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  • Klaff, Rami, 1971- (författare)
  • Disease-Specific Survival in Prostate Cancer Patients Results from the Scandinavian Prostate Cancer Group (SPCG) Trial No. 5 and Regional Cancer Register Data
  • 2016
  • Doktorsavhandling (övrigt vetenskapligt)abstract
    • <p><strong>Introduction</strong></p><p>Prostate cancer (PCa) is the most common cancer among men in Sweden. The clinical course varies considerably, which makes it difficult to predict the prognosis in the individual case. In order to explore the early as well as the late course of the disease, large study groups and population-based cohorts are necessary.</p><p>Aims</p><ul><li>To explore factors that influence the long-term outcome of men with low-risk tumours in a population-based register, to predict the long-term course, and to assess the mortality rate for men with prostate cancer (Paper I)</li><li>To analyse long-term outcome and to investigate factors associated with long-term survival in patients with metastases to the skeleton (Paper II)</li><li>To analyse early androgen deprivation treatment (ADT) failure and to define clinical predictors associated with short survival due to early ADT failure in prostate cancer patients with bone metastases (Paper III)</li><li>To analyse the prognostic significance of the extent of bone metastases in relation to other pretreatment variables in prostate cancer patients, and to explore the impact of bone metastases on quality-of-life (Paper IV)</li></ul><p><strong>Material and methods</strong></p><p>The study groups were assembled from The South East Region Prostate Cancer Register (SERPCR), and The Scandinavian Prostate Cancer Group (SPCG) Trial No. 5. In the first study, prognostic factors and long-term disease-specific mortality rates of low-risk prostate cancer patients from the early PSA era were analysed. In the second study, patient-related factors, quality-of-life (QoL) and long-term survival in 915 PCa patients with bone metastases (M1b) under ADT, were analysed. In Study III factors predicting primary failure to respond to ADT were identified. Study IV explored the impact of the extent of bone metastases on survival and QoL for these men.</p><p><strong>Result and conclusions</strong></p><p>The long-term disease-specific mortality of low-risk localised PCa is low, but the annual mortality rate gradually increases. This indicates that some tumours slowly develop into lethal cancer, particularly in men 70 years or older and with a PSA level ≥ 4 μg/L. From the SPCG Trial No. 5, a subgroup of patients with M1b disease and favourable set of predictive factors survived more than 10 years under ADT with an acceptable QoL. Independent predictors of long-term survival were identified as performance status (PS) &lt; 2, limited extent of bone metastases, and a PSA level &lt; 231 μg/L at the time of enrolment in the trial. However, four independent clinical predictors of early ADT failure could be defined. Men exhibiting these features should be considered for an alternative treatment. Patient grouping based on three categories of extent of bone metastases related to PS, haemoglobin, and QoL at presentation, as independent predictors of mortality, may provide improved accuracy of prognosis.</p>
  • Aljabery, Firas (författare)
  • Staging and tumor biological mechanisms of lymph node metastasis in invasive urinary bladder cancer
  • 2017
  • Doktorsavhandling (övrigt vetenskapligt)abstract
    • <p><strong>Aim: </strong>To study the possibility of detecting lymph node metastasis in locally advanced urinary bladder cancer (UBC) treated with radical cystectomy (RC) by using preoperative positron emission tomography/computed tomography (PET/CT) and peroperative sentinel node biopsy (SNB) technique. We also investigate the clinical significance of macrophage traits expression by cancer cells, M2-macrophage infiltration (MI) in tumor stroma and the immunohistochemical expression of biomarkers in cancer cells in relation to clinicopathologic data.</p><p><strong>Patients and Methods: </strong>We studied prospectively 122 patients with UBC, pathological stage pT1–pT4 treated with RC and pelvic lymph node dissection (PLND) during 2005–2011 at the Department of Urology, Linköping University Hospital. In the first study, we compared the results of preoperative PET/CT and conventional CT with the findings of postoperative histopathological evaluation of lymph nodes (LNs). In the second study we investigated the value of SNB technique for detecting pathological LNs during RC in patients with UBC. W also examined the significance of the primary tumor location in the bladder in predicting the site of LN metastases, and the prognostic significance of lympho-vascular invasion (LVI) and lymph node metastasis density (LNMD) on survival. In the third study, we investigate the clinical significance of macrophage infiltration (MI) in tumor stroma and macrophage-traits expression by tumor cells. In the fourth study, we investigate the cell cycle suppression proteins p53, p21, pRb, p16, p14 ARF as well as tumors proliferative protein Ki67 and DNA repair protein ERCC1 expression in cancer cells. The results were compared with clinical and pathological characteristics and outcome.</p><p><strong>Results: </strong>Prior to RC, PET/CT was used to detect LN metastasis in 54 patients. PET/CT had 41% sensitivity, 86% specificity, 58% PPV, and 76% NPV, whereas the corresponding figures for conventional CT were 41%, 89%, 64%, and 77%. SNB was performed during RC in 103 patients. A median number of 29 (range 7–68) nodes per patient were examined. SNs were detected in 83 out of 103 patients (81%). The sensitivity and specificity for detecting metastatic disease by SNB varied among LN stations, with average values of 67% -90%. LNMD or ≥8% and LVI were significantly related to shorter survival. In 103 patients, MI was high in 33% of cases, while moderate and low infiltration occurred in 42% and 25% of tumors respectively. Patients with tumors containing high and moderate compared to low MI had low rate of LN metastases (P=0.06) and improved survival (P=0.06), although not at significant level. The expression of different tumor suppression proteins was altered in 47-91% of the patients. There were no significant association between cancer specific survival (CSS) and any of the studied biomarkers. In case of altered p14ARF, ERCC1 or p21, CSS was low in case of low p53 immunostaining but increased in case of p53 accumulation, although not at a significant level, indicating a possible protective effect of p53 accumulation in these cases.</p><p><strong>Conclusion: </strong>PET/ CT provided no improvement over conventional CT in detection and localization of regional LN metastases in bladder cancer. It is possible to detect the SN but the technique is not a reliable for perioperative localization of LN metastases; however, LVI and LNMD at a cut-off level of 8% had significant prognostic values. MI in the tumor microenvironment but not CD163 expression in tumor cells seems to be synergistic with the immune response against urinary bladder cancer. Our results further indicate that altered p53 might have protective effect on survival in case of altered p14ARF, p21, or ERCC1 indicating an interaction between these biomarkers.</p>
  • Loftås, Per, 1964- (författare)
  • Response to neoadjuvant treatment in rectal cancer surgery
  • 2016
  • Doktorsavhandling (övrigt vetenskapligt)abstract
    • <p>Rectal cancer is one of the three most common malignancies in Sweden with an annual incidence of about 2000 cases. Current treatment consists of surgical resection of the rectum including the loco-regional lymph nodes in the mesorectum. In advanced cases, neoadjuvant chemo-radiotherapy (CRT) prior to the operative treatment reduces local recurrences and enables surgery. The neoadjuvant treatment can also eradicate the tumour completely, i.e. complete response. This research project was designed to investigate the effects of preoperative radiotherapy/ CRT and analyze methods to predict response to CRT.</p><p>Study I investigated the expression of the FXYD-3 protein with immunohistochemistry in rectal cancer, with or without preoperative radiotherapy. The results from the total cohort showed that, strong FXYD-3 expression was correlated to infiltrative tumour growth (p = 0.02). In the radiotherapy group, strong FXYD-3 expression was related to an unfavourable prognosis (p = 0.02). Tumours with strong FXYD-3 expression had less tumour necrosis (p = 0.02) after radiotherapy. FXYD-3 expression in the primary tumour was increased compared to normal mucosa (p=0.008). We concluded that FXYD-3 expression was a prognostic factor in patients receiving preoperative radiotherapy for rectal cancer.</p><p>Study II investigated FXYD-3 expression in tumours that developed local recurrences following surgery and compared this with expression in tumours that did not develop local recurrences. There was no difference in the expression of FXYD-3 between the group that developed local recurrences and the group that did not develop local recurrences. There was no difference in survival between those with strong or weak FXYD-3 expression. We concluded that this study could not confirm the findings from study 1 i.e. that FXYD-3 expression has prognostic significance in rectal cancer.</p><p>Study III was a register-based study on the incidence and effects of complete response to neoadjuvant treatment. Eight per cent of the patients with adequate CRT to achieve complete response also had a complete histological response of the luminal tumor in the resected bowel. Sixteen per cent of that group had remaining lymph node metastases in the operative specimen. Chemotherapy together with radiotherapy doubled the chance of complete response in the luminal tumour. Patients with remaining lymph node metastases had a lower survival rate compared to those without. We concluded that residual nodal involvement after neoadjuvant treatment was an important factor for reduced survival after complete response in the luminal tumour.</p><p>Study IV followed up the results from the previous study by re-evaluating magnetic resonance imaging (MRI)- images in patients with complete tumour response. Two experienced MRI radiologists performed blinded re-staging of post CRT MR- images from patients with complete response in the luminal tumour. One group with lymph node metastases and another one without were studied and the results compared with the pathology reports. The sensitivity, specificity, and positive and negative predicted values for correct staging of positive lymph nodes was 37%, 84%, 70% and 57%. The size of the largest lymph node (4.5 mm, p=0.04) seemed to indicate presence of a tumour positive lymph node. We concluded that MRI couldn’t correctly stage patients for lymph node metastases in patients with complete response to CRT in the luminal tumour.</p>
  • Sjöholm, H, et al. (författare)
  • Necrosis of malignant gliomas after intratumoral injection of 201Tl in vivo in the rat
  • 1995
  • Ingår i: Anti-Cancer Drugs. - Rapid Communications. - 0959-4973. ; 6:1, s. 109-114
  • Tidskriftsartikel (refereegranskat)abstract
    • Fourteen adult Fischer 344 rats were inoculated in vivo unilaterally in the caudate nucleus in the brain with malignant RG 2 glioma cells. By 3 weeks a tumor with a diameter of 3-6 mm normally develops. Ten animals which survived the repeated periods of anesthesia and thallium (Tl) injections (intratumorally three times of 201Tl, 15-23 days after inoculation) showed a prolonged retention of radioactivity at the site of injection with no uptake in other organs except for the kidneys. Singular circumscribed necroses were found post-mortem at the site of injection, comprising malignant glioma tumor tissue, which in six animals was absent, in three animals was markedly reduced in size compared with controls and in one animal had the expected size. In four animals metastases were found in distant locations in the brain; in three of these cases there was a retention of radioactivity in the tumor. The selective necrotizing effect on the tumor cells is interpreted as mainly due to emission of Auger electrons from intracellularly accumulated 201Tl, giving rise to very high energy deposition in the vicinity of the cell nucleus. The results should also have implications for the treatment of human malignant gliomas.
  • Eriksson, Erik M, et al. (författare)
  • Participation in a Swedish cervical cancer screening program among women with psychiatric diagnoses: a population-based cohort study.
  • 2019
  • Ingår i: BMC public health. - 1471-2458. ; 19:1
  • Tidskriftsartikel (refereegranskat)abstract
    • In Sweden, organized screening programs have significantly reduced the incidence of cervical cancer. For cancers overall, however, women with psychiatric diagnoses have lower survival rates than other women. This study explores whether women with psychiatric diagnoses participate in cervical cancer screening programs to a lesser extent than women on average, and whether there are disparities between psychiatric diagnostic groups based on grades of severity.
  • Ericson Lindquist, Kajsa (författare)
  • Tumors associated with Hereditary Nonpolyposis Colorectal Cancer: Defective Mismatch Repair and Familial Risk of Cancer
  • 2005
  • Doktorsavhandling (övrigt vetenskapligt)abstract
    • Popular Abstract in Swedish Defekt mismatch-reparation och familjär cancerrisk Cancer är på cellnivå en genetisk sjukdom. Förändringar i cellens arvsmassa (DNA) drabbar tre huvudtyper av gener; onkgener, tumörsuppressorgener och DNA-reparationsgener. Onkgener är en grupp gener som befrämjar cellens tillväxt. Vid cancerutveckling aktiveras onkgener via mutation eller genom ökat uttryck, vilket leder till ökad tillväxt. Tumörsuppressorgener hämmar normalt celldelning, bromsar cellcykeln, styr defekta celler till programmerad celldöd och verkar för stabilitet i genomet. När båda kopiorna av en tumörsuppressorgen inaktiveras förloras dess funktion, vilket befrämjar tumörbildning. Normalt finns alla gener i dubbel uppsättning, en kopia från vardera föräldern. Vid ärftlig cancer finns den första erforderliga DNA-förändringen (mutationen) i kroppens alla celler (konstitutionell mutation), medan icke-ärftlig (sporadisk) cancer uppkommer genom förvärvade (somatiska) mutationer av båda kopiorna. DNA-reparationsgener motverkar att förändringar i arvsmassan uppstår genom att ta hand om spontana mutationer vid celldelning via cellens olika DNA-reparationssystem. Defekt DNA-reparation är en tumörbiologisk mekanism som styr utvecklingen i flera vanliga tumörtyper, bl. a. i en andel av tjocktarmscancer och livmodercancer. Dessutom karakteriserar defekt DNA-reparation av typen mismatch repair (MMR) specifikt de tumörer som uppkommer genom det ärftliga syndromet hereditär nonpolyposis colorektal cancer (HNPCC). I MMR-systemet samverkar sex olika proteiner och vid HNPCC är någon av MMR-generna MLH1, MSH2, MSH6 eller PMS2 defekta. Personer som bär en av mutation i någon av dessa gener löper ca 90% risk att drabbas av cancer, vanligast i tjock-/ändtarm och livmoder, men även i njurbäcken/urinledare, tunntarm eller äggstockar. Tumörer som uppkommit via defekt MMR karakteriseras av så kallad mikrosatellitinstabilitet (MSI) och immunhistokemisk förlust av det defekta MMR-proteinets uttryck. Denna avhandlings fyra första delarbeten innefattar tumörbiologiska studier i vilka vi har undersökt förekomst av defekt MMR i olika tumörtyper associerade med HNPCC. I arbete I studerades individer med fyra primära (separat uppkomna) tumörer varav minst två i tjocktarm eller ändtarm. Defekt MMR förekom i 41% av tumörerna. Hos 17/45 patienter (38%) var samma MMR protein förlorat i flera tumörer. Studien visade en ökad frekvens MMR-defekter vid multipla tumörer och HNPCC är en diagnos som bör övervägas hos patienter som drabbas av flera tumörer. I arbete II undersöktes defekt MMR i tunntarmscancer, vilket förekom i 18% av fallen. MMR defekter var något vanligare bland de unga patienterna. Fynden visar att MMR-defekter i tunntarmscancer är ungefär lika vanliga som i tjocktarmscancer. I arbete III studerades cancer i de övre urinvägarna, dvs. i njurbäcken och urinledare. MSI och/eller immunhistokemisk MMR-proteinförlust påvisades i cirka 5% av fallen. Trots en ökad risk för cancer i urinvägarna hos individer med HNPCC indikerar studien att endast en liten andel av tumörer i de övre urinvägarna uppkommer via defekt MMR. I arbete IV påvisades att defekt MMR också kan förekomma i sarkom, en ovanlig tumörform som uppkommer i kroppens stödjevävnader. Denna tumörtyp är normalt inte associerad med ärftlighet, men en koppling mellan sarkom och HNPCC finns sannolikt. I Sverige sker en rapportering av alla cancerdiagnoser till ett nationellt cancerregister. Det finns även ett familjeregister där individers barn kan identifieras. Genom att länka cancerregister och familjeregister till varandra kan cancerrisker hos barn till föräldrar med cancer räknas ut. Delarbete V är en epidemiologisk studie (en studie av samband och riskfaktorer i en befolkning) där vi beräknat cancerrisker hos individer vars föräldrar drabbats av de cancertyper som är vanligast vid HNPCC. Analyserna visade att barn till personer med någon HNPCC-associerad diagnos löper en förhöjd risk att själva drabbas av cancer, framför allt i samma organ som föräldern. Störst cancerrisk har de barn vars föräldrar fått sin tumör före 50 års ålder, barn som har både en förälder och ett syskon med cancer och barn vars förälder utvecklat flera primära tumörer. I studien påvisades ett starkt samband mellan canceruppkomst och HNPCC-associerad tumör hos en förälder och resultaten bekräftar vikten av att ta hänsyn till förekomst av flera olika tumörtyper när HNPCC övervägs som diagnos. Studien visade även att flera primära tumörer hos en individ är en stark riskfaktor för ärftlighet, jämförbar med tumörförekomst hos flera individer i familjen. Sammanfattningsvis har vi i arbetena I-V · påvisat defekt MMR i hög frekvens hos individer som utvecklat flera primära cancrar · visat att defekt MMR förekommer i samma frekvens i tunntarmscancer som i tjocktarmscancer · funnit låg andel defekt MMR i cancer i de övre urinvägarna · visat att defekt MMR förekommer i mjukdelssarkom samt · beräknat cancerrisker hos individer vars föräldrar utvecklat HNPCC-relaterad cancer
  • Duell, Eric J., et al. (författare)
  • Menstrual and reproductive factors in women, genetic variation in CYP17A1, and pancreatic cancer risk in the European prospective investigation into cancer and nutrition (EPIC) cohort
  • 2013
  • Ingår i: International Journal of Cancer. - 0020-7136 .- 1097-0215. ; 132:9, s. 2164-2175
  • Tidskriftsartikel (refereegranskat)abstract
    • Menstrual and reproductive factors and exogenous hormone use have been investigated as pancreatic cancer risk factors in case-control and cohort studies, but results have been inconsistent. We conducted a prospective examination of menstrual and reproductive factors, exogenous hormone use and pancreatic cancer risk (based on 304 cases) in 328,610 women from the EPIC cohort. Then, in a case-control study nested within the EPIC cohort, we examined 12 single nucleotide polymorphisms (SNPs) in CYP17A1 (an essential gene in sex steroid metabolism) for association with pancreatic cancer in women and men (324 cases and 353 controls). Of all factors analyzed, only younger age at menarche (<12 vs. 13 years) was moderately associated with an increased risk of pancreatic cancer in the full cohort; however, this result was marginally significant (HR = 1.44; 95% CI = 0.992.10). CYP17A1 rs619824 was associated with HRT use (p value = 0.037) in control women; however, none of the SNPs alone, in combination, or as haplotypes were associated with pancreatic cancer risk. In conclusion, with the possible exception of an early age of menarche, none of the menstrual and reproductive factors, and none of the 12 common genetic variants we evaluated at the CYP17A1 locus makes a substantial contribution to pancreatic cancer susceptibility in the EPIC cohort.
  • H., Olsson, et al. (författare)
  • Worse breast cancer prognosis in insulin treated diabetic patients - A population based registry study in Sweden
  • 2015
  • Ingår i: 37th San Antonio Breast Cancer Symposium,San Antonio, Texas, United States,2014-12-09 - 2014-12-13. - American Association for Cancer Research Inc..
  • Konferensbidrag (refereegranskat)abstract
    • Background. Diabetes may be linked to incidence of different tumor diseases and prognosis through various mechanisms such as the disease itself, hyperglycemia, obesity and anti-diabetes therapy. Material and methods. The study includes all women with BC diagnosed in Sweden between 2000 through 2008 (n=54406). The women had no previous cancer diagnosis during the period of 1958-1999. Dates of birth, BC diagnosis and TNM-stage where directly extracted from the cancer registry. The women's anti-diabetes therapy was gathered from the Swedish Prescribed Drug Registry. Information regarding the cause of death and date of death was obtained from the Cause of Death Registry and tbe Swedish Population Register up until the 31st of December 2012 and 31st of December 2013 respectively. Analyses have been restricted to patients receiving insulin therapy (n=2463) and their breast cancer prognosis has been calculated in comparison with breast cancer patients without diabetes. All analyses were adjusted for TNM-stage and age at diagnosis. Results. Patients with insulin treated diabetes had a worse prognosis compared with other women with breast cancer (HR 1.7, 95%CI 1.5-2.0). The worse prognosis could be seen both for patients with ER+ and ER- tumors. The worst prognosis was seen for patients treated with NPH insulins (HR 2.8, 95% CI 2.4-3.3) while patients treated with long-acting insulin analogs had an intermediate prognosis (HR 1.6, 95% CI 1.2-2.2). Those women treated with NPH insulins and metformin had a slightly worse prognosis (HR 1.4, 95% CI 1.0-1.8). The results for breast cancer specific survival and total survival were similar. Conclusion. Our results imply that insulin treated breast cancer patients have a worse survival compared with other women with breast cancer regardless of tumor stage. Metformin therapy may partially counteract the association.
  • Assel, M. J., et al. (författare)
  • Long-term prediction of prostate cancer diagnosis and death using PSA and obesity related anthropometrics at early middle age : : Data from the malmö preventive project
  • 2018
  • Ingår i: Oncotarget. - Impact Journals, LLC. - 1949-2553. ; 9:5, s. 5778-5785
  • Tidskriftsartikel (refereegranskat)abstract
    • Objectives: To evaluate whether anthropometric parameters add to PSA measurements in middle-aged men for risk assessment of prostate cancer (PCa) diagnosis and death. Results: After adjusting for PSA, both BMI and weight were significantly associated with an increased risk of PCa death with the odds of a death corresponding to a 10 kg/m2 or 10 kg increase being 1.58 (95% CI 1.10, 2.28; p = 0.013) and 1.14 (95% CI 1.02, 1.26; p = 0.016) times greater, respectively. AUCs did not meaningfully increase with the addition of weight or BMI to prediction models including PSA. Materials and Methods: In 1974 to 1986, 22,444 Swedish men aged 44 to 50 enrolled in Malmö Preventive Project, Sweden, and provided blood samples and anthropometric data. Rates of PSA screening in the cohort were very low. Documentation of PCa diagnosis and disease-specific death up to 2014 was retrieved through national registries. Among men with anthropometric measurements available at baseline, a total of 1692 men diagnosed with PCa were matched to 4190 controls, and 464 men who died of disease were matched to 1390 controls. Multivariable conditional logistic regression was used to determine whether diagnosis or death from PCa were associated with weight and body mass index (BMI) at adulthood after adjusting for PSA. Conclusions: Men with higher BMI and weight at early middle age have an increased risk of PCa diagnosis and death after adjusting for PSA. However, in a multivariable numerical statistical model, BMI and weight do not importantly improve the predictive accuracy of PSA. Risk-stratification of screening should be based on PSA without reference to anthropometrics.
  • Allum, W., et al. (författare)
  • ECCO essential requirements for quality cancer care: Oesophageal and gastric cancer
  • 2018
  • Ingår i: Critical reviews in oncology/hematology. - 1040-8428. ; 122, s. 179-193
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: ECCO essential requirements for quality cancer care (ERQCC) are checklists and explanations of organisation and actions that are necessary to give high-quality care to patients who have a specific type of cancer. They are written by European experts representing all disciplines involved in cancer care. ERQCC papers give oncology teams, patients, policymakers and managers an overview of the elements needed in any healthcare system to provide high quality of care throughout the patient journey. References are made to clinical guidelines and other resources where appropriate, and the focus is on care in Europe. Oesophageal and gastric: essential requirements for quality care: • Oesophageal and gastric (OG) cancers are a challenging tumour group with a poor prognosis and wide variation in outcomes among European countries. Increasing numbers of older people are contracting the diseases, and treatments and care pathways are becoming more complex in both curative and palliative settings.• High-quality care can only be a carried out in specialised OG cancer units or centres which have both a core multidisciplinary team and an extended team of allied professionals, and which are subject to quality and audit procedures. Such units or centres are far from universal in all European countries.• It is essential that, to meet European aspirations for comprehensive cancer control, healthcare organisations implement the essential requirements in this paper, paying particular attention to multidisciplinarity and patient-centred pathways from diagnosis, to treatment, to survivorship. Conclusion: Taken together, the information presented in this paper provides a comprehensive description of the essential requirements for establishing a high-quality OG cancer service. The ERQCC expert group is aware that it is not possible to propose a ‘one size fits all’ system for all countries, but urges that access to multidisciplinary units or centres must be guaranteed for all those with OG cancer.
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