Colorectal rectal cancer (CRC) is the 3rd most common cancer in men, the 2nd most common cancer in women, and the 4th leading cause of cancer death. Lack of screening or delayed screening for CRC is the major cause of undiagnosed cancers that become malignant and eventually become fatal. Nurses at the project site are not in compliance with CRC screening guidelines due to inadequate knowledge of the screening guidelines recommended by the American Cancer Society, which creates a gap in practice. The purpose of this project was to develop staff education on CRC screening guidelines. The practice focused question addressed if evidence-based education regarding CRC screening could be an effective means for nurse education, according to a panel of local experts. A pre-test evaluation of knowledge regarding CRC screening was administered to nursing staff from the site. The John Hopkins evidence-based practice model guided the development of the staff education program, using the results of the pre-test, evidence-based practice literature and guidelines. The project team, consisting of a physician and medical support staff, evaluated the education program, plan for delivery, and plan for evaluation of learning through an anonymous Likert-style evaluation survey. The 3 team members also completed program evaluation surveys, and 100% agreed or strongly agreed that the program objectives were met. The project was limited to planning only and the education program materials, along with plans for later implementation and evaluation of learning through pre- and post-tests, were handed over to the project site for delivery at a later date. The CRC screening education will become part of the yearly staff competencies, leading to appropriate screening of the site’s patient population. This education project has the potential to promote positive social change by saving lives and improving the quality of those lives.

Le renouvellement de l’épithélium intestinal repose sur la prolifération incessante de cellules souches intestinales (CSI) capables de régénérer l’intégralité de l’épithélium en 3 à 5 jours. Des altérations de ces dernières sont à l’origine de la transformation tumorale. L’étude des mécanismes impliqués dans la protection des CSI face à différents stress est donc essentielle pour mieux comprendre l’homéostasie et les pathologies intestinales. Dans un modèle de souris prédisposées à développer des tumeurs suite à la perte du gène Apc, notre équipe a pu précédemment démontrer une activation de l’autophagie nécessaire à la croissance tumorale. Nos travaux visent à étudier le rôle de ce processus catabolique dans l’homéostasie des CSI. Pour ce faire, nous utilisons des modèles murins génétiquement modifiés et des cultures d’organoïdes afin d’étudier les effets de l’inhibition de l’autophagie dans l’homéostasie intestinale et en particulier dans les CSI.Nos travaux indiquent que l’inhibition de l’autophagie par l’invalidation du gène Atg7 conduit à une activation de p53 et de l’apoptose spécifique des CSI. L’invalidation simultanée du gène Tp53 empêche la mort des CSI déficientes en autophagie. De plus, au long terme, ces souris développent des tumeurs, contrairement aux souris invalidées uniquement pour les gènes Atg7 ou Tp53. Nous avons donc émis l’hypothèse que l’inhibition de l’autophagie sensibilisait les CSI à l’apoptose suite à une accumulation de dommages cytotoxiques. Par une analyse d’expressions géniques des CSI issues de cryptes contrôles et invalidées pour le gène Atg7, nous avons mis en évidence une altération des réponses associées au stress oxydant et à la réparation de l’ADN. Confirmant ces signatures, nous avons observé des dommages de l’ADN dans les cryptes déficientes en autophagie et un défaut de réparation de ces dommages suite à une irradiation. Nous observons également une accumulation d’espèces réactives de l’oxygène dans les CSI déficientes en autophagie associée à une atténuation de la réponse antioxidante médiée par NRF2. Des traitements antibiotiques à large-spectre ou antioxydants améliorent la survie des CSI déficientes en autophagie et soutiennent l’influence des espèces réactives de l’oxygène et de la flore intestinale sur la mort des CSI. Nos travaux indiquent donc un rôle important de l’autophagie dans la protection et le maintien des CSI, de par son contrôle des espèces réactives de l’oxygène, du microenvironnement bactérien et des voies de réparation de l’ADN. / The renewal of the intestinal epithelium relies on the continuous proliferation of stem cells capable of regenerating the entire epithelium every 3 to 5 days. These intestinal stem cells (ISC) are thought to be the cell of origin for colorectal cancer. Thus, characterizing the mechanisms involved the protection of ISC against different stresses is key to understanding both intestinal homeostasis and tumor development. In tumoral tissue from mice predisposed to intestinal tumor development following the loss of the tumor suppressor gene Apc, our laboratory previously showed an upregulation of autophagy required for tumor growth. Our work aims to understand the role this catabolic mechanism in the homeostasis of ISC. To this end, we use genetically modified mouse models and intestinal organoid culture to study the effects of autophagy inhibition in intestinal homeostasis and in particular in ISC.We found that the inhibition of autophagy upon deletion of the gene Atg7 results in p53 activation and apoptosis of ISC specifically. The simultaneous deletion of Tp53 prevents the death of autophagy-deficient ISC. Moreover, over time, mice deficient for both Atg7 and Tp53 develop tumors, contrary to those deficient for either Atg7 or Tp53 alone. We therefore hypothesized that the inhibition of autophagy sensitizes ISC to p53-mediated apoptosis as a result of accumulated pro-tumorigenic damages. Transcriptomic analysis on sorted control or Atg7-deficient ISC revealed aterations in oxidative stress and DNA damage responses. Confirming these signatures, we observed DNA damages in autophagy-deficient crypts along with a defect in the repair of induced damages following irradiation. We additionally observed an accumulation of reactive oxygen species in autophagy-deficient ISC linked to a downregulation of the NRF2-mediated antioxidant response. Wide-spectrum antibiotic or antioxidant treatments improve the survival of autophagy-deficient ISC and support the contribution of both reactive oxygen species and the intestinal microbiota to the death of ISC. Our work therefore reveals we find an important function of autophagy in the integrity and maintenance of ISC by controlling reactive oxygen species, the microbial microenvironment and DNA repair pathways.

Le cancer colorectal (CRC) est l'un des cancers les plus agressifs. Afin de rechercher de nouveaux marqueurs de progression de ce cancer, des puces tout transcriptome et épissage, ainsi que des puces microARNs, ont été précédemment utilisées au laboratoire.Dans une première partie, l’analyse des données transcriptomiques a permis de trouver un ensemble de transcrits dérégulés dans les adénomes et dans le CRC, dont la surexpression de TIMP1, associée à la diminution de rétention de l’intron 3, par rapport à la muqueuse normale. Ce transcrit aberrant n’est pas sujet au mécanisme de dégradation active des ARNm («Nonsense-Mediated mRNA Decay »). Nous avons alors analysé les mécanismes d’épissage de TIMP1, ce qui nous a conduits à identifier hnRNPA1 comme un régulateur important, à la fois in vitro et in vivo, de la rétention de l’intron 3 de TIMP1, via sa fixation au début de l’exon 4. Le rôle de TIMP1i3 (+) dans la progression du CRC reste à identifier.Dans une seconde partie, l’analyse des données de la puce microARNs (miRs) a permis de trouver un ensemble de miRs dérégulés dans les CRC. Nous avons sélectionné des gènes codant des facteurs d’épissage dont l’expression était modifiée au cours de la progression cancéreuse, en tant que cibles possibles de certains de ces miRs. Six interactions ont été montrées (PRMT5/miR145; SRSF6/miR375; RBMX/miR23a; RBMX/miR24; RBMX/miR125a5p; SRSF11/miR143).En utilisant la technique de « Luciferase Reporter Gene Assay » couplée à la mutagenèse dirigée, nous avons montré que le miR145 régule négativement l’expression de PRMT5 par interaction avec la région 3’ non traduite du gène. Du fait du contrôle de la machinerie d’épissage des ARN prémessagers par PRMT5, nous proposons que miR145 pourrait être un régulateur général de l’épissage. / Colorectal cancer (CRC) is one of the most vaggressive cancers in the world. In order to look for new markers in progression of this cancer, all transcriptome and splice chips, as well as microRNA chips, have been previously used in the laboratory.In the first part of my thesis, transcriptomic data analysis revealed a set of deregulated transcripts in adenoma and in CRC, including overexpression of TIMP1, associated with the decrease of intron 3 retention, compared to normal mucosae. This aberrant transcript is not subject to the active mechanism of mRNAs degradation ("Nonsense-Mediated mRNA Decay"). Then we analysed the splicing mechanisms of TIMP1, which led us to identify hnRNPA1 as a major regulator, both in vitro and in vivo, of TIMP1 intron 3 retention via its binding in the beginning of exon 4. TIMP1i3 (+) role in the progression of CRC remains to be identified.In a second part, the analysis of microRNA data (miRs) revealed a set of deregulated miRs in CRC. The aim was to identify target genes for these miRs.We selected genes encoding splice factors whose expression was modified during cancer progression as possible targets for some of these miRs. Six interactions were shown (PRMT5/miR145; SRSF6/miR375; RBMX/miR23a; RBMX/miR24; RBMX/miR125a5p; SRSF11/miR143).Using the "Luciferase Reporter Gene Assay" technique coupled with site directed mutagenesis, we have shown that miR145 negatively regulated the expression of PRMT5 by interaction with its 3’untranslated translated region. Due to the control of the premessenger RNA splicing machinery by PRMT5, we propose that miR145 could be a general splicing regulator.

Le cancer colorectal (CCR) est le premier cancer digestif dans les pays occidentaux. Malgré les progrès thérapeutiques réalisés au cours des deux dernières décennies, la survie relative à 5 ans ne dépasse pas 56%, et s’abaisse à 11,3% pour les patients métastatiques. Le pronostic est lié au stade de développement de la maladie au moment du diagnostic. Les décès sont en rapport avec une résistance primaire de la masse tumorale aux thérapies, ou la survenue de récidive, en rapport avec une maladie microscopique résiduelle, non contrôlée par les thérapies systémiques adjuvantes. Le travail réalisé au sein de notre laboratoire portant sur deux voies de signalisation met en leurs rôles dans le CCR : les neurotrophines (NTs, facteurs de croissance impliqués dans la survie des cellules cancéreuses) et l’autophagie (processus de recyclage cellulaire impliqué dans la résistance au stress). Le but de cette étude a été d’analyser la part de ces deux voies dans la survie des cellules du cancer colo-rectal et l’impact de leur inhibition sur le devenir cellulaire et l’évolution tumorale. L’étude a été menée sur deux lignées cellulaires provenant du même patient : SW480 (tumeur primaire) et SW620 (invasion ganglionnaire), aussi utilisées pour la réalisation de greffes sous cutanées sur le modèle murin Nude. De plus, la présence de principales protéines des NTs (TrkB) et de l’autophagie (LC3) a été analysée dans les tissus de patients. Des travaux précédents menés sur des cultures de CCR ont montré que la surexpression de TrkB était associée à la survie cellulaire. Nous avons donc choisi d’inhiber la voie des NTs avec le K252a (100nM). Sur culture cellulaire de CCR, in vitro, l’inactivation de la voie PI3K / AKT, induit une activation de l’autophagie. A l’opposé, le blocage du flux autophagique par une approche pharmacologique (avec la chloroquine, CQ ; 25µM) ou par une approche transcriptomique (siRNA anti-ATG5) induit une suractivation de la signalisation des NTs, via le couple TrkB/BDNF. Ainsi, les deux voies de survie se compensent mutuellement et la double inhibition permet l’amélioration de l’effet des simples traitements. L’utilisation des deux inhibiteurs in vivo induit une réduction spectaculaire du volume tumoral (voire même la disparition dans certains cas). Finalement, la présence de la forme active du TrkB (phospho TrkB) et de la forme active de la LC3 (LC3II), démontrant l’activation de ces deux voies dans les tissus de patients, a été observée. L’ensemble de ces résultats montre que l’activation des voies des NTs et de l’autophagie contribue à la survie des cellules de CCR. L’approche qui consiste à la double inhibition des NTs et de l’autophagie pourrait être un point majeur pour le développement de nouvelles thérapies dans le CCR. / Colorectal cancer (CRC) is the first digestive cancer in occidental countries. Despite effective therapies, cases of resistance and/or recurrence exist. Our laboratory works on two signaling pathways regulating balance between survival and cell death: neurotrophins (NTs, growth factors involved in cancer cells survival) and autophagy (cellular recycling involved in stress resistance). The aim of this study was to investigate relationship between these two pathways and the impact of their inhibition on cell fate and tumor evolution.Studies were performed on two CRC cell lines derived from the same patient: SW480 (primary tumor) and SW620 (node invasion), also used for subcutaneous xenografts on Nude mouse model. In addition, presence of major proteins of NTs (TrkB) and autophagy (LC3) were assessed in patient’s tissues.Previous work showed that TrkB overexpression is associated with pro-survival signaling in CRC cell. So, we choose to inhibit NTs pathway with K252a (100 nM). As expected, inactivation of the PI3K / AKT pathway was observed and CRC cells were able to activate autophagy. At the opposite, blocking autophagic flux by pharmacologic approach (chloroquine; CQ; 25µM) or by transcriptomic approach (siRNA against ATG5) induced over-activation of the NTs pathway, via TrkB/BDNF. Thus, both survival pathways compensate each other. Moreover, dual inhibition allowed improving the effect of single treatment through a significant reduction of metabolic activity. The using of both inhibitors in vivo induces a spectacular reduction of tumor volume (or even disappearance in some cases). Presence of active form of TrkB (phospho TrkB) and active form of LC3 (LC3-II) demonstrating activation of these two pathways, in patient’s tissues have been observed. Taken together, our results showed that activation of NTs and autophagy contribute to CRC cell survival. The approach consisting of dual inhibition of NTs and autophagy could be a major point for new CRC therapies development.

L’altération des mécanismes impliqués dans l’homéostasie intestinale peut conduire au développement de cancers colorectaux (CCR). Les CCR se situent au 2nd rang des décès par cancer en France et il est donc nécessaire d’améliorer nos connaissances pour mieux les soigner. L’objectif de ces travaux était de comprendre les mécanismes impliqués dans l’homéostasie intestinale par le biais de la Cadhérine atypique MUCDHL dont l’expression semble diminuée dans les CCR. Les conséquences de cette perte et le mode d’action de MUCDHL restent mal connus. Ainsi, l’étude d’une large cohorte de patients et d’un modèle murin a permis de confirmer que la perte de MUCDHL aggrave la tumorigenèse intestinale. De plus, la caractérisation de l’interaction entre MUCDHL et la β-caténine a montré que le mode d’action de MUCDHL est plus complexe qu’une simple séquestration membranaire de la β-caténine impliquant différentes voies de signalisation. Enfin ces travaux ont permis d’identifier des interactants de MUCDHL. Les résultats montrent pour la première fois le rôle de suppresseur de tumeurs de MUCDHL dans le côlon et apportent des informations sur sa régulation et son mode d’action. / The alteration of mechanisms involved in intestinal homeostasis leads to the development of colorectal cancer (CRC). In France, CRC is the second leading cause of cancer mortality, and it is therefore necessary to improve our knowledge to treat it better. The objective of this project was to understand more precisely mechanisms involved in intestinal homeostasis through the atypical Cadherin MUCDHL whose expression seems decreased in CRC. However, the consequences of this loss, as well as the mode of action and the molecular relays of MUCDHL were largely unknown. Thus, the study of a large cohort of patients and of a murine model confirmed that the loss of MUCDHL enhances intestinal tumorigenesis. In addition, the functional characterization of the interaction between MUCDHL and β-catenin showed that the mode of action of MUCDHL is more complex than a simple membrane sequestration of β-catenin involving different signaling pathways. Finally, new interactants of MUCDHL were identified. The results obtained through this work show, for the first time, the tumor suppressor role of MUCDHL in the colon, and provide informations about its regulation and mode of action.

Introduction to the issue: Colorectal cancer is Europe's second most common malignant disease. Among the influential risk factors of colorectal cancer are the intake of high energy foods, animal fats, lack of fiber, excessive alcohol consumption, nicotinism, lack of physical activity, and obesity. Research methodology: Empirical research was carried out using qualitative research. The purposefully selected research sample consisted of fifteen informants after colorectal cancer surgery. Data collection took place through semi-structured interviews. The data were processed by the method of thematic analysis. The aim of the diploma thesis: The aim of the diploma thesis was to reveal the life habits of informants after colorectal cancer surgery, discover how the diagnosis of colorectal cancer has changed the way they look at their lifestyle, finding motivation and overcome the barriers to a lifestyle change. The outcomes: Despite the illness and knowledge of risk factors, the informants were rather satisfied with their current lifestyle and did not plan to change it. A healthy lifestyle was considered financially unaffordable. When deciding on a change, the informants were prevented from having a social aspect, the absence of friends who would share a sports activity with them. Environmental and...

The Wnt signaling pathway represents the principal evolutionarily conserved signaling cascade found in all multicellular organisms. It plays a key role not only in many processes during embryogenesis, but also in maintaining tissue homeostasis and regeneration. By contrast, mutations in genes encoding components of the pathway often result in increased activation of Wnt signaling and underlie onset of many human diseases, particularly cancer. The canonical Wnt signaling pathway is essential for proliferation and maintenance of the pluripotent state of intestinal stem cells and thus for homeostatic renewal of the intestinal epithelium. However, aberrant (hyper)activation of the Wnt signaling pathway is the initial step in development of intestinal neoplasia. Understanding the causes and identifying the consequences of the Wnt signaling hyperactivation is crucial for deciphering mechanisms leading to malignant transformation. Although the canonical Wnt signaling pathway has been the subject of scientific studies for several decades, all regulatory mechanisms and consequences of its hyperactivation have not been completely elucidated yet. During my PhD studies, I focused on understanding function(s) of some components and target genes of this signaling cascade. In this theses, results of my first...

Background: Uptake of screening remains crucial in the prevention of both the incidence of colorectal cancer (CRC) and its mortality. Objectives: To estimate the prevalence of CRC screening and identify chronic conditions that predict CRC screening uptake among US adults using the 2012 National Health Interview Survey (NHIS) data. Materials and Methods: A cross-sectional analysis of the 2012 NHIS data. Chronic conditions examined were hypertension, cancer history, arthritis, ulcer, and high cholesterol level. A total of 21,511 participants were included in the analysis. Weighted univariate and multiple logistic regression analyses in SAS ver. 9.2 were used to estimate the odds ratios (ORs) with 95% confidence intervals (CIs). Results: The overall prevalence of CRC screening was 19%. The prevalence of CRC screening in adults with cancer history, hypertension, ulcer, high cholesterol, and arthritis was significantly higher than those without the chronic conditions (26% vs.18%, 23% vs.16%, 25% vs.18%, 23% vs. 16%, and 23% vs. 17%, respectively). After adjusting for potential factors, hypertension (OR=1.18, 95%CI=1.08-1.30), ulcer (OR=1.28, 95%CI=1.10-1.48), high cholesterol (OR=1.25, 95%CI=1.14-1.39), and arthritis (OR=1.24, 95%CI=1.12-1.37) were all positively associated with CRC screening (p<0.05). Females were less likely to screen for CRC than to males (OR=0.72; 95% CI=0.65-0.80). Compared to young adults (18-44 years), screening was significantly higher in middle-aged (45-64 years) and elder adults (65+) (OR=2.60, 95%CI=2.11-3.21 and OR=2.67, 95%CI=2.13-3.33, respectively). African Americans were more likely to screen for CRC compared to their white counterparts (OR=1.61, 95% CI=1.44-1.81). Conclusions: We have found significant associations between chronic conditions and CRC screening uptake. We also found higher uptake of CRC screen in African Americans than Whites, in contrast to earlier findings.

Kolorektalcancer (CRC) är en av de vanligaste förekommande cancerformerna i världen och är även den näst dödligaste typen. Vid immunohistokemiska (IHC) analyser använder man sig av markörer som cytokeratin 20 (CK20) och caudal-typ homeobox 2 (CDX2) för diagnostisering av CRC. En ytterligare markör som kan användas är special AT-rikt sekvensbindningsprotein 2 (SATB2). SATB2 är ett DNA-bindande protein som finns mellan 70-97% hos CRC-fall. Ett automatiserat färgningsinstrument, BenchMark Ultra använder IHC, där analysprincipen går ut på att den inmärkta sekundära antikroppen med pepparrotsperoxidas (HRP) binder till den primära antikroppen och dess antigen. I närvaro av 3’3-diaminobenzindine (DAB) bildas en brun färgprodukt tillsammans med väteperoxidaset (H2O2) i HRP. Syftet med arbetet var att framställa ett färgningsprotokoll för SATB2 och se hur detta protokoll fungerar vid riktiga patientfall. Två klossar med två tarmvävnader på varje och en testkontroll snittades, färgades med BenchMark Ultra och monterades för mikroskopi. Samma procedur utfördes med patientfallen. Resultatet visade att preparaten med SATB2-antikroppsspädningen 1:200 fungerade bäst med värmebehandling vid både ultraView respektive OptiView DAB. Proteasbehandling gav ospecifik infärgning. Det valda optimala protokollet med SATB2-antikroppsspädning på 1:200, värmebehandling 36 min i ultraView DAB kördes på patientfallen. Resultatet jämfördes med tidigare genomförda IHC-analyser med positivitet för CK20 och CDX2. SATB2 utföll positiv för båda patientfallen, vilket indikera på att protokollet fungerar. Slutsatsen kom blev att optimala protokollet för SATB2 är spädning på 1:200 och värmebehandling 36 min i ultraView DAB. Med detta kan SATB2 införas som ett tillägg till CK20 och CDX2 vid diagnostisering av CRC i rutinverksamheten. / Colorectal cancer (CRC) is a common and the second most deadly cancer form in the world. With immunohistochemistry (IHC) analyses, biomarkers as cytokeratine 20 (CK20) and caudal type homeobox 2 (CDX2) are used for diagnosing CRC. Another biomarker that can be used is special AT-rich sequence binding protein 2 (SATB2). SATB2 is a DNA-binding protein that is found in 70-90% of CRC cases. BenchMark Ultra is an automatic staining instrument which uses IHC. The principle is that a marked secondary antibody with horse radish peroxidase (HRP) binds to the primary antibody and it’s antigen. Peroxidase (H2O2) in HRP produces a brown color with 3’3-diaminobenzindine (DAB). The aim of this study was to create a protocol for SATB2 and see how it can be used in real cases. Two embedded colon samples and a test control were cut, stained and mounted on slides for microscopy. Same process was carried out with the patient cases. Results showed samples with SATB2-antibody dilution 1:200 worked best with heat treatment in both detection kits. The protease treatment gave non-specific staining. The optimal protocol with SATB2-antibody dilution 1:200 and heat treatment for 36 min with ultraView DAB were tested on patient cases. The results of the patient cases were compared with previous conducted staining with CK20 and CDX2, SATB2 was positive for both cases. In conclusion, the protocol with dilution 1:200 and heat treatment for 36 min with ultraView DAB suited best for SATB2. SATB2 will be introduced as an additional antibody for diagnosis of CRC.

Bakgrund: Kolorektal cancer är den tredje vanligaste cancersjukdomen i Sverige, vars symtom och behandling kan ha negativa följder i det dagliga livet och medföra nedsatt livskvalité, vilket ställer stora krav på sjuksköterskan att uppmärksamma nuvarande och potentiella kort- och långsiktiga behov. Genom ökad kunskap och förståelse för personers upplevelse av att leva med kolorektal cancer kan sjuksköterskan främja deras egenvård och därmed deras livskvalité.Syfte: Studien syftar till att beskriva personers upplevelse av att leva med kolorektal cancer.Metod: Studien har genomförts som en litteraturöversikt och baseras på tolv vetenskapliga artiklar med kvalitativ metod. Datasökning har gjorts i databaserna PubMed och Cinahl.Resultat: I resultatet framkom två huvudkategorier som beskriver personers upplevelse av att leva med kolorektal cancer: Upplevelse av att leva ett begränsat liv och Upplevelse av egenvårdsstöd.Slutsats: Att leva med kolorektal cancer medför sociala begränsningar och känslomässiga reaktioner till följd av förändrade avföringsvanor, stomi, fatigue och sexuell dysfunktion, där socialt stöd i vardagen har betydelse för egenvård och hantering av dessa begränsningar. Genom att tillämpa ett salutogent och holistiskt förhållningssätt kan sjuksköterskan få kunskap och uppfattning om personens upplevda begräsningar och egenvårdsbehov för att kunna erbjuda stöd som främjar den enskilda personens egenvårdsförmåga och livskvalité. / Background: Colorectal cancer is the third most common cancer in Sweden, whose symptoms and treatment can have a negative consequence in daily life and lead to reduced quality of life, which places great demands on the nurse to pay attention to current and potential short- and long-term needs. Through increased knowledge and understanding of people's experience of living with colorectal cancer, the nurse can promote their self-care and thus their quality of life.Aim: The study aims to describe people's experience of living with colorectal cancer.Method: The study has been conducted as a literature review and is based on twelve scientific articles with a qualitative method. Data search has been done in the PubMed and Cinahl databases.Results: The results revealed two main categories that describe people's experience of living with colorectal cancer: Experience of living a limited life and Experience of self-care support.Conclusion: Living with colorectal cancer causes social limitations and emotional reactions due to changed bowel habits, stoma, fatigue, and sexual dysfunction, where social support in everyday life is important for self-care and management of these limitations. By applying a salutogenic and holistic approach, the nurse can gain knowledge and perception of the person's perceived limitations and self-care needs to be able to offer support that promotes the individual's self-care ability and quality of life.