4 resultados para prostatacancer


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Syftet med denna systematiska litteraturstudie var att beskriva männens upplevelser av livskvalitet vid prostatacancer samt deras behov av stöd från sjuksköterskan och närstående. Studiens resultat grundade sig på 17 vetenskapliga artiklar av både kvalitativ samt kvantitativ ansats. Artiklarna söktes med hjälp av valda sökord via Högskolan Dalarnas databaser. Artiklarna kvalitetgranskades utifrån modifierade granskningsmallar. Resultatet visade att män med prostatacancer upplevde urininkontinens som den svåraste emotionella upplevelsen och de kände stor frustration över att inte kunna kontrollera sin vattenkastning. Männen negligerade sina kroppar på grund av sina inkontinensbesvär. Männen beskrev även att de upplevde en saknad efter lust för sexuell samvaro speciellt de yngre männen som uttryckte förtvivlan över sin nedsatta erektionsförmåga. Männen upplevde förändringarna i sin identitet och maskulinitet som mycket smärtsamma. I stödet från sjuksköterskan beskrev männen att de kände en saknad efter att få diskutera existentiella frågor och tankar med sjuksköterskan medan andra män upplevde att sjuksköterskan bemötte deras behov av stöd. Männen kände sig lugna när de samtalat med sjuksköterskan. I stödet från närstående uppskattade männen sin partners omtanke och förståelse. De förlitade sig främst på sin partner och familj som fanns vid deras sida för att tillsammans dela de djupaste tankar och funderingar.

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Syftet med denna systematiska litteraturstudie var att undersöka hur patienter med prostatacancer upplever stöd och information från vården och närstående. Resultaten i studien grundades på 15 vetenskapliga artiklar av både kvalitativ och kvantitativ ansats. Sökningar gjordes via Högskolan Dalarnas sökmotor Elin@dalarna och databaserna Blackwell synergy, Cinahl, Weiley och PubMed. Via granskningsmallar kvalitetsgranskades artiklarna, utgivna 1999-2009. Artiklarna var på engelska och etiskt godkända. Det uppsatsförfattarna funnit efter sina litteraturstudier var att vården gällande stöd och information såg väldigt olika ut inom vården. Det beror naturligtvis på patientens behov av hjälp och dennes fas i sjukdomen. Patienterna sökte stöd och information hos familj och bekanta som hade erfarenhet av prostatacancer. Deltagarna upplevde dessa som bra källor till stöd och information. Resultatet visade även på att det fanns stödgrupper och att deltagare upplevde dessa som positivt, men att flera deltagare inte visste att dessa stödgrupper existerade.

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Narratives about life-changing events like cancer have become more common in today’s society. The purpose of the present study was to investigate whether gender patterns in society can also be found in pathographies about cancer, and further to investigate how gender is expressed in these cancer related narratives. Questions were posed on characteristics of the autobiographical cancer narratives, how gender is constructed by the authors of these narratives, and what these narratives say about gender structures’ liability to change in the individuals affected by this disease. The material consisted of two Swedish pathographies about breast cancer, written by women, and two Swedish pathographies about prostate cancer, written by men. These works were published in the first decade of the present century. Narrative interpretation was used as the analysis method. The results show that gender patterns expressed in these narratives mainly follow conventional standards. Gender structures appear to be resistant to change in men and women diagnosed with cancer. The narratives by the women authors appear though to be somewhat more open to using the notions of manhood than was sees in narratives by the male authors regarding norms of femininity.

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Hereditary non-polyposis colorectal carcinoma (HNPCC; Lynch syndrome) is among the most common hereditary cancers in man and a model of cancers arising through deficient DNA mismatch repair (MMR). It is inherited in a dominant manner with predisposing germline mutations in the MMR genes, mainly MLH1, MSH2, MSH6 and PMS2. Both copies of the MMR gene need to be inactivated for cancer development. Since Lynch syndrome family members are born with one defective copy of one of the MMR genes in their germline, they only need to acquire a so called second hit to inactivate the MMR gene. Hence, they usually develop cancer at an early age. MMR gene inactivation leads to accumulation of mutations particularly in short repeat tracts, known as microsatellites, causing microsatellite instability (MSI). MSI is the hallmark of Lynch syndrome tumors, but is present in approximately 15% of sporadic tumors as well. There are several possible mechanisms of somatic inactivation (i.e. the second hit ) of MMR genes, for instance deletion of the wild-type copy, leading to loss of heterozygosity (LOH), methylation of promoter regions necessary for gene transcription, or mitotic recombination or gene conversion. In the Lynch syndrome tumors carrying germline mutations in the MMR gene, LOH was found to be the most frequent mechanism of somatic inactivation in the present study. We also studied MLH1/MSH2 deletion carriers and found that somatic mutations identical to the ones in the germline occurred frequently in colorectal cancers and were also present in extracolonic Lynch syndrome-associated tumors. Chromosome-specific marker analysis implied that gene conversion, rather than mitotic recombination or deletion of the respective gene locus accounted for wild-type inactivation. Lynch syndrome patients are predisposed to certain types of cancers, the most common ones being colorectal, endometrial and gastric cancer. Gastric cancer and uroepithelial tumors of bladder and ureter were observed to be true Lynch syndrome tumors with MMR deficiency as the driving force of tumorigenesis. Brain tumors and kidney carcinoma, on the other hand, were mostly MSS, implying the possibility of alternative routes of tumor development. These results present possible implications in clinical cancer surveillance. In about one-third of families suspected of Lynch syndrome, mutations in MMR genes are not found, and we therefore looked for alternative mechanisms of predisposition. According to our results, large genomic deletions, mainly in MSH2, and germline epimutations in MLH1, together explain a significant fraction of point mutation-negative families suspected of Lynch syndrome and are associated with characteristic clinical and family features. Our findings have important implications in the diagnosis and management of Lynch syndrome families.