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Background Colorectal cancer (CRC) is leading malignant tumors to occur mainly in industrialized countries, where it exhibits one of the highest mortality rates. Up to 80% of all CRCs characterize a chromosomal instability (CIN) phenotype. The main challenge faced by scientist is to reveal the mechanism of CIN development. An often proposed model is defects in DNA repair in terms of efficiency and genetic variations that modulate the response to stimuli from the environment. The objectives of this research were to determine whether nucleotide excision repair (NER) might affect CRC risk. Materials and Methods The first part of the study concerns NER efficiency. In the second part we selected 2 common single nucleotide polymorphisms within genes involved in NER (Xeroderma pigmentosum group C (XPC) Lys939Gln, Xeroderma pigmentosum group D (XPD) Lys751Gln) to determine the relation between them and CRC risk. The restriction fragment length polymorphism-polymerase chain reaction method was used for genotyping of 221 CRC patients vs. 270 cancer-free individuals. The isotopic labeling in vitro assay was used to evaluate NER capacity in lymphocytes and tissue protein extracts. Results We observed a significantly decreased level of NER capacity (P = .025) in lymphocytes delivered from CRC patients compared with healthy ones. Polymorphism screening points to higher CRC risk for the Gln939Gln genotype (P = .02) and Gln allele (P = .002) of the XPC gene. Conclusion Taken together, our findings suggest a potential role for NER in CRC.

Introduction The development of patient rights and increasing number of lawsuits based on medical malpractice make medical doctors constantly improve knowledge regarding the acceptability of changing the scope of operation. This is particularly important when patients have expressed their refusal to changing the scope and type of procedure (ESTP) or no informed consent (IC) has been obtained from the patient prior to the procedure. Material and methods The method of study comprised content analysis of existing legislation. The current jurisprudence and doctrine were confronted with existing regulations. An algorithm of correct formal procedures was elaborated. Results The doctor has right to realize ESTP when the patient has not given the consent to it or the refusal expressed by him was not fully conscious. Healthcare providers are absolutely prohibited from realizing ESTP when patient objected to any changes being thoroughly informed by the physician prior to the operation. When patient refuses possible ESTP, the doctor has the right to withdraw from performing surgery but should inform the patient about other places, where a similar procedure can be provided.

// Malgorzata Mrowicka 1 , Jerzy Mrowicki 1 , Michal Mik 2 , Radoslaw Wojtczak 1 , Lukasz Dziki 2 , Adam Dziki 2 and Ireneusz Majsterek 1 1 Department of Clinical Chemistry and Biochemistry, Medical University of Lodz, Hallera 1 Square, Lodz 90-647, Poland 2 Chair of Surgery, Department of General and Colorectal Surgery, Medical University of Lodz, Hallera 1 Square, Lodz 90-647, Poland Correspondence to: Malgorzata Mrowicka, email: malgorzata.mrowicka@umed.lodz.pl Keywords: inflammatory bowel diseases; genetic polymorphism; antioxidant enzyme activity; oxidative stress Received: August 11, 2017 Accepted: October 28, 2017 Published: November 27, 2017 ABSTRACT Purpose: The main aim of this study was investigate the association between the genetic polymorphism of antioxidant enzyme genes: SOD1, CAT and GSHPX1 and the risk of inflammatory bowel disease (IBD), including Crohn’s disease and ulcerative colitis in the Polish population. Methods: A total of 445 subjects including 200 patients with IBD and 245 controls were allowed in this study. We determined activity of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx1) and examination their association with the SNPs of respective genes ( SOD1 +35A/C, CAT C-262T and GSHPX1 Pro197Leu). RFLP technique was used to determine the selected genes polymorphisms. Antioxidant enzymes activity were evaluated in erythrocyte hemolysate of 23 patients with non-active IBD and 30 healthy participants. Results: The A/C genotype and the C allele frequencies of A/C polymorphism of SOD1 gene were significantly associated with the reduced risk of IBD (OR=0.43; 95% CI 0.23; 0.83). Alike, C/T (OR=0.45; 95% CI= 0.29; 0.70) and T/T genotype (OR=0.43; 95% CI= 0.21; 0.87) of GSHPX1 gene polymorphism diminished the susceptibility to IBD. A significant decrease of CAT ( P =0.028) and increase of GPx1 ( P =0.025) enzyme activities were seen in IBD patients compared to control. Conclusions: Our data confirm dysregulated antioxidant capacity in patients suffering from IBD. Both, the SOD1 A/C genotype as well as GSHPX1 C/T and T/T genotypes may be associated with a reduction risk of IBD in the Polish population.

Purpose: To assess the prognostic value of postoperative C-reactive protein (CRP) and neutrophil to lymphocyte ratio (NLR) in the development of anastomotic leak (AL) in patients after surgery for colorectal cancer (CRC). Methods: Patients operated on for CRC between 2010 and 2014 were enrolled into the study. The sensitivity, specificity, positive predictive value (PPV) and negative predictive values (NPVs) were calculated for the CRP and NLR measured on the 4th postoperative day (POD). Results: Among 724 patients, AL was diagnosed in 33 (4.6%). The accuracy of CRP in the detection of AL using area under curve was 0.83 with the optimal cut-off value of 180 mg/L, sensitivity 75%, specificity 91%, PPV 52% and NPV 87%. Also, NLR on POD4 was higher in the AL group: 9.03 ± 4.13 vs. 4.45 ± 2.25; p = 0.0012; sensitivity 69%, specificity 78%, PPV 49%, NPV 88% at cut-off point of 6.5. Moreover, CRP and NLR on POD4 were significantly higher in patients who died in the postoperative period: 239 ± 24 mg/L vs. 199 ± 41 mg/L; p = 0.034 and 10.71 ± 2.08 vs. 8.65 ± 4.67; p = 0.029, respectively). Conclusions: CRP and NLR on POD4 possess the ability to predict the development of AL and postoperative mortality after CRC operation. Based on our results, high NPV might be indicative of patients with low risk of AL in their postoperative period.

Introduction Our aim was to determine the effect of the single nucleotide polymorphisms (SNP) –93G>A of the MLH1 gene (rs1800734) and Gly322Asp of the MSH2 gene (rs4987188) on the risk of colon cancer (CC) and identify any relationship with clinical factors. Material and methods The study included 144 unrelated patients with sporadic CC (71 males; mean age: 61.7 ±11 years) and 151 control patients (74 males; mean age: 63 ±11 years). DNA was extracted from peripheral blood lymphocytes, and genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism. Results In our population, the homozygous G/G genotype of the –93G>AMLH1 gene increased the risk of sporadic CC (OR = 2.07; 95% CI: 1.11–3.83; p < 0.02). For A/G and A/A genotypes, the MLH1-93G>A polymorphism was significantly more common in women (p = 0.034). The SNP demonstrated differences in allele distribution according to the location of the tumor, i.e. right vs. left side (p = 0.014), and disease recurrence (p = 0.022). Significant differences were found in the occurrence of Gly322Asp of MSH2 with regard to primary and recurrent disease (p = 0.001). Conclusions The –93G>AMLH1 polymorphism plays an important role in evaluating the risk of sporadic CC. It can also be used as an indicator in some patients with left-sided and recurrent tumors. MSH2 Gly322Asp is a potential marker in patients with risk of recurrence.

As a result of reactive oxygen species operation, cell damage occurs in both cellular organelles and molecules, including DNA. Oxidative damage within the genetic material can lead to accumulation of mutations and consequently to cancer transformation. OGG1 glycosylase, a component of the Base Excision Repair (BER) system, is one of the enzymes that prevents excessive accumulation of 8-oxoguanine (8-oxG), the most common compound formed by oxidative DNA damage. In case of structural changes of OGG1 resulting from polymorphic variants, we can observe a significant increase in the concentration of 8-oxG. Linking individual polymorphisms to DNA repair systems with increased risk of colorectal cancer will allow patients to be classified as high risk and included in a prophylactic program. The aim of the study was to determine the level of oxidative DNA damage and to analyze the distribution of Ser326Cys polymorphism of the OGG1 gene in a group of patients with colorectal cancer and in a control group in the Polish population. Material and methodology. DNA was isolated from the blood of 174 patients with colorectal cancer. The control group consisted of 176 healthy individuals. The level of oxidative damage was determined by analyzing the amount of 8-oxguanine using the HT 8-oxo-dG ELISA II Kit. Genotyping was performed via the TaqMan method. Results. The obtained results indicate that Ser326Cys polymorphism of the OGG1 gene increases the risk of RJG and is associated with significantly increased levels of 8-oxoguanine. Conclusions. Based on the results obtained, we conclude that Ser326Cys polymorphism of the OGG1 gene may modulate the risk of colorectal cancer by increasing the level of oxidative DNA damage.

Aim The objectives were to recognize the risk factors for surgical site infections (SSIs) after surgery due to colorectal cancer and to assess the impact of mechanical bowel preparation (MBP) and oral antibiotic prophylaxis (ABX) on SSIs. Methods Records from two colorectal centers were used. Risk factors of SSIs were categorized into patient-, disease-, and treatment-dependent. Results A group of 2240 patients was included. SSIs were noted in 364 patients (16.3 %). MBP+/ABX+ was connected with a lower incidence of anastomotic leak (AL) and organ-space SSIs: 2.4 vs. 6.3 %; p = 0.008 and 3.6 vs. 7.2 %; p = 0.017, respectively. Patient-dependent factors: obesity increased the risk of skin superficial SSIs, adjusted OR 1.53 (1.47–1.59 95 % confidence interval (95 % CI)), and deep incisional SSIs 1.42 (1.39–1.45 95 % CI). Disease-dependent factors: rectal cancer was associated with a higher risk of skin superficial and deep incisional SSIs, adjusted OR 1.28 (1.22–1.34 95 % CI) and 1.13 (1.09–1.15 95 % CI). Treatment-dependent factors: MBP+/ABX+ was associated with a lower risk of organ-space SSIs, adjusted OR 0.53 (0.44–0.59 95 % CI). Radiotherapy increased the risk of organ-space SSIs, adjusted OR 1.78 (1.75–1.80 95 % CI). The risk of organ-space SSIs was the highest after low anterior resection, adjusted OR 1.62 (1.60–1.64 95 % CI). Conclusions If possible, MBP and ABX should always be administered to decrease the risk of AL and organ-space SSIs. Factors strictly related to the treatment mostly increased the risk of organ-space SSIs.

Despite many years of experience with laparoscopic procedures in rectal cancer, the superiority of minimally invasive approaches has been questioned especially in recent years. This article is a short review of the current knowledge about laparoscopic approaches in comparison to conventional modalities in patients with rectal cancer. To present the current state of the knowledge, we focused on reports that were published in the last few years and compared them to multicenter trials and meta-analyses published last year. Our analysis mainly applied to the primary end-points of these trials. We also included expert opinions that have been published in the last several months.

Aim This study aimed to assess the influence of the C-reactive protein (CRP) level on the early outcome after elective colorectal resection. Method Patients with colorectal cancer operated on between 2006 and 2013 were identified retrospectively. They were divided into a study group operated on between 2010 and 2013 when CRP was measured routinely on the fourth postoperative day and a control group operated on between 2006 and 2009 when the CRP level was not measured routinely. Mortality, intra-abdominal septic complications (IASC), abscesses and anastomotic leakage (AL), the need for reoperation, the interval from index surgery to relaparotomy, length of hospital stay and imaging studies were compared by multivariate analysis. Results A total of 1189 patients were assessed, including 598 (50.3%) in the study group (mean age 61.3 ± 13 years; 282 female) and 591 (49.7%) in the control group (mean age 61.8 ± 11 years; 267 female). There were seven (1.2%) postoperative deaths in the study group and nine (1.5%) in the control group (P = 0.598). Abdominal ultrasound (US) was performed more often in the study group [97 (16.2%) vs 71 (12.0%); P = 0.037]. In the study group the interval to diagnosis of IASC was shorter than in the control group (5.7 ± 1.5 days vs 7.3 ± 1.3 days; P = 0.029). The decision to reoperate was also made earlier in the study group (6.2 ± 1.7 days vs 7.4 ± 2.8 days; P = 0.043). Conclusion Routine measurement of CRP can help to make an earlier diagnosis of IASC and earlier decision for relaparotomy, without any influence on mortality or length of hospital stay.

DNA oxidative lesions are widely considered as a potential risk factor for colorectal cancer development. The aim of this work was to determine the role of the efficiency of base excision repair, both in lymphocytes and in epithelial tissue, in patients with CRC and healthy subjects. SNPs were identified within genes responsible for steps following glycosylase action in BER, and patients and healthy subjects were genotyped. A radioisotopic BER assay was used for assessing repair efficiency and TaqMan for genotyping. Decreased BER activity was observed in lymphocyte extract from CRC patients and in cancer tissue extract, compared to healthy subjects. In addition, polymorphisms ofEXO1,LIG3, andPolBmay modulate the risk of colorectal cancer by decreasing (PolB) or increasing (LIG3andEXO1) the chance of malignant transformation.

Non-specific Inflammatory Bowel Diseases (IBD) are particularly troublesome diseases affecting the human digestive tract, in particular the intestine. These diseases manifest themselves in chronic intestinal inflammation that is difficult to control, with periods of uncontrolled exacerbations and self-reminiscent occurrences. Depending on the symptoms and their location in the human gastrointestinal tract, these diseases may occur in various forms. Among the two most common forms of these diseases, Ulcerative Colitis (UC), and Crohn's Disease (CD) can be distinguished. Although the underlying cause of activation as well as the subsequent development of these diseases is not clearly defined, these disorders are known to have autoimmune background. The pathogenesis of IBD is associated with chronic idiopathic, recurrent, inflammatory-mediated gastrointestinal inflammation. The disease may be caused by changes in genes caused by various factors or family genetic predisposition. Exposure to a range of environmental risk factors may lead to disease activation in susceptible individuals. Many of the various factors mentioned in the article, which people are exposed to in their lives, may influence the development of these diseases.

Purpose The main aim of this study was investigate the association between the genetic polymorphism of antioxidant enzyme genes: SOD1, CAT and GSHPX1 and the risk of inflammatory bowel disease (IBD), including Crohn’s disease and ulcerative colitis in the Polish population. Methods A total of 445 subjects including 200 patients with IBD and 245 controls were allowed in this study. We determined activity of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx1) and examination their association with the SNPs of respective genes (SOD1 +35A/C, CAT C-262T and GSHPX1 Pro197Leu). RFLP technique was used to determine the selected genes polymorphisms. Antioxidant enzymes activity were evaluated in erythrocyte hemolysate of 23 patients with non-active IBD and 30 healthy participants. Results The A/C genotype and the C allele frequencies of A/C polymorphism of SOD1 gene were significantly associated with the reduced risk of IBD (OR=0.43; 95% CI 0.23; 0.83). Alike, C/T (OR=0.45; 95% CI= 0.29; 0.70) and T/T genotype (OR=0.43; 95% CI= 0.21; 0.87) of GSHPX1 gene polymorphism diminished the susceptibility to IBD. A significant decrease of CAT (P=0.028) and increase of GPx1 (P=0.025) enzyme activities were seen in IBD patients compared to control. Conclusions Our data confirm dysregulated antioxidant capacity in patients suffering from IBD. Both, the SOD1 A/C genotype as well as GSHPX1 C/T and T/T genotypes may be associated with a reduction risk of IBD in the Polish population.

AIM The aim of this study was to assess the expression of vascular endothelial growth factor (VEGF) as a key proangiogenic factor and determine whether there is any correlation between its expression and clinical symptoms or endoscopic changes in patients with chronic radiation proctitis (ChRP). METHOD Fifty patients who had all undergone radiotherapy for prostate, cervical or uterine cancer were included in the study (37 women, 13 men). There was a control group of 20 patients (9 women, 11 men). The Radiation Therapy Oncology Group/European Organization for Research and Treatment of Cancer (RTOG/EORTC) scoring system was used for grading the severity of the proctitis. Endoscopic scoring of late rectal mucosal damage was performed using Gilinsky's classification. Serum levels of VEGF were analysed by the enzyme-linked immunosorbent assay method. RESULTS Most patients presented with Grade 1 symptoms. Endoscopic assessment showed that most patients had Grade 1 late rectal mucosal damage. The predominant endoscopic finding was the presence of telangiectasia. Assessment of VEGF correlation between the control group and the degrees of endoscopic changes showed statistically significant differences for all three degrees (P

The aim of the study was to assess the clinical and functional results of surgical treatment of female patients with rectal prolapse. In the period of 2003–2010, the group of 86 female patients (mean age of 67 ± 10) underwent surgery due to rectal prolapse. The group of 24 patients (27.9 %) suffered from mild anal incontinence. They were operated on with open sutured rectopexy (18 pts), Altemeier (45 pts) and Delorme procedure (23 pts). Prior to surgery and after operation, clinical and function results were obtained. The follow-up period amounted to 32 ± 11 months. In perineal approaches, we found mortality in one patient (1.4 %, Delorme) and anastomotic leak in four patients (5.9 %). The recurrence rate in the perineal group was 11.8 % (eight patients). We noted one recurrence in the rectopexy group (5.6 %). The Altemeier procedure revealed the most significant impact on the function of the anal sphincter muscles and resting pressures (42 ± 7 vs 53 ± 9 cm H2O; p = 0.0082). If anterior levatoroplasty was added, the benefits referred also to squeeze pressures (41 ± 8 vs 58 ± 9 cm H2O; p = 0.006 and 42 ± 10 vs 56 ± 9 cm H2O; p = 0.01). In the treatment of rectal prolapse, there is still no consensus about the operation of choice. Selection of the appropriate method should be based on clinical findings and patients’ comorbidities to obtain maximal benefits and minimize the postoperative risk and failures.

Oxidative damage has been implicated in the pathogenesis of colorectal cancer (CRC). The base excision repair (BER) pathway is the major DNA repair pathway for oxidative DNA damage and genetic variation associated with impaired BER might thus increase a risk of CRC. In this work, we evaluated associations between the repair efficiency of oxidative DNA lesions and single-nucleotide polymorphisms of BER genes: the 194Trp/Arg and the 399Arg/Gln XRCC1, the 326Ser/Cys OGG1 and the 324Gln/His MUTYH and CRC occurrence in a Polish population. These polymorphisms were genotyped in 182 CRC patients and 245 control subjects, using a PCR-RFLP approach. The level of oxidative damage and DNA repair capacity in lymphocytes and CRC tissue samples was evaluated by comet assay using FPG and Nth glycosidases. The 326Ser/Cys OGG1 and the 324Gln/His as well as the 324His/His MUTYH genotypes were found to be associated with an increased CRC risk, while no association was found for the XRCC1 gene polymorphisms. It was also demonstrated the reduced capacity of oxidative damage repair in CRC patients in comparison to healthy controls. Moreover, the decrease efficiency of DNA repair were correlated with the 399Gln/Gln XRCC1 and the 324His/His MUTYH genotypes occurrence in CRC patients. The results obtained in our study indicated an association of OGG1 and MUTYH genes polymorphisms involved in oxidative DNA lesions repair with the risk occurrence of colorectal cancer in Polish patients. It was also found that studied polymorphisms might affect DNA repair capacity suggesting their role in CRC pathogenesis. Finally, we conclude that BER pathway may be an important target for the diagnosis and treatment of colorectal patients.

Background Numerous data have shown that progressive loss of human trabecular meshwork (TM) cells may be connected with oxidative stress. This hypothesis may suggest an association of base excision repair with the risk of primary open angle glaucoma development. Purpose The aim of this study was to evaluate the role of the 399Arg/Gln XRCC1 , the 194 Arg/Trp XRCC1 , the 326SerCys OGG1 , and the 324Gln/His MUTYH gene polymorphisms with clinical parameters and the risk for development of POAG. Methods Our research included 170 patients with POAG and 193 healthy controls. Gene polymorphisms were investigated by PCR-RFLP. The Heidelberg Retinal Tomography (HRT) clinical parameters were also analyzed. Results The 399Arg/Gln genotype of the XRCC1 gene was associated with an increased risk for POAG (OR 2.50; 95% CI, 1.54–4.07, P = 0.0002). The 399Gln/Gln XRCC1 genotype may increase the risk for POAG progression according to clinical parameters such as cup/disk ratio (c/d) (OR 1.93; 95% CI, 1–3.73, P = 0.04) and Rim area (RA factor) (OR 3.88; 95% CI, 1.01–14.82, P = 0.04). Moreover, an association was found of retinal nerve-fiber layer (RNFL factor) with the 399Arg/Gln XRCC1 genotype distribution and POAG progression (OR 2.46; 95% CI, 1.06–5.68, P = 0.03). In contrast, analysis of the 324Gln/His MUTYH gene polymorphism distribution in the patient group according to RA factor showed that it may reduce the progression of POAG (OR 0.14; 95% CI, 0.02–0.89, P = 0.05). Our current study demonstrates an association between the 326Ser/Cys OGG1 gene polymorphism and the 326Cys allele of the OGG1 gene, and progression of POAG. In addition, the presence of the 326His allele of the MUTYH gene may increase the risk for POAG progression, according to the VF parameter (OR 2.57; 95% CI, 1.47–4.57, P = 0.0001). Conclusion We suggest that the 399Arg/Gln genotype and the 399Gln allele of the XRCC1 gene may be risk factors for POAG development. Moreover, we postulate that the 399 Arg/Gln XRCC1 , the 326 Ser/Cys OGG1 and the 324 Gln/His MUTYH genes polymorphisms may be associated with progression of POAG.

Methotrexate (MTX) and 6-mercaptopurine (6MP) are the most commonly used drugs in the therapy of childhood acute lymphoblastic leukaemia (ALL). The main genotoxic effect of MTX resulting from inhibition of thymidylate synthase is mis-incorporation of uracil into DNA, which is considered essential for the effectiveness of the Protocol M in ALL IC BFM 2002/EURO LB 2002 regimens. In this study, we investigated the level of basal and induced DNA damage as well as the effectiveness of DNA repair in lymphocytes of children with ALL at four time-points during therapy with MTX and 6MP. To assess DNA damage and the efficacy of DNA repair we used the modified alkaline comet assay with uracil DNA glycosylase (Udg) and endonuclease III (EndoIII). In addition, we examined the induction of apoptosis in the lymphocytes of the patients during treatment. Finally, we compared the activity of base-excision repair (BER), involved in removal of both uracil and oxidized bases from DNA in lymphocytes of children with ALL and lymphocytes of healthy children. BER efficiency was estimated in an in vitro assay with cellular extracts and plasmid substrates of heteroduplex DNA with an AP-site. Our results indicate that there is a significant decrease in the efficacy of DNA repair associated with an increased level of uracil in DNA and induction of apoptosis during therapy. Moreover, it was found that the BER capacity was decreased in the lymphocytes of ALL patients in contrast to that in lymphocytes of healthy children. Thus, we suggest that an impairment of the BER pathway may play a role in the pathogenesis and therapy of childhood ALL.

Background: colorectal cancer (CRC) is one of the most common cancers in developed countries. Annually, over one million of new cases in the world are recorded. Majority of CRCs occur sporadically with dominant phenotype of chromosomal instability (CIN). Permanent exposure to DNA damaging agents such as ionizing radiation result in DNA double-stranded breaks, which create favorable conditions for chromosomal aberration to arise. Homologous recombination repair (HRR) is the leading process engaged in maintaining of the genome integrity. RAD51 protein was recognized as crucial in HRR. Single nucleotide polymorphisms are the primary source of genetic variation which presence in the RAD51 promoter region can affect on its expression and consequently modulate HR efficiency. Objectives: The aim of this study was to analyze the distribution of genotypes and allele frequencies of -4791A/T and -4601A/G RAD51 gene polymorphisms, followed by an assessment of their relationship with the risk of CRC. Material and methods: The study included 115 patients with confirmed CRC. Control group was consisted of 118 cancer-free individuals with a negative family history. The genotypes were identified by PCR-RFLP method. Conclusion: This study revealed statistically significant association between appearance of G/A genotype in position -4601 of RAD51 gene and CRC risk.

Introduction In cases of haemorrhoidal disease resistant to conservative treatment, surgical treatment is necessary to relieve the symptoms. Aim To investigate the current methods used by Polish surgeons. Material and methods Surveys were distributed to members of the Association of Polish Surgeons (APS), in which participants were asked a number of closed-ended questions regarding haemorrhoidal disease and the way they treated suffering patients Results Out of the 1523 members of APS who received questionnaires, responses were received from 807 (52.9%) members. The Milligan-Morgan technique was indicated by 72.5% of surgeons as a leading surgical treatment, followed by Ligasure (15.5%), Ferguson (3.5%), DGHL (3.5%), other methods (3.5%), Parks (1.7%), and Longo (0%). The majority of participants (93%) indicated from 0 to 1 life threatening complications, 5% – from 2 to 3, and 2% > 4. A total of 83% of participants use a single dose of antibiotics prior to surgery. Conclusions The Milligan-Morgan technique is the preferred method. The majority of procedures are performed in regional hospitals and university departments, and less commonly in private practices. The vast majority of surgeons in Poland are not convinced about the stapler technique, justifying this fact with the possibility of developing serious complications

Participation of DNA repair systems in the pathogenesis of cancer has been a suspected phenomenon for a long time. Decreased efficiency in DNA repair translates to their ability to fix and consequently leads to mutations and the process of carcinogenesis. Linking individual polymorphisms of DNA repair systems with an increased risk of colorectal cancer will allow the classification of patients to high-risk groups and their placement under preventive program.The aim of the study was to determine the effect of XPF gene polymorphism Ser835Ser on increasing the risk of colorectal cancer in the Polish population.Material and methods. as the material blood collected from 146 patients diagnosed with colon cancer was used. The control group consisted of 149 healthy subjects. Genotyping was performed by Taq- Man method.Results. The results indicate that genotype TCC/TCT is associated with an decreased risk of colorectal cancer (OR 0.574; CI 95% 0.335-0.984; p=0.043).Conclusions. Based on these results, we conclude that the XPF gene polymorphism Ser835Ser may be associated with a decreased risk of colorectal cancer

Background: Primary open-angle glaucoma (POAG) is the main cause of irreversible blindness worldwide. Matrix metalloproteinases (MMPs) and their regulators (TIMPs and ILs) have been extensively studied as POAG risk factors. Recent reports have showed several single-nucleotide polymorphisms (SNPs) for MMPs, TIMPs and ILs encoding genes in patients with POAG. The aim of this study was to investigate association of the -1607 1G/2G MMP1, -the 1562 C/T MMP9, the -82 A/G MMP12, the -511 C/T IL-1β and the 372 T/C TIMP1 gene polymorphisms with POAG occurrence and to investigate their impact on main clinical features. Material and methods: In the present case–control study, we examined group of 511 unrelated Caucasian subjects consist of 255 patients with POAG (mean age 70 ± 15) and 256 controls (mean age 67 ± 16). Determination of genes polymorphic variants was made using polymerase chain reaction–restriction fragment length polymorphism technique (PCR-RFLP). The odds ratios (ORs) and 95% confidence intervals (CIs) for each genotype and allele were calculated. Results: Presented study showed statistically significant increase in the POAG development risk of the -1607 2G/2G MMP1 genotype (OR 1.75; 95% CI, 1.11–2.75; p = 0.014) and for the -1607 2G MMP1 allele (OR 1.35; 95% CI, 1.05–1.73; p = 0.017), as well as for the -1562 C/T MMP9 genotype (OR 1.74; 95% CI, 1.17–2.59; p = 0.006) and the -1562 T MMP9 allele (OR 1.55; 95% CI, 1.10–2.17; p = 0.012) in patients with POAG in comparison with healthy control group. We also observed positive association of the -511 T/T IL-1β genotype (OR 2.60; 95% CI, 1.41–4.80; p = 0.002) as well as the -511 T IL-1β allele occurrence with an increased POAG development risk (OR 1.47; 95% CI, 1.13–1.90; p = 0.003). Furthermore, we found an association of the -1607 1G/2G MMP1, -1562 C/T MMP9 (anova, p

Inflammatory bowel disease (IBD) are characterized recurrent inflammation of gastrointestinal tract. The etiology and pathogenesis this disease is currently unclear, but it has become evident that immune and genetic factors are involved in this process. The aim of this study was to determine whether gene polymorphisms: MIF-173 G/C; CXCL12-801 G/A and CXCR4 C/T exon 2 position of rs2228014 is associated with susceptibility to IBD. A total of 286 patients were examined with IBD, including 152 patients with ulcerative colitis and 134 with Crohn’s disease (CD) and 220 healthy subjects were recruited from the Polish population. Genotyping for polymorphisms in CXCL12/CXCR4 and MIF was performed by RFLP-PCR. Statistical significance was found for polymorphisms CXCR4, a receptor gene for CXCL12 genotypes and alleles in CD and for genotype C/T and T allele in ulcerative colitis with respect to control. This confirms the effect of CXCL12 gene. The interplay between CXCL12 and its receptor CXCR4 affects homeostasis and inflammation in the intestinal mucosa. Three-gene analysis in CD confirmed the association of genotype GGGGCT. Statistical analysis of clinical data of patients with ulcerative colitis showed significant differences in the distribution of genotype C/T and T allele for CXCR4 in the left-side colitis. Having CXCR4/CXCL12 chemokine axis polymorphisms may predispose to the development of IBD. Activation can also be their defensive reaction to the long-lasting inflammation.

Cancer cell invasion is a key element in metastasis that requires integrins for adhesion/de-adhesion, as well as matrix metalloproteinases (MMPs) for focalized proteolysis. Herein we show that MMP-2 is up-regulated in resected colorectal tumors and degrades β1 integrins with the release of fragments containing the β1 I-domain. The β1 cleavage pattern is similar to that produced by digestion of α5β1 and α2β1 with MMP-2. Two such fragments, at 25 and 75 kDa, were identified after immunoprecipitation, with monoclonal antibody BD610468 reacting with the NH(2)-terminal I-like ectodomain followed by SDS-PAGE and microsequencing using electrospray (ISI-Q-TOF-Micromass) spectrometry. Cleavage of the β1 integrin can be abolished by inhibition of MMP-2 activity; it can be induced by up-regulation of MMP-2 expression, as exemplified by HT29 colon cancer cells transfected with pCMV6-XL5-MMP-2. Co-immunoprecipitation studies of colon cancer cells showed that the β1 integrin subunit is associated with MMP-2. The MMP-2-mediated shedding of the I-like domain from β1 integrins resulted in decreased adhesion of colon cancer cells to collagen and fibronectin, thus abolishing their receptivity. Furthermore, such cells showed enhanced motility as evaluated by a "wound healing-like" assay and time-lapse microscopy, indicating their increased invasiveness. Altogether, our data demonstrate that MMP-2 amplifies the motility of colon cancer cells, not only by digesting the extracellular matrix components in the vicinity of cancer cells but also by inactivating their major β1 integrin receptors.

Inflammatory bowel diseases (IBD) and colorectal cancer (CRC) are disorders that originate from immune disturbances. In our study, we evaluated the association between the -251 T/A interleukin (IL)-8 and the -1112 C/T IL-13 polymorphisms, the risk of IBD, and CRC development. Genotypes were determined by PCR-restriction fragment length polymorphism in 191 patients with CRC, 150 subjects with IBD, and 205 healthy controls. We found an association between CRC and the presence of the -251 TA genotype and A allele of the IL-8 gene (odds ratios [ORs] 2.28 and 1.65). A similar relationship was observed between these polymorphic variants and ulcerative colitis (OR 2.05 for the -251 TA genotype and OR 1.47 for the -251 A allele) as well as Crohn's disease (ORs 3.11 and 1.56, respectively). Our research also revealed that the CT and TT genotypes of the IL-13 -1112 C/T polymorphism may be connected with a higher risk of CRC (ORs 2.28 and 1.65). The same genotypes affected the susceptibility of IBD (ORs 2.26 and 3.72). Our data showed that the IL-8 -251 T/A and IL-13 -1112 C/T polymorphisms might be associated with the IBD and CRC occurrence and might be used as predictive factors of these diseases in a Polish population.

Chronic rhinosinusitis with nasal polyps is strongly associated with other diseases, including asthma and allergy. The following study tested the association of the −765G/C polymorphism of cyclooxygenase-2 (COX-2) encoding gene and the −14C/G polymorphism of protooncogen MET (MET) encoding gene with a risk of chronic rhinosinusitis with nasal polyps in a Polish population. One hundred ninety-five patients of chronic rhinosinusitis with nasal polyps as well as 200 sex-, age-, and ethnicity-matched control subjects without chronic sinusitis and nasal polyps were enrolled in this study. Among the group of patients, 63 subjects were diagnosed with allergy and 65 subjects with asthma, respectively. DNA was isolated from peripheral blood lymphocytes of patients as well as controls, and gene polymorphisms were analyzed by restriction fragment length polymorphism–polymerase chain reaction (RFLP-PCR). Ten percent of the samples have been confirmed by a second method single-strand conformation polymorphism (SSCP)-PCR. We reported that the −765G/C COX-2 (odds ratio [OR] 7.79; 95% confidence interval [CI] 4.88–12.4, p

UNLABELLED Inflammatory bowel diseases (IBD) are disorders originated from immune disturbances. The AIM OF THE STUDY was to evaluate the association between the -2518 A/G MCP-1 polymorphism and the risk of IBD development. MATERIAL AND METHODS Genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. Study group consisted of 197 subjects with IBD (120 with ulcerative colitis and 77 with Crohn's disease) as well as 210 healthy controls. RESULTS The presence of the -2518 G/G MCP-1 genotype in the investigated groups seems to be connected with higher risk of inflammatory bowel disease as well as Crohn's disease only (OR 2.26; 95% CI 1.44-3.54 and OR 2.08; 95% CI 1.21-3.46, respectively). CONCLUSIONS Our data showed that the -2518 A/G MCP-1 polymorphism might be associated with the IBD occurrence and might be used as predictive factor of these diseases in a Polish population.

Head and neck cancers (head and neck squamous cell carcinomas [HNSCC]) are a heterogeneous group of neoplasms with varying presenting symptoms, treatment, and expected outcome. There is a need to find an effective way of its treatment at the molecular level. Thus, we should identify the mechanism of cancer cell response to damaging agents' activity, especially at DNA level. Our major goal was to evaluate the efficacy of DNA double strand breaks (DSBs) repair in HTB-43 and SCC-25 cancer cell lines as well as lymphocytes taken from HNSCC patients and healthy donors. The DNA repair efficiency was measured by neutral comet assay as well as extrachromosomal assay for DNA DSBs repair (TAK assay). We determined the levels of two main pathways of DNA DSBs—nonhomologous end joining (NHEJ) and homologous recombination repair (HRR). Neutral comet assay was used for evaluation of DNA DSBs repair after treatment with genotoxic agents. DNA DSBs induced by gamma radiation were repaired slower in lymphocytes from HNSCC patients than in lymphocytes from healthy controls. HTB-43 and SCC-25 cancer cell lines have higher efficacy of NHEJ and HRR than lymphocytes taken from patients as well as control subjects. Our results confirm the necessity of further studies on the mechanisms of DNA DSBs repair to provide insight into the molecular basis of head and neck cancer, which will allow us to improve methods of HNSCC treatment.

Nasal polyps are strongly associated with a risk of chronic rhinosinusitis development as well as other obstruction including asthma and allergy. The following study tested the association of the 140A/G polymorphism of lactoferine (LF) encoding gene and the -33C/G polymorphism of osteoblast-specific factor-2 (OSF-2) encoding gene with a risk of chronic rhinosinusitis with nasal polyps in a Polish population. One hundred ninety five patients of chronic rhinosinusitis with nasal polyps as well as 200 sex, age and ethnicity matched control subjects without chronic sinusitis and nasal polyps were enrolled in this study. Among the group of patients 63 subjects were diagnosed with allergy and 65 subjects with asthma, respectively. DNA was isolated from peripheral blood lymphocytes of patients as well as controls and gene polymorphisms were analyzed by restriction fragments length polymorphism polymerase chain reaction (RFLP-PCR). We reported that the 140A/G LF (OR 4.78; 95% CI 3.07-7.24), the -33C/G OSF-2 OR 3.48; 95% CI 2.19-5.52) and the -33G/G OSF-2 (OR 16.45; 95% CI 6.71-40.30) genotypes were associated with an increased risk of chronic rhinosinusitis with nasal polyps among analyzed group of patients. Moreover, the group of patients without allergy or asthma indicated the association of the -33C/G (OR 3.72; 95% CI 2.24-6.19 and OR 15.11; 95% CI 5.91-38.6) and -33G/G (OR 3.73; 95% CI 2.24-6.19 and OR 14.07; 95% CI 5.47-36.16) genotypes of the OSF-2 as wells as 140A/G (OR 3.89; 95% CI 2.40-6.31 and OR 3.62; 95% CI 2.45-5.34) genotype of OSF-2 with an increased risk of chronic rhinosinusitis with nasal polyps. Finally, it was also found that the selected group of patients with allergy or asthma indicated a very strong association of the -33C/G (OR 2.40; 95% CI 1.23-4.69 and OR 2.40; 95% CI 1.23-4.69, respectively) and -33G/G (OR 16.01; 95% CI 5.77-44.41 and OR 17.90; 95% CI 6.53-49.05, respectively) genotypes of the OSF-2 as wells as 140A/G (OR 3.22; 95% CI 1.74-6.11 and OR 3.25; 95% CI 1.75-6.04, respectively) genotypes with an increased risk of chronic rhinosinusitis with nasal polyps. Thus, our results suggest that LF and OSF-2 gene polymorphisms may have deep impact on the risk of rhinosinusitis nasal polyps' formation which may also depend on asthma or allergy. Our results showed that the 140A/G polymorphism of LF gene and the -33C/G polymorphism of the OSF-2 gene may be associated with the risk of chronic rhinosinusitis with nasal polyps in a Polish population.

Tobacco smoking is one of the major risk factors in pathogenesis of head and neck squamous cell carcinomas (HNSCC). Many of the chemical compounds present in tobacco are well-known carcinogens which form adducts with DNA. Cells remove these adducts mainly by the nucleotide excision repair pathway (NER). NER also eliminates a broad spectrum of pyrimidine dimers (CPD) and photo-products (6-4PP) induced by UV-radiation or DNA cross-links after cisplatin anti-cancer treatment. In this study DNA damage and repair was examined in peripheral blood lymphocytes obtained from 20 HNSCC patients and 20 healthy controls as well as HTB-43 larynx and SSC-25 tongue cancer cell lines. DNA repair kinetics in the examined cells after cisplatin or UV-radiation treatment were investigated using alkaline comet assay during 240min of post-treatment incubation. MTT assay was used to analyse cell viability and the Annexin V-FITC kit specific for kinase-3 was employed to determine apoptosis after treating the cells with UV-radiation at dose range from 0.5 to 60J/m(2). NER capability was assessed in vitro with cell extracts by the use of a bacterial plasmid irradiated with UV-light as a substrate for the repair. The results show that lymphocytes from HNSCC patients and HTB-43 or SSC-25 cancer cells were more sensitive to genotoxic treatment with UV-radiation and displayed impaired DNA repair. Also evidenced was a higher rate of apoptosis induction after UV-radiation treatment of lymphocytes from the HNSCC patients and the HTB-43 cancer cells than after treatment of those from healthy donors. Finally, our results showed that there was a significant decrease in NER capacity in HTB-43 or SSC-25 cancer cells as well as in peripheral blood lymphocytes of HNSCC patients compared to controls. In conclusion, we suggest that the impaired NER pathway might be a critical factor in pathogenesis of head and neck cancer.

UBC9 (E2) SUMO conjugating enzyme plays an important role in the maintenance of genome stability and integrity. In the present work we examined the association between the c.73GA (Val25Met) polymorphism of the UBC9 gene (rs11553473) and efficacy of DNA double-strand breaks (DSBs) repair (DRE) in breast cancer patients. We determined the level of endogenous (basal) and exogenous (induced by γ-irradiation) DSBs and efficacy of their repair in peripheral blood lymphocytes of 57 breast cancer patients and 70 healthy individuals. DNA damage and repair were studied by neutral comet assay. Genotypes were determined in DNA from peripheral blood lymphocytes by allele-specific PCR (ASO-PCR). We also correlated genotypes with the clinical characteristics of breast cancer patients. We observed a strong association between breast cancer occurrence and the variant allele carried genotypes in patients with elevated level of basal as well as induced DNA damage (OR 6.74, 95% CI 2.27-20.0 and OR 5.33, 95% CI 1.81-15.7, respectively). We also found statistically significant (p0.05) difference in DRE related to the c.73GA polymorphism of the UBC9 gene in breast cancer patients. Carriers of variant allele have decreased DNA DRE as compared to wild type genotype carriers. We did not find any association with the UBC9 gene polymorphism and estrogen and progesterone receptor status. The variant allele of the UBC9 gene polymorphism was strongly inversely related to HER negative breast cancer patients (OR 0.03, 95% CI 0.00-0.23). Our results suggest that the c.73GA polymorphism of the UBC9 gene may affect DNA DSBs repair efficacy in breast cancer patients.

Purpose: The aim of this study was to investigate the association of a 11 nucleotide deletion, the c.469+46_56del mutation, in the intron of the homeobox MSX1 gene and breast cancer occurrence and characteristics. Methods: The mutation was genotyped in peripheral blood lymphocytes of 200 breast cancer patients and 203 controls by single-strand conformational PCR and DNA sequencing. Results: The del/del variant of the c.469+46_56del mutation increased the risk of breast cancer occurrence (OR 2.20; 95% CI 1.41–3.44, p < 0.05). We did not observe any association between genotypes of this mutation and lymph node status, Bloom–Richardson grading, estrogen and progesterone receptors and HER2 expression. Conclusions: The del/del genotype of the c.469+46_56del mutation in the MSX1 gene may be associated with the increased risk of breast cancer in Polish population and may be considered as an early marker in this disease.

Primary anorectal melanoma is a rare entity with a poor prognosis accounting for approximately 0.1-4.6% of anal tumours and 0.5-1.6% of all melanomas. Almost 60% of patients have already disseminated disease at initial diagnosis.We report four cases of anorectal melanoma treated at our department from November 2006 to September 2008, as well as a review of the literature.There were two females and two males, of median age 69 years (range: 59-81 years). Most frequent complaints were rectal bleeding and/or anorectal pain. Three of our four patients had amelanotic melanomas. We found the positive expression of S-100 protein and HMB-45 in two patients and melanin A cells in one case. Abdominoperineal resection was performed in two patients, colostomy in one patient and a wide local excision also in one case. Three patients died on account of dissemination of melanoma, one patient is still alive.Anal melanoma remains a deadly problem. Clear guidelines for the therapy of anorectal melanoma have not been established. This mainly results from the rarity of this tumour. Treatment is based on retrospective studies, which report a limited number of cases.

Objective Novel treatments for colorectal cancer (CRC) include chemoprevention. Nonsteroidal anti-inflammatory drugs (NSAIDs) were the first to be studied and an inverse association was proven between their use and the development of invasive CRC. The numerous side effects of NSAIDs led, however, to the search for safer drugs. These have included Coxibs (selective COX-2 inhibitors). In this study, the role of coxibs in the chemoprevention of CRC is reviewed. Results Numerous in-vitro and in-vivo experiments have shown the effectiveness of coxibs in the chemoprevention of CRC. These have led to the registration of celecoxib by the USA Food and Drug Administration for the treatment of familial adenomatous polyposis. Further studies of coxibs have revealed an increased risk of serious cardiovascular events when compared with placebo. This finding has considerably decreased the opportunities for chemoprevention of CRC. Conclusion The multi-directional activity of coxibs, which was the reason for their effectiveness against CRC development may be the key to proposing a new target area for chemoprevention. It has been shown that celecoxib partly inhibits the activity of NF-κB, transcription factor involved in inflammation and carcinogenesis pathways. Modulation of its activation may be the future of effective CRC chemoprevention.

XRCC2 and XRCC3 proteins are structurally and functionally related to RAD51 which play an important role in the homologous recombination, the process frequently involved in cancer transformation. In our previous work we show that the 135G>C polymorphism (rs1801320) of the RAD51 gene can modify the effect of the Thr241Met polymorphism (rs861539) of the XRCC3 gene. We tested the association between the 135G>C polymorphism of the RAD51 gene, the Thr241Met polymorphism of the XRCC3 gene and the Arg188His polymorphism (rs3218536) of the XRCC2 gene and colorectal cancer risk and clinicopathological parameters. Polymorphisms were evaluated by restriction fragment length polymorphism polymerase chain reaction (RFLP-PCR) in 100 patients with invasive adenocarcinoma of the colon and in 100 sex, age and ethnicity matched cancer–free controls. We stratified the patients by genotypes, tumour Duke’s and TNM stage and calculated the linkage of each genotype with each stratum. Carriers of Arg188Arg/Me241tMet, His188His/Thr241Thr and His188His/G135G genotypes had an increased risk of colorectal cancer occurrence (OR 5.70, 95% CI 1.10–29.5; OR 12.4, 95% CI 1.63–94.9; OR 5.88, 95% CI 1.21–28.5, respectively). The C135C genotype decreased the risk of colorectal cancer singly (OR 0.06, 95% CI 0.02–0.22) as well as in combination with other two polymorphisms. TNM and Duke’s staging were not related to any of these polymorphisms. Our results suggest that the 135G>C polymorphism of the RAD51 gene can be an independent marker of colorectal cancer risk. The Thr241Met polymorphism of the XRCC3 gene and the Arg188His polymorphism of the XRCC2 gene can modify the risk of colorectal cancer. Electronic supplementary material The online version of this article (doi:10.1007/s11033-010-0430-6) contains supplementary material, which is available to authorized users.

Aim : Identification of the incidence of relaparotomy after operations for colorectal cancer and finding out factors influencing the incidence of relaparotomy and risk of mortality. Method : In the period from 2008 to 2012 the group of patients electively operated on for colorectal cancer was analysed. The database of the surgical department was reviewed retrospectively to search relaparotomies performed in perioperative period. We compared the risk of mortality and of reoperations according to clinical and demographic pre- and postoperative factors, tumour location and extend of surgery. Results : The group of 1674 patients was electively operated on for colorectal cancer and 121 (7.2%) relaparotomies were identified and analysed (77 males, 44 females, mean age of 65.1). In the whole group the risk of relaparotomy was higher in males OR 1.68; 95%CI 1.15–2.47; p = 0.008 and in patients with ASA III/IV OR 1.54; 95% CI 1.05–2.27; p = 0.027. The overall mortality rate was higher in patients after relaparotomy than after the only initial procedure 13.2% vs. 1.4%; with higher risk of mortality OR 9.78; 95%CI 4.97–19.29; p = 0.0008. The rate of anastomotic leak requiring reoperation was 2.7%. In resection procedures the incidence of reoperation was significantly higher 8.1% vs. 3.5%; p = 0.007, without any influence on mortality OR 0.7; 95%CI 0.14–3.49; p = 0.656. In reoperated patients mortality rate was the highest if the tumour was primary located in left colon than in the rectum an right colon (44.4% vs. 10.9% vs. 6.7%; p = 0.04). Anastomotic leak significantly increased the risk of mortality OR 2.95; 95%CI 1.00–8.39; p = 0.048. The risk of mortality was also higher in patients at age >65 OR 7.70; 95%CI 1.67–35.57; p = 0.009 and when ASA score was III or IV OR 5.83; 95%CI 1.58–21.60; p = 0.008. Conclusion : Patients after relaparotomy for complications of colorectal cancer surgery are at very high risk of mortality. Particularly male gender, older age, poor general condition and anastomotic complications are the risk factors of high mortality.