i.e. likelihood of cure, stage of disease, and treatment options) highest, and information about psychosocial aspects and self-care lowest. These findings are in accordance with the results from studies of women diagnosed with other types of cancer, which used the same methodology. © 2004 Elsevier Ltd. All rights reserved.
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2.
  • Carlsson, Maria, 1958-, et al. (författare)
  • Treatment modality affects long-term quality of life in gynaecological cancer.
  • 2000
  • Ingår i: Anticancer Research. - : The International Institute of Anticancer Research. - 0250-7005 .- 1791-7530. ; 20:1B, s. 563-568
  • Tidskriftsartikel (refereegranskat)abstract
    • In order to survey the side effects after cancer treatment, quality of life data were collected from females in clinical remission. MATERIALS AND METHODS The study was cross-sectional; every patient that visited the outpatient clinic during a period of three months was asked to anonymously complete the EORTC QLQ-C30 questionnaire and five additional specific questions related to gynaecological cancer. RESULTS In total, 235 patients (90%) returned the questionnaire. In general, both the levels of functioning and symptomatology were time-dependent. Patients with short treatment-free intervals reported more problems than the others. When using treatment modality as an independent variable in the statistical calculations, a treatment-related effect on functioning and symptomatology was demonstrated (p < 0.05 to p < 0.001). Patients previously treated with chemotherapy had poorer role- and cognitive functioning and more problems with fatigue, nausea, vomiting, dyspnoea, constipation and financial problems, compared with those not treated with chemotherapy (p < 0.05 to p < 0.01). Those patients who had been treated with external radiotherapy and/or brachytherapy had significantly more problems with flatulence and diarrhoea (p < 0.05 to p < 0.001). In conclusion, patients who underwent treatment for gynaecological cancer reported long-term side effects also many years after finishing treatment. The problems where related to treatment modality which should be considered, especially when planning adjuvant treatment.
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3.
  • Planck, Maria (författare)
  • Hereditary Nonpolyposis Colorectal Cancer - Molecular Genetics and Biology of Associated Tumors
  • 2002
  • Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
    • This thesis focuses on one of the most common types of hereditary cancer, hereditary nonpolyposis colorectal cancer (HNPCC). This syndrome is characterized by an autosomal dominant inheritance, an increased risk for several types of cancer (especially cancer of the colorectum, small bowel, endometrium, ovary and urinary tract), early age at diagnosis, and frequent development of multiple primary malignancies. HNPCC is caused by a germline mutation in one of several DNA mismatch-repair (MMR) genes. In paper I, we screened 16 families with suspected HNPCC for germline MMR gene mutations and found a diverse spectrum of mutations, involving the MMR genes MLH1, MSH2 and MSH6. A defective MMR is associated with microsatellite instability (MSI) in the tumor tissue and with somatic mutations in repeated sequences in several cancer-associated genes. In paper II, we studied the occurrence of such alterations in 24 tumors from 14 individuals in an HNPCC family with a germline MSH2 mutation and found an extensive intra- and inter-individual variation. Paper III demonstrates intratumoral heterogeneity of repeat-mutations in 10 macroscopically different areas of a colon carcinoma in a patient with a germline MLH1 mutation. The variation in the somatic mutations in repeat-containing genes suggests that these alterations are important for tumor progression rather than initiation and that the accumulation of mutations, rather than the specific alterations, drives HNPCC tumorigenesis. MMR defects play a role also in the development of sporadic (non-hereditary) cancer and are found in about 15% of colon cancers. In paper IV, we investigated rectal cancer patients regarding a family history of cancer and MSI in the tumor tissue. Only 3/165 (2%) of the tumors had MSI and all 3 patients were found to carry germline HNPCC-causing mutations. We conclude that MSI is rare in rectal cancer, but, when present, strongly indicates HNPCC. In paper V, we studied MSI and immunohistochemical expression of the MMR proteins in small bowel adenocarcinomas and found MSI in 11/70 (16%) tumors, 7 of which showed loss of MMR expression. Defective MMR thus contributes to small bowel carcinogenesis in a fraction of the tumors similar to colon cancer. In paper VI, we studied a population-based series of women who developed the two most common cancer types in HNPCC, colorectal cancer and endometrial cancer, before age 50. MSI was demonstrated in 75% of the tumors and concordant loss of the same MMR protein in both tumors, suggesting an underlying MMR gene mutation, was found in 12/27 patients. In summary, this thesis presents novel HNPCC-causing mutations, demonstrates variability among somatic mutations in repeat-containing genes in HNPCC-tumors, delineates the contribution of defective MMR in rectal cancer and small bowel cancer and points to a high risk of HNPCC among women with colorectal and endometrial cancer at young age.
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5.
  • Villman, Kenneth, et al. (författare)
  • Topoisomerase II-α expression in different cell cycle phases in fresh human breast carcinomas
  • 2002
  • Ingår i: Modern Pathology. - Baltimore : Lippincott Williams & Wilkins. - 0893-3952 .- 1530-0285. ; 15:5, s. 486-491
  • Tidskriftsartikel (refereegranskat)abstract
    • Topoisomerase II-alfa (topo IIalfa) is the key target enzyme for the topoisomerase inhibitor class of anti-cancer drugs. In normal cells, topo IIalfa is expressed predominantly in the S/G2/M phase of the cell cycle. In malignant cells, in vitro studies have indicated that the expression of topo IIalfa is both higher and less dependent on proliferation state in the cell. We studied fresh specimens from 50 cases of primary breast cancer. The expression of topo IIalfa in different cell cycle phases was analyzed with two-parameter flow cytometry using the monoclonal antibody SWT3D1 and propidium iodide staining. The expression of topo IIalfa was significantly higher in the S/G2/M phase of the cell cycle than in the G0/G1 phase in both DNA diploid and DNA nondiploid tumors. In 18 of 21 diploid tumors, and in 25 of 29 nondiploid tumors, >50% of the topo IIalfa–positive cells were in the G0/G1 phase. This significant expression of topo IIalfa in the G0/G1 phase of the cell cycle may have clinically important implications for treatment efficacy of topoisomerase II inhibitors.
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6.
  • Jestin, P, et al. (författare)
  • Elective surgery for colorectal cancer in a defined Swedish population.
  • 2004
  • Ingår i: European Journal of Surgical Oncology. - : Elsevier BV. - 0748-7983 .- 1532-2157. ; 30:1, s. 26-33
  • Tidskriftsartikel (refereegranskat)abstract
    • AIMS: The aim of this study was to describe variability in compliance to clinical guidelines in colorectal cancer surgery related to hospital structure.METHODS: All patients registered in the databases of the Regional Oncologic Centre, operated upon electively for colon cancer between the start of the register in 1997 until 2000 (n=1771) and for rectal cancer between the start of the register in 1995 until 2000 (n=1841) were selected for analysis.RESULTS: There was no difference in 5-year survival rate between colon and rectal cancer (mean follow-up 2.6 and 3.0 years, respectively; p=0.22). There was a significant difference in frequency of preoperative liver scan depending on hospital category with an increase in colon cancer from 39 to 46% (p=0.02) and in rectal cancer from 42 to 64% (p<0.001). For colon cancer there was no difference, according to hospital category, in quotient sigmoid and high anterior resection to left-sided resection. Furthermore, high anterior resection was more common at university and general district hospitals (8%) compared with district hospitals (4%) (p=0.01). Sphincter-saving surgery was more common at university hospitals and district general hospitals than at district hospitals (low anterior/abdomino-perineal resection quotients 2.3, 2.4 and 1.6, respectively; p<0.001).CONCLUSIONS: Population-based audit forms an appropriate and valuable basis for quality assurance projects. In addition to describing compliance to guidelines and pointing to process steps that can be improved, such investigations may also indicate changes due to scientific development. Linked to case-costing data, such results may form an important basis for decisions about modifications in health care.
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7.
  • Rösch, Frank, et al. (författare)
  • Radiolanthanides in nuclear medicine.
  • 2004
  • Ingår i: Metal ions in biological systems. - 0161-5149. ; 42, s. 77-108
  • Forskningsöversikt (refereegranskat)
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8.
  • Kadar, Lianna (författare)
  • Body Protein and its Change in Patients During Anti-Tumor Treatment
  • 2001
  • Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
    • The purpose of this study was to investigate how total body protein and its fraction of body weight (body protein fraction) change in cancer patients during different anti-tumor treatments, and to see if these changes have any clinical significance in the form of prognostic value or correlation with disease course and tumor response. In 84 patients, 28 with lung cancer, 24 with gastrointestinal tumors, 30 with breast cancer, 1 with non-Hodgkin lymphoma and 1 with kidney cancer, the total amount of body nitrogen was measured using an in vivo prompt gamma neutron activation technique. Using the relationship 1 g nitrogen to 6.25 g protein, the amount of total body protein was calculated. The measurements of body protein and body weight were made during the period of radiation, cytostatic or hormone treatment. Each patient was his or her own control. The precision of the method for measurement of body protein was ±5% (1 SD). In patients with lung cancer, we noted a significant correlation between changes in total body protein during radiotherapy and the recurrence-free interval and overall survival. Patients, in whom body protein decreased, had a significantly shorter time to tumor recurrence than those in whom body protein increased or remained constant. In patients with gastrointestinal tumors we noted a significant difference between the changes in body protein fraction in the patients with loco-regional disease and the patients with metastasized disease, in whom the changes were greatest. Finally, in patients with metastasized breast cancer there was no significant correlation between change in body protein fraction and tumor response. The conclusions are that the amount of body protein in cancer patients changes during the disease and anti-tumor treatment. The amount of body protein in patients with lung cancer has a prognostic value, as a decrease of body protein is an indicator of tumor invasion and early metastasis as well as a decreased overall survival. In patients with gastrointestinal tumors a correlation between change in body protein fraction and course of the disease was seen.
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9.
  • Koul, Anjila (författare)
  • Molecular Genetic Alterations In Endometrial And Ovarian Cancers
  • 2001
  • Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
    • Endometrial cancer is the most common gynecological cancer diagnosed in western countries. Complex atypical hyperplasia (CAH) reflects a state of hyperestrinism and its role as a precursor lesion of this cancer is established. Endometrial cancers arising in association with CAH are reported in women of younger age, with early stage disease, favorable histological types, higher progesterone receptor levels and clinically better survival prognosis. However, the molecular events delineated in these two pathogenetic types are less known. Hereditary nonpolyposis colon cancer is caused by germline mutations in DNA mismatch repair (MMR) genes, and associated mainly with cancer in the colon, while endometrial and ovarian cancer are the most common extracolonic malignancies in these patients. Tumors from mutation carriers are characterized by an microsatellite instability (MSI) phenotype, and a subset of sporadic colon cancer demonstrates MSI and somatic mutations in MMR genes. MSI is also reported in a subset of sporadic endometrial cancers, although without identifiable mutation in MMR genes. In this study, endometrial cancers histologically checked for presence/absence of CAH were analyzed for mutations in the TP53, PTEN, KRAS, B-catenin, CDKN2A, BRCA1, and BRCA2 genes, as well as for their DNA ploidy and MSI. Two thirds of the endometrial tumors included in the study contained mutation in either of the seven genes analyzed, but very few cases with coexisting mutations were recorded, suggesting alternate genetic pathways in tumorigenesis. We found that PTEN, KRAS, B-catenin, and TP53 mutations were present in tumors both with and without CAH. PTEN mutations associated with MSI and DNA diploidy, while TP53 mutations related to DNA nondiploidy. Approximately 90% of all endometrial cancers are diagnosed in surgical stage disease I and II, with a five-year survival of 85% to 70%, respectively. A consensus opinion regarding useful prognostic markers to identify a “high-risk” subset among these patients is, however, lacking. In this study, TP53 alterations (mutation or protein overexpression) correlated to several clinicopathological markers of poor prognosis in endometrial cancer, and decreased progression-free survival in both early and advanced stage disease. However, DNA nondiploidy seemed to be an even better marker of poor prognosis in patients with early stage disease (I-II). The strongest risk factor for ovarian cancer is a positive family history of ovarian or breast cancer. While the majority of familial cases are associated with germline BRCA1 or BRCA2 mutation, the frequency of mutations in cases unselected for family history is still unclear. In the present pilot study of ovarian tumors, we detected a surprisingly high frequency of both germline and somatic BRCA-gene mutations, emphasizing the importance of extended analysis of population-based series of patients to determine the true contribution of these predisposing genes to the overall incidence of ovarian cancer in this population. BRCA-gene mutations strongly associated with a serous/seropapillary histological type. Unexpectedly, BRCA1 mutations were seen in two cases of ovarian cancer with brain metastasis.
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