Serum Selenium Concentration as a Potential Diagnostic Marker for Early-Stage Colorectal Cancer: A Comparative Study.

BACKGROUND Selenium deficiency is an established risk factor for colorectal cancer. The aim of the present study was to determine selenium levels in blood samples obtained from colorectal cancer patients compared with the levels of this element in the blood of patients who had undergone hernia repair and cholecystectomy. MATERIAL AND METHODS The study group consisted of 49 patients diagnosed with colorectal cancer at our institution. The comparison group consisted of 29 and 26 patients undergoing hernia repair and cholecystectomy, respectively. The histological staging level was evaluated on a 4-grade scale. Serum selenium concentration was quantified by inductively coupled mass spectrometry using methane to reduce polyatomic interference. RESULTS Colorectal cancer patients had significantly lower serum selenium concentration than the comparison patients (67.24±15.55 µg/L vs 78.81±12.93 µg/L; P<0.001), and selenium concentration was below the reference range in a high percentage of colorectal cancer patients. However, among the colorectal cancer patients, no significant difference in cancer grading was observed according to selenium concentration (P=0.235). Serum selenium concentration in the patients was evaluated on the basis of 5 independent variables (R=0.6250): age (P=0.011), number of leukocytes (P=0.010), family history of cancer (P=0.045), dietary supplements (P=0.023), and exposure to chemical factors (P=0.057). CONCLUSIONS This study supports findings from previous studies that low serum selenium levels are associated with colorectal cancer and that selenium deficiency may be a risk factor for colorectal cancer.

Microencapsulated sodium butyrate administered to patients with diverticulosis decreases incidence of diverticulitis--a prospective randomized study.

BACKGROUND: Microencapsulated sodium butyrate (MSB) has been previously associated with anti-inflammatory and regenerative properties regarding large bowel mucosa. We aimed to examine a role of MSB in patients with diverticulosis, hypothesizing its potential for reduction of diverticulitis episodes and diverticulitis prevention. METHODS: Seventy-three patients with diverticulosis (diagnosed in colonoscopy or/and barium enema or/and CT colography) were recruited for the study and randomized. The investigated group was administered MSB 300 mg daily; the control group was administered placebo. After 12 months, a total of 52 patients completed the study and were subject to analysis (30 subjects and 22 controls). During the study, the number of episodes of diverticulitis (symptomatic diagnosis with acute pain, fever, and leukocytosis), hospitalizations, and surgery performed for diverticulitis were recorded. Additionally, a question regarding subjective improvement of symptoms reflected changes in quality of life during the analysis. RESULTS: After 12 months, the study group noted a significantly decreased number of diverticulitis episodes in comparison to the control group. The subjective quality of life in the study group was higher than in the control group. There were no side effects of the MSB during the therapy. CONCLUSIONS: MSB reduces the frequency of diverticulitis episodes, is safe, and improves the quality of life. It can play a role in the prevention of diverticulitis.

High Resolution Melting analysis as a rapid and efficient method of screening for small mutations in the STK11 gene in patients with Peutz-Jeghers syndrome.

BACKGROUND: Peutz-Jeghers syndrome (PJS) is a rare hereditary syndrome characterized by the occurrence of hamartomatous polyps in the gastrointestinal tract, mucocutaneous pigmentation and increased risk of cancer in multiple internal organs. Depending on the studied population, its incidence has been estimated to range from 1:200 000 even up to 1:50 000 births. Being an autosomal disease, PJS is caused in most cases by mutations in the STK11 gene. METHODS: The majority of causative DNA changes identified in patients with PJS are small mutations and, therefore, developing a method of their detection is a key aspect in the advancement of genetic diagnostics of PJS patients. We designed 13 pairs of primers, which amplify at the same temperature and enable examination of all coding exons of the STK11 gene by the HRM analysis. RESULTS: In our group of 41 families with PJS small mutations of the STK11 gene were detected in 22 families (54%). In the remaining cases all of the coding exons were sequenced. However, this has not allowed to detect any additional mutations. CONCLUSIONS: The developed methodology is a rapid and cost-effective screening tool for small mutations in PJS patients and makes it possible to detect all the STK11 gene sequence changes occurring in this group.

Expression and DNA methylation levels of prolyl hydroxylases PHD1, PHD2, PHD3 and asparaginyl hydroxylase FIH in colorectal cancer.

BACKGROUND: Colorectal cancer (CRC) is one of the most common and comprehensively studied malignancies. Hypoxic conditions during formation of CRC may support the development of more aggressive cancers. Hypoxia inducible factor (HIF), a major player in cancerous tissue adaptation to hypoxia, is negatively regulated by the family of prolyl hydroxylase enzymes (PHD1, PHD2, PHD3) and asparaginyl hydroxylase, called factor inhibiting HIF (FIH). METHODS: PHD1, PHD2, PHD3 and FIH gene expression was evaluated using quantitative RT-PCR and western blotting in primary colonic adenocarcinoma and adjacent histopathologically unchanged colonic mucosa from patients who underwent radical surgical resection of the colon (n=90), and the same methods were used for assessment of PHD3 gene expression in HCT116 and DLD-1 CRC cell lines. DNA methylation levels of the CpG island in the promoter regulatory region of PHD1, PHD2, PHD3 and FIH were assessed using bisulfite DNA sequencing and high resolution melting analysis (HRM) for patients and HRM analysis for CRC cell lines. RESULTS: We found significantly lower levels of PHD1, PHD2 and PHD3 transcripts (p=0.00026; p<0.00001; p<0.00001) and proteins (p=0.004164; p=0.0071; p<0.00001) in primary cancerous than in histopathologically unchanged tissues. Despite this, we did not observe statistically significant differences in FIH transcript levels between cancerous and histopathologically unchanged colorectal tissue, but we found a significantly increased level of FIH protein in CRC (p=0.0169). The reduced PHD3 expression was correlated with significantly increased DNA methylation in the CpG island of the PHD3 promoter regulatory region (p<0.0001). We did not observe DNA methylation in the CpG island of the PHD1, PHD2 or FIH promoter in cancerous and histopathologically unchanged colorectal tissue. We also showed that 5-Aza-2'-deoxycytidine induced DNA demethylation leading to increased PHD3 transcript and protein level in HCT116 cells. CONCLUSION: We demonstrated that reduced PHD3 expression in cancerous tissue was accompanied by methylation of the CpG rich region located within the first exon and intron of the PHD3 gene. The diminished expression of PHD1 and PHD2 and elevated level of FIH protein in cancerous tissue compared to histopathologically unchanged colonic mucosa was not associated with DNA methylation within the CpG islands of the PHD1, PHD2 and FIH genes.

Familial adenomatous polyposis of the colon.

Familial adenomatous polyposis (FAP) is a well-defined autosomal dominant predisposition to the development of polyposis in the colon and rectum at unusually early ages. The first symptoms of FAP are diarrhea and blood in the stool. Weight loss and weaknesses occur after the development of advanced tumour. The incidence of the FAP disorder is one per 10000 newborns. There are high levels of heterogeneity with regard to the number and timing of the occurrence of polyps. The classical form of FAP is characterized by the presence of more than 100 polyps, which appear in the second decade of life. The average time of occurrence of polyps is 15 years. The earliest symptoms of polyposis have been observed in a three-year-old child. The polyps are characterized by large potential for the development towards malignant tumour. Malignancy can occur from late childhood onwards. Attenuated adenomatous polyposis coli is characterized by a more benign course of disease in contrast to classical FAP. The occurrence of FAP is associated with mutations in the APC tumour suppressor gene, which was described in 1991. The APC gene is located on chromosome 5q21 and is involved in cell proliferation control. A recessive form of adenomatous polyposis is caused by mutations in the base excision repair gene - MUTYH gene. The MUTYH gene is involved in repairing DNA lesions as a result of oxidative DNA damage. MUTYH associated polyposis (MAP) is a predisposition to the development of polyps of the colon but the number of polyps is lower in comparison to classical FAP. The high risks of cancer observed in these two diseases make them important medical issues. Molecular studies of colonic polyposis have been performed in Poland for over fifteen years. A DNA Bank for Polish FAP patients was established at the Institute of Human Genetics in Poznan in which DNA samples from 600 FAP families have been collected.

Hamartomatous polyposis syndromes.

Hamartomas are tumour-like malformations, consisting of disorganized normal tissues, typical of the site of tumour manifestation. Familial manifestation of hamartomatous polyps can be noted in juvenile polyposis syndrome (JPS), Peutz-Jeghers' syndrome (PJS), hereditary mixed polyposis syndrome (HMPS) and PTEN hamartoma tumour syndrome (PHTS). All the aforementioned syndromes are inherited in an autosomal dominant manner and form a rather heterogenous group both in respect to the number and localization of polyps and the risk of cancer development in the alimentary tract and other organs. Individual syndromes of hamartomatous polyposis frequently manifest similar symptoms, particularly during the early stage of the diseases when in several cases their clinical pictures do not allow for differential diagnosis. The correct diagnosis of the disease using molecular methods allows treatment to be implemented earlier and therefore more effectively since it is followed by a strict monitoring of organs that manifest a predisposition for neoplastic transformation.

Surgical removal of Aquafilling localized to different sites.

<b><br>Introduction:</b> Aquafilling, a widely used soft-tissue filler since 2005, shows multiple adverse effects, necessitating the development of effective methods for its removal. We present a surgical method for removal of Aquafilling present in the breasts, breasts with migration to the chest and/or the abdomen, and the buttocks, and elaborate and discuss the advantages of this method.</br> <b><br>Aim:</b> The aim of this study was to present a surgical method for removal of Aquafilling (soft-tissue filler) present in the breasts, breasts with migration to the chest and/or the abdomen, and the buttocks, and to elaborate the advantages of this proposed technique.</br> <b><br>Materials and methods:</b> The surgical Aquafilling removal method described here was used in 25 patients (age, 21-53 years). The technique was used to remove Aquafilling present in the breasts (14 patients), breasts with migration to the chest and/or the abdomen (7 patients), and the buttocks (3 patients). The detailed course of Aquafilling removal surgery and postoperative treatment for these three types of cases is described.</br> <b><br>Results:</b> Surgical removal of Aquafilling with the described method did not cause any of the previously described ailments in each patient, excluding one patient who only showed significant pain reduction in both breasts preceding each menstruation cycle.</br> <b><br>Conclusions:</b> The method described herein can be recommended for removal of Aquafilling present in the breasts, breasts with migration to the chest and/or the abdomen, and buttocks, since it allowed thorough Aquafilling removal and decreased the local inflammatory state and the risk of potential carcinogenesis.</br>.

Evaluation of CD10 expression as a diagnostic marker for colorectal cancer.

Aim: We aimed to determine the potential of CD10 as a marker for the early diagnosis of adenocarcinoma of the colon. Background: Adenocarcinoma is diagnosed in one out of 20 individuals in the USA and western European countries. Its prognosis and treatment depend largely on the severity of the disease at the time of diagnosis. Additional new biological markers are being sought that can help diagnose colon cancer at an early stage. One such marker present in both serum and tumor tissue is CD10. Methods: CD10 concentrations were tested by ELISA and immunohistochemistry in serum and tissue samples, respectively, from 113 patients diagnosed histopathologically and treated for adenocarcinoma of the colon. Additionally, the ROC curve with optimal cut-off point based on Youden's criterion was calculated for CD10. Results: Serum concentrations of CD10 and its tissue expression in patients diagnosed with adenocarcinoma of the colon correlate with cancer staging based on the Astler-Coller-Dukes classification. To ascertain the optimal cut-off point for CD10 as a predictor of belonging to the study group, ROC curve was prepared for CD10. Optimal cut-off point for CD10 was 0.57, with prediction of belonging to the study group for CD10 ≥ 0.57. Conclusion: CD10 can be a useful marker in the early diagnosis of adenocarcinoma of the colon.

Decreased expression of 17ß-hydroxysteroid dehydrogenase type 1 is associated with DNA hypermethylation in colorectal cancer located in the proximal colon.

BACKGROUND: The importance of 17ß-estradiol (E2) in the prevention of large bowel tumorigenesis has been shown in many epidemiological studies. Extragonadal E2 may form by the aromatase pathway from androstenedione or the sulfatase pathway from estrone (E1) sulfate followed by E1 reduction to E2 by 17-ß-hydroxysteroid dehydrogenase (HSD17B1), so HSD17B1 gene expression may play an important role in the production of E2 in peripheral tissue, including the colon. METHODS: HSD17B1 expression was analyzed in colorectal cancer cell lines (HT29, SW707) and primary colonic adenocarcinoma tissues collected from fifty two patients who underwent radical colon surgical resection. Histopathologically unchanged colonic mucosa located at least 10-20 cm away from the cancerous lesions was obtained from the same patients. Expression level of HSD17B1 using quantitative PCR and western blot were evaluated. DNA methylation level in the 5' flanking region of HSD17B1 CpG rich region was assessed using bisulfite DNA sequencing and HRM analysis. The influence of DNA methylation on HSD17B1 expression was further evaluated by ChIP analysis in HT29 and SW707 cell lines. The conversion of estrone (E1) in to E2 was determined by electrochemiluminescence method. RESULTS: We found a significant decrease in HSD17B1 transcript (p = 0.0016) and protein (p = 0.0028) levels in colorectal cancer (CRC) from the proximal but not distal colon and rectum. This reduced HSD17B1 expression was associated with significantly increased DNA methylation (p = 0.003) in the CpG rich region located in the 5' flanking sequence of the HSD17B1 gene in CRC in the proximal but not distal colon and rectum. We also showed that 5-dAzaC induced demethylation of the 5' flanking region of HSD17B1, leading to increased occupation of the promoter by Polymerase II, and increased transcript and protein levels in HT29 and SW707 CRC cells, which contributed to the increase in E2 formation. CONCLUSIONS: Our results showed that reduced HSD17B1 expression can be associated with DNA methylation in the 5' flanking region of HSD17B1 in CRC from the proximal colon.

The prognosis of clinical course and the analysis of the frequency of the inflammation and dysplasia in the intestinal J-pouch at the patients after restorative proctocolectomy due to FAP.

PURPOSE: The main operative method in familial adenomatous polyposis (FAP) patients is restorative proctocolectomy with "J"-shaped pouch and temporary loop ileostomy. The aim of the study was the analysis of the frequency of the dysplasia and inflammation in the intestinal pouch and prognosis of the clinical course in FAP patients after restorative proctocolectomy. METHODS: A group of 165 FAP patients (86 females and 79 males, mean age 22.49 ± 12) subjected to a restorative proctocolectomy in the years 1985-2009 was analyzed. Clinical data coming from follow-up observation in the period of 2004-2009 were evaluated. In all patients, clinical examination and endoscopy with polypectomy and/or biopsy of pouch mucosa were done. RESULTS: The mean time of pouchitis occurrence after an ileal pouch-anal anastomosis was 6 months. Mean time for low-grade dysplasia was 14 months. The time difference of low-grade dysplasia after the above procedure as compared to pouchitis alone was substantial. Mean time for high-grade dysplasia was 16 months and for neoplasia even 19 months. It was estimated that early pouchitis happening within the first year after surgery occurs in 5% of patients, low-grade dysplasia 4 years later in 7% of cases, high-grade dysplasia 7 years later in around 10% of patients and neoplasia 14 years after surgery in 15% of cases. CONCLUSIONS: In conclusion, the Polyposis Registry encompassing whole country is the best way of controlling FAP patients. The regular lifelong endoscopic monitoring gives the opportunity of the early detection of the dysplasia and can protect against neoplasia.

The diameter of the ileal J-pouch-anal anastomosis as an important risk factor of pouchitis - clinical observations.

BACKGROUND: Patients' quality of life after restorative proctocolectomy depends on the potential complications. Stricture of the ileal pouch-anal anastomosis is one of the complications following restorative proctocolectomy. MATERIAL/METHODS: We analyzed the correlation between the diameter of the anastomosis and clinical parameters, including pouchitis disease activity index (PDAI), the activity of fecal M2-pyruvate kinase and maximum tolerable volume of the pouch. The study group consisted of 31 patients in whom covering ileostomy had been closed 72 ± 50 months before enrolement to the study. Restorative proctocolectomy for ulcerative colitis or familial adenomatous polyposis coli had been performed in this group. RESULTS: The study did not show any correlation between the diameter of the anastomosis and primary indication for surgery, the time elapsed after restoration of the bowel continuity, the activity of fecal M2-pyruvate kinase, or maximum tolerable volume. However, meaningful correlations between the stricture of the anastomosis and the presence and activity of pouchitis, together with the ileal villi atrophy, were detected. CONCLUSIONS: Stricture of the anastomosis appears to be an important factor increasing the incidence of pouchitis, and is independent of the underlying condition and time after the operation. Dilation of the anastomosis and prevention of stricture should constitute a permanent element of postoperative follow-up.

Crohn's Disease Susceptibility and Onset Are Strongly Related to Three NOD2 Gene Haplotypes.

The genetic background and the determinants influencing the disease form, course, and onset of inflammatory bowel disease (IBD) remain unresolved. We aimed to determine the NOD2 gene haplotypes and their relationship with IBD occurrence, clinical presentation, and onset, analyzing a cohort of 578 patients with IBD, including children, and 888 controls. Imaging or endoscopy with a histopathological confirmation was used to diagnose IBD. Genotyping was performed to assess the differences in genotypic and allelic frequencies. Linkage disequilibrium was analyzed, and associations between haplotypes and clinical data were evaluated. We emphasized the prevalence of risk alleles in all analyzed loci in patients with Crohn disease (CD). Interestingly, c.2722G>C and c.3019_3020insC alleles were also overrepresented in ulcerative colitis (UC). T-C-G-C-insC, T-C-G-T-insC, and T-T-G-T-wt haplotypes were correlated with the late-onset form of CD (OR = 23.01, 5.09, and 17.71, respectively), while T-T-G-T-wt and C-C-G-T-wt were prevalent only in CD children (OR = 29.36, and 12.93, respectively; p-value = 0.001). In conclusion, the presence of c.3019_3020insC along with c.802C>T occurred as the most fundamental contributing diplotype in late-onset CD form, while in CD children, the mutual allele in all predisposing haplotypes was the c.2798 + 158T. Identifying the unique, high-impact haplotypes supports further studies of the NOD2 gene, including haplotypic backgrounds.

Multifocal colorectal cancer in ulcerative colitis patient with sclerosing cholangitis - case report.

<b>Introduction:</b> U lcerative colitis (CU) is an inflammatory disease predisposing to colorectal cancer. Colorectal cancer in ulcerative colitis is more often metachronous or synchronous. <br><b>Case report:</b> In this case report we present a patient with multifocal colorectal cancer in the course of CU and operative treatment that was implemented. Additionallyprimary sclerosing cholangitis was diagnosed in this patient post-operatively.

[Pulmonary embolism as a first manifestation of synchronous occurrence of two neoplasms]. / Zatorowosc plucna jako pierwszy objaw synchronicznego zachorowania na dwa nowotwory.

A case of 67-year-old man with a first episode of acute, unprovoked venous thromboembolism (VTE). Screening for cancer revealed coexistence of two neoplasms: colon sigmoid cancer (operated on 6 weeks after pulmonary embolism onset), and multiple myeloma (treated successfully with thalidomide and dexamethasone). Low molecular weight heparin use as VTE treatment was followed by thromboprophylaxis for myeloma therapy. During a 30-month follow-up period, neither new thromboembolic complications nor cancer recurrence were observed. Overlapping different prothrombotic mechanisms of double malignancy might result in detection of both neoplasms at early stage.

The relationship between the symptom of fatigue and the functioning of patients with inflammatory bowel diseases after surgery.

INTRODUCTION: The occurrence of fatigue in patients suffering from inflammatory bowel diseases (IBD) is influenced by pain, frequent bowel movements, stress associated with symptoms and time of their occurrence reaction of surroundings, fear for their own health, sleep disturbances, side effects of pharmacological treatment, physical and mental exhaustion, hindered social contacts and difficulties at work. AIM: To evaluate the fatigue and the assessment of functioning of patients with IBD, who were treated surgically. MATERIAL AND METHODS: To evaluate the functioning of patients, a Polish version of the Inflammatory Bowel Disease Questionnaire was used. To evaluate the occurrence of fatigue in studied subjects, a Polish version of the Functional Assessment of Chronic Illness Therapy - Fatigue Scale was used. The activity of disease was evaluated with the use of the Crohn's Disease Activity Index for patients with Crohn's disease (CD) and the Clinical Activity Index for patients with ulcerative colitis (UC). RESULTS: Before surgery, there was no significant difference between CD and UC patients, with regard to the mean FACIT-F (28.76 for CD and 28.76 for UC, p = 0.72). Also, after surgery, there was no significant difference between CD and UC patients, with regard to the mean FACIT-F (14.8 for CD and 16.0 for UC, p = 0.71). The IBD patients who underwent surgery for CD and UC had significantly lower FACIT-F scores compared to the patients before the surgery (p = 0.001 and p = 0.0001, respectively). IBD patients who underwent surgery for CD and UC had significantly better functioning and higher IBDQ total scores compared to the patients before the surgery. CONCLUSIONS: Surgical treatment significantly reduces the fatigue symptom in patients with IBD. The severity of fatigue correlates with disease activity and functioning in the respective areas.

MicroRNA regulation in colorectal cancer tissue and serum.

Colorectal cancer is recognized as the fourth leading cause of cancer-related deaths worldwide. Thus, there is ongoing search for potential new biomarkers allowing quicker and less invasive detection of the disease and prediction of the treatment outcome. Therefore, the aim of our study was to identify colorectal cancer specific miRNAs expressed in cancerous and healthy tissue from the same patient and to further correlate the presence of the same miRNAs in the circulation as potential biomarkers for diagnosis. In the current study we detected a set of 40 miRNAs differentially regulated in tumor tissue when comparing with healthy tissue. Additionally, we found 8 miRNAs differentially regulated in serum of colorectal cancer patients. Interestingly, there was no overlap in miRNAs regulated in tissue and serum, suggesting that serum regulated miRNAs may be not actively secreted from colorectal tumor cells. However, four of differentially expressed miRNAs, including miR-21, miR-17, miR-20a and miR-32 represent the miRNAs characteristic for different tumor types, including breast, colon, lung, pancreas, prostate and stomach cancer. This finding suggests important groups of miRNAs which can be further validated as markers for diagnosis of tumor tissue and regulation of carcinogenesis.

Health-related quality of life assessment among patients with inflammatory bowel diseases after surgery - review.

Aim of the work was to review systematically the published literature addressing whether quality of life (QoL) and health-related QoL (HRQoL) are influenced by surgery among patients with inflammatory bowel disease (IBD). Electronic databases and published articles were searched to identify relevant studies published in the years 1990-2015. Then, a multistep selection was undertaken to identify articles that met specific selection criteria, such us specific key-words (IBD, HRQoL, ulcerative colitis (UC), Crohn's disease (CD), and surgery), and the population was assessed (studies concerning patients < 18 years old were excluded). The review included 27 studies that were evaluated in the context of the influence of surgery on QoL and HRQoL. Concluding, with the increase in the incidence of IBD, monitoring of QoL is an important indicator of the health effects at each stage of the surgical treatment.

Checklist in colorectal surgery - proposal of experts of the Polish Club of Coloproctology and National Consultant in general surgery.

A checklist is a collection of information that helps reduce the risk of failure due to limitations in human memory and attention. In surgery, the first Surgical Safety Checklist (SSC), created under the supervision of WHO (World Health Organization), was established in 2007 and covers three stages related to the patient's stay in the operating theater and operation: 1. Prior to initiation (induction) of anesthesia; 2. before cutting the skin; 3. before the patient leaves the operating room Colorectal surgery is particularly at high risk for complications and relatively high mortality. Elimination or, more likely, reducing the risk of complications by standardizing perioperative procedures may be particularly important in this group. The introduction of "dedicated" colorectal checklist surgery seems to be justified. The checklist proposed by the authors in colorectal surgery is divided into four stages, in which conscientious completion of checklists is intended to reduce the potential risk of complications due to hospitalization and surgical treatment. The presented checklist is obviously not closed, as a new publications or recommendations appear, some points may be modified, new issues may be added to the checklist. At present, however, it is a tool considering the well-known and confirmed elements of intraoperative procedures, the compliance of which may significantly reduce the rate of adverse events or surgical complications.

Significance of intratissue estrogen concentration coupled with estrogen receptors levels in colorectal cancer prognosis.

Dysregulation of estrogen related pathways is implicated colorectal cancer (CRC) development. However, significance of intratissue concentration of estrone (E1) and 17ß-estradiol (E2) in relation to estrogen receptor (ESR) expression level was not addressed so far. Herein, we measured E1 and E2 intratissue concentration using liquid chromatography electrospray ionization tandem mass spectrometry (ESI LC/MS) and mRNA levels of ESR1 and ESR2 using RT-qPCR in cancerous and histopathologically unchanged tissue from 75 and 110 CRC patients, respectively. The obtained results were associated with clinicopathological factors, expression of estrogen dependent genes (CTNNB1, CCND1) and prognostic significance. We found no statistically significant differences in E1 or E2 concentration between cancerous tissue and histopathologically unchanged counterparts. Moreover, mRNA levels of ESR1 and ESR2 were significantly decreased in cancerous tissue compared with histopathologically unchanged (p=0.00001). Log rank analysis revealed no benefit of low E1 to E2 ratio, high E1, E2 concentration or ESR1, ESR2 mRNA level for patients' overall (OS) and disease free survival (DFS). Interestingly, we have observed that patients with low ESR1 mRNA level coupled with low E1 intratissue concentration had a significant decrease in DFS compared with group of patients with high ESR1 mRNA level and high E1 concentration (HR=0.16, 95% CI 0.02-1.05; p=0.06). Furthermore, patients with low E1 concentration and low ESR1 transcript had significantly higher CTNNB1 and CCND1 mRNA level compare with subgroup with high level of both grouping factors. Our study indicates a potential value of estrogen intratissue concentration and its receptor expression level for CRC patients' prognosis.