Incidence Of Colon Cancer Research Articles

Heavy-ion radiation-induced colitis and colorectal carcinogenesis in Il10-/- mice display co-activation of β-catenin and NF-κB signaling.

Space radiation-induced gastrointestinal (GI) cancer risk models for future interplanetary astronauts are being developed that primarily rely on quantitative animal model studies to assess radiation-quality effects of heavy-ion space radiation exposure in relation to γ-rays. While current GI-cancer risk estimation efforts are focused on sporadic GI-cancer mouse models, emerging in-vivo data on heavy-ion radiation-induced long-term GI-inflammation are indicative of a higher but undetermined risk of GI-inflammation associated cancers, such as colitis-associated cancer (CAC). Therefore, we aimed to assess radiation quality effects on colonic inflammation, colon cancer incidence, and associated signaling events using an in-vivo CAC model i.e., Il10-/- mice. Male Il10-/- mice (8-10 weeks, n = 12/group) were irradiated with either sham, γ-rays or heavy-ions (28Si or 56Fe), and histopathological assessments for colitis and CAC were conducted at 2.5 months post-exposure. qPCR analysis for inflammation associated gene transcripts (Ptges and Tgfb1), and in-situ staining for markers of cell-proliferation (phospho-histone H3), oncogenesis (active-β-catenin, and cyclin D1), and inflammation (phospho-p65NF-κB, iNOS, and COX2) were performed. Significantly higher colitis and CAC frequency were noted after heavy-ion exposure, relative to γ and control mice. Higher CAC incidence after heavy-ion exposure was associated with greater activation of β-catenin and NF-κB signaling marked by induced expression of common downstream inflammatory (iNOS and COX2) and pro-proliferative (Cyclin D1) targets. In summary, IR-induced colitis and CAC incidence in Il10-/- mice depends on radiation quality and display co-activation of β-catenin and NF-κB signaling.

Evidence-based surgical management for early colon cancer

In recent years, the incidence of early colon cancer (ECC) in China showed a rising trend. Accurate definition of ECC is of great significance for disease assessment, treatment decision-making and prognosis judgment. Although endoscopic resection has become an option in the treatment of ECC, surgical intervention is still needed for tumor residue and high risk pT1 tumors in order to prevent recurrence and metastasis. There is no consensus on indication, timing, radical resection range and tumor location of ECC surgery. The innovation of laparoscopic surgical techniques strongly promoted the progress of ECC minimally invasive surgery. Postoperative follow-up should be systematic, standardized and individualized, based on the stratification of ECC recurrence risk factors.

Optimized surgical tactics for localized colon cancer (literature review)

Malignant tumors have long occupied a special place in medicine and many researchers in different areas focused their attention on these disorders. Particular attention should be paid to gastrointestinal tumors with colon cancer being the most common among them. Moreover, the incidence of colon cancer is constantly growing. Despite the extensive experience in surgical treatment for colon cancer, we are still in search for new optimal methods that can increase overall and relapse-free survival without increasing the incidence of intra- and post-operative complications that are always associated with the volume of surgery. Recently, there has been a stable trend towards organ-sparing techniques. Segmental resections have become widely used in patients with localized cancer of the left colon and are now considered as an alternative to traditional left hemicolectomy. These two techniques demonstrated no significant differences in long-term outcomes. Then segmental resections became widely used in patients with localized tumors of the right colon and middle third of the transverse colon. These surgeries demonstrated their efficacy and good long-term outcomes. As for caecal cancer, the literature on this subject is too scant to make any conclusions about the rationality and feasibility of ileocecal resections. This implies that the utility of the method and its potential implications should be evaluated in further studies, including prospective ones that will compare both short-term and long-term outcomes. This literature review analyzes anatomical and physiological characteristics of right and left colon tumors, outlines generally accepted standards of lymphadenectomy, and summarizes the information on novel surgical techniques for colorectal cancer.

Variation of Saponins in Sanguisorba officinalis L. before and after Processing (Paozhi) and Its Effects on Colon Cancer Cells In Vitro.

The incidence of colon cancer is increasing year over year, seriously affecting human health and quality of life in recent years. However, traditional Chinese medicine (TCM) has been utilized for the treatment of colon cancer. S. officinalis Saponins (S-Saponins), the potential compound of TCM, displays multiple biological activities in colon cancer treatment. In our study, ultra-high-performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS) combined with multivariate statistical analysis were performed to analyze and identify raw and processed saponins. Then, MTT and cell migration assays were used to preliminarily explore the effects of saponins in vitro on colon cancer cells. The results showed that 29 differential saponins compounds under Paozhi were identified by UHPLC-MS/MS. Moreover, in vitro validation showed that Sprocessed better inhibited the proliferation and migration of colon cancer cells than Sraw. This study provides a basis for the determination of the chemical fundamentals of the efficacy changes during Paozhi through inferring the changes in saponin components and its possible transformation mechanisms before and after processing S. officinalis. Meanwhile, it also provides new insights into potential bioactive ingredients for the treatment of colon cancer.

EPH144 The Impact of COVID-19 Pandemic on the Detection and Management of Cancer: A German Claims Data Analysis

The COVID-19 pandemic impacted the German healthcare system comprehensively. It is being widely discussed whether there was also a negative effect on cancer care, but evidence to quantify such an effect is lacking. This analysis aims to investigate the pandemic impact on the detection and management of breast cancer (BC), colon cancer (CC), lung cancer (LC), and prostate cancer (PC) in Germany. The analysis was based on anonymized claims data from a German statutory health insurance (AOK PLUS). Incidence was defined as at least one inpatient or two outpatient diagnoses of one of the four cancer types after a 24-month pre-index period without any cancer diagnoses. Standardized cumulative incidences and the proportions of patients with a metastatic diagnosis within the first three months after incident diagnosis were compared between 2019 and 2020. Differences in the time to treatment initiation (surgery, radiation, or systemic anticancer treatment) between 2019 and 2020 were investigated using Kaplan-Meier estimation. The standardized cumulative incidence of BC, CC, and LC in 2020 were significantly lower compared to 2019 (BC: 0.040%/0.038%; CC: 0.045%/0.037%; LC: 0.028%/0.025%; all p<0.001), while similar incidence of PC was observed (0.036%/0.036%; p>0.001). In all groups, the proportion of patients with metastases at the time of incident diagnosis did not differ considerably between the years. The time to treatment initiation after incident diagnosis did not differ significantly between 2019 and 2020 in the investigated populations. In incident BC/CC/LC/PC patients, the median time to therapy start was 42/47/59/90 days in 2019 versus 40/47/56/94 days in 2020 (HR [95%-CI]: 1.01 [0.92-1.10]/1.02 [0.92-1.3]/1.06 [0.94-1.20]/0.97 [0.88-1.07]). Significantly fewer patients were diagnosed with BC, CC, and LC in 2020 compared to 2019, possibly due to lower cancer screening rates. However, cancer therapy initiation and timing in newly diagnosed patients in 2020 were not substantially different from the pre-pandemic year.

Abstract B024: Deconvolution by scRNAseq, scATACseq and functional genomics of impact of a relevant high risk diet on stem cells and homeostasis

Abstract Dietary patterns are major determinants of sporadic colon cancer incidence, the vast majority of the disease. NWD1 is a unique purified rodent diet that establishes mouse exposure to key nutrients recapitulating levels linked to higher risk in human, and is the only mouse model that develops sporadic intestinal and colon tumors, reflecting the etiology, incidence, frequency and lag with developmental age of the human disease. NWD1 fed mice reflect human metabolic syndrome with chronic inflammation, exhibit elevated Wnt signaling throughout the small and large intestinal mucosa and altered lineage marker expression, but Lgr5hi cells are suppressed in their lineage tracing, accumulation of mutations, and efficiency in tumor initiation. Alternate cells are mobilized to maintain the mucosa with increased efficiency to cause tumors. Deconvolving impact of NWD1 using scRNAseq, scATACseq and functional genomics provided novel insight into mechanisms elevating risk for sporadic tumors. NWD1 extensively, rapidly, and reversibly reprogrammed Lgr5hi stem cells, down-regulating Ppargc1a expression that altered mitochondrial structure and function and suppressed Oxphos and the TCA cycle. Ppargc1a genetic knockout in Lgr5hi cells recapitulated the dietary effects, and NWD1 or Ppargc1a inactivation repressed developmental maturation of Lgr5hi cell progeny as cells progressed through progenitor cell compartments. In compensation, mobilized Bmi1+, Ascl2hi cells maintained and adapted the mucosa. In parallel, NWD1 altered Ppargc1a chromatin structure in stem cells, and also for genes adapting enterocytes to the diet, independently confirming NWD1 epigenetic reprogramming of stem and differentiated cells. Importantly, pathways of antigen processing and presentation were elevated, especially in mature enterocytes, a pathogenic mechanism causing human chronic low-level pro-tumorigenic inflammation in IBD, also present in NWD1 fed mice. Fundamental conclusions: 1) plasticity of cells to function as stem cells mediates physiological adaptation of the mucosa. Thus, the human mucosa is in constant flux in response to its environment, supporting historic concepts of homeostasis by Claude Bernard and Walter Cannon as a continual process of tissue adaptation to its environment, not a single optimized state. 2) our data and the literature suggest that failure to recapitulate key human nutritional exposures contributes to why human stem cells reach crypt clonality in 6 years, 50-fold longer than the 6 weeks in the mouse. Thus, better modeling of human nutritional exposures in the mouse more accurately reflects human mechanisms of homeostasis and pathogenesis. 3) Complexity of cell reprogramming reported for the earliest premalignant human colon tumors is already present in the mucosa at nutritional risk for tumor development. 4) Oncogenic mutations provide a competitive advantage to intestinal stem cells in tumorigenesis, but the competition takes place on a playing field sculpted by the nutritional environment, a major determinant of who wins. Citation Format: Jiahn Choi, Xusheng Zhang, Wenge Li, Michele Houston, Karina Peregrina, Robert Dubin, Kenny Ye, Leonard H. Augenlicht. Deconvolution by scRNAseq, scATACseq and functional genomics of impact of a relevant high risk diet on stem cells and homeostasis [abstract]. In: Proceedings of the AACR Special Conference on Colorectal Cancer; 2022 Oct 1-4; Portland, OR. Philadelphia (PA): AACR; Cancer Res 2022;82(23 Suppl_1):Abstract nr B024.

Bile acids as carcinogens in the colon and at other sites in the gastrointestinal system.

Colon cancer incidence is associated with a high-fat diet. Such a diet is linked to elevated levels of bile acids in the gastrointestinal system and the circulation. Secondary bile acids are produced by microorganisms present at high concentrations in the colon. Recent prospective studies and a retrospective study in humans associate high circulating blood levels of secondary bile acids with increased risk of colon cancer. Feeding mice a diet containing a secondary bile acid, so their feces have the bile acid at a level comparable to that in the feces of humans on a high-fat diet, also causes colon cancer in the mice. Studies using human cells grown in culture illuminate some mechanisms by which bile acids cause cancer. In human cells, bile acids cause oxidative stress leading to oxidative DNA damage. Increased DNA damage increases the occurrence of mutations and epimutations, some of which provide a cellular growth advantage such as apoptosis resistance. Cells with such mutations/epimutations increase by natural selection. Apoptosis, or programmed cell death, is a beneficial process that eliminates cells with unrepaired DNA damage, whereas apoptosis-resistant cells are able to survive DNA damage using inaccurate repair processes. This results in apoptosis-resistant cells having more frequent mutations/epimutations, some of which are carcinogenic. The experiments on cultured human cells have provided a basis for understanding at the molecular level the human studies that recently reported an association of bile acids with colon cancer, and the mouse studies showing directly that bile acids cause colon cancer. Similar, but more limited, findings of an association of dietary bile acids with other cancers of the gastrointestinal system suggest that understanding the role of bile acids in colon carcinogenesis may contribute to understanding carcinogenesis in other organs.

Reproductive Factors in Relation to Incidence of Lung and Colorectal Cancers in a Cohort of Norwegian Women: The HUNT Study.

The roles of reproductive factors in the etiology of lung and colorectal cancers, among the most common cancers in women, are unclear. We aimed to explore whether female reproductive factors were associated with the incidence of lung and colorectal cancers. We followed up 33 314 cancer-free women who participated in the HUNT Study in Norway from 1995-1997 to 2018. A large panel of reproductive factors were self-reported at baseline. Incident lung and colorectal cancer cases were ascertained from the Cancer Registry of Norway. Cox regression models were used to estimate hazard ratios (HRs) with 95% CIs after adjustment for important confounders. During a median follow-up interval of 22.2 years, 467 women developed lung cancer (including 169 lung adenocarcinoma), 660 developed colon cancer, and 211 had rectal cancer. Early menarche (≤12 years) was associated with an increased incidence of lung adenocarcinoma (HR 1.43; 95% CI, 1.02-2.03). Women with one or no child had an increased colon cancer incidence (HR 1.26; 95% CI, 1.03-1.54). Hormone therapy appeared to be associated with a decreased incidence of rectal cancer (HR 0.68; 95% CI, 0.44-1.04). Results in the subgroup of postmenopausal women were similar or strengthened. Other reproductive factors were not related to the risk of lung, colon, and rectal cancers. Certain reproductive factors might play a role in the etiology of lung and colorectal cancers. Further investigations are warranted to study if they are causal associations.

Integration of stool microbiota, proteome and amino acid profiles to discriminate patients with adenomas and colorectal cancer

ABSTRACT Background Screening for colorectal cancer (CRC) reduces its mortality but has limited sensitivity and specificity. Aims We aimed to explore potential biomarker panels for CRC and adenoma detection and to gain insight into the interaction between gut microbiota and human metabolism in the presence of these lesions. Methods This multicenter case-control cohort was performed between February 2016 and November 2019. Consecutive patients ≥18 years with a scheduled colonoscopy were asked to participate and divided into three age, gender, body-mass index and smoking status-matched subgroups: CRC (n = 12), adenomas (n = 21) and controls (n = 20). Participants collected fecal samples prior to bowel preparation on which proteome (LC-MS/MS), microbiota (16S rRNA profiling) and amino acid (HPLC) composition were assessed. Best predictive markers were combined to create diagnostic biomarker panels. Pearson correlation-based analysis on selected markers was performed to create networks of all platforms. Results Combining omics platforms provided new panels which outperformed hemoglobin in this cohort, currently used for screening (AUC 0.98, 0.95 and 0.87 for CRC vs controls, adenoma vs controls and CRC vs adenoma, respectively). Integration of data sets revealed markers associated with increased blood excretion, stress- and inflammatory responses and pointed toward downregulation of epithelial integrity. Conclusions Integrating fecal microbiota, proteome and amino acids platforms provides for new biomarker panels that may improve noninvasive screening for adenomas and CRC, and may subsequently lead to lower incidence and mortality of colon cancer.

Impact of Carcinoid and Appendiceal Site Inclusion on Early Onset Colon Cancer Incidence Rate Analysis in the United States

Early onset colorectal cancer incidence rates (IR) are rising in the United States.1 Prior early onset colorectal cancer Surveillance Epidemiology and End Results (SEER) studies have combined adenocarcinomas and carcinoids (neuroendocrine tumors) under the umbrella term “colorectal cancer,” which can bias IR interpretations given that only adenocarcinomas are the target of national screening initiatives. Our recent study using SEER 18 demonstrated that both colon and rectal carcinoids are rising at a higher rate than adenocarcinomas in young patients, which underscores the importance of analyzing these subtypes independently if we want to obtain an accurate depiction of colorectal cancer (adenocarcinoma) rates.

Colon Cancer Incidence and Mortality: Trends from the Pennsylvania Cancer Registry across 3 Decades

Colon Cancer Incidence and Mortality: Trends from the Pennsylvania Cancer Registry across 3 Decades

S305 Changes in Colorectal Cancer Incidence Associated With Medicaid Expansion: An Analysis of the National Cancer Database

Introduction: The Affordable Care Act (ACA), enacted in 2010, increased insurance coverage for states that expanded Medicaid, but its impact across the United States on Colorectal Cancer (CRC) detection remains unclear. The National Cancer Database (NCDB) is a hospital-based cancer registry that captures approximately 75% of diagnosed cancers in the U.S. and Puerto Rico. This study used the NCDB to investigate the changes in the frequency of colon cancer incidence before and after Medicaid expansion. Methods: We compared all adult cases of CRC in the NCDB using ICD-codes from pre-Medicaid expansion in 2006-2009 to the period after full state participation in 2015-2018. Information on patient demographics (age, sex, race, insurance status, educational attainment, residential location, Charlson-Deyo Comorbidity Score (CDCS), staging at diagnosis) were queried. United States census data from 2010 and 2020 were used to standardize CRC incidence. Chi-square and t-test analysis were performed using SPSS v.28. Results: With the ACA, the proportion of those without insurance dropped from only 3.3% to 3.0% in the NCDB database. The total incidence of CRC was 569,659 patients for the two study periods. There were 86.4 cases per 100,000 diagnosed pre-Medicaid expansion and 92.5 cases per 100,000 post-Medicaid expansion. Patients diagnosed after expansion were younger 65.6±12.4 y vs 67.1±12.7 y. In the post-Medicaid expansion period, there was an increase in the incidence of CRC in males (52.7% vs 50.5%), Non-Hispanic Black (12.4% vs 11.5%) and Hispanic patients (6.9% vs 4.8%), patients with lower educational attainment (22.6% vs 21.6%), and patients with greater comorbidities via CDCS (5.0% vs 2.9%). Though there were statistically significant differences in income and residential location, these findings were not clinically significant. There was a slight shift in the incidence of CRC diagnosed at a later stage post-expansion. Results are summarized in Table. Conclusion: Medicaid expansion was associated with an increase in the incidence of CRC diagnosis despite a very modest drop in the proportion uninsured. The age of diagnosis decreased post-Medicaid expansion. There was also an increase in the proportion of males, minorities, patients with lower educational attainment, and those with a greater number of comorbid conditions. CRC was not found at an earlier stage of diagnosis despite an increase in the access to medical care. These findings highlight the impact of expanding health insurance coverage for all. Table 1. - Comparison of Patient Characteristics between Pre-Medicaid Expansion (2006-2009) and Post-Medicaid Expansion (2015-2018) Factors Pre-Expansion (2006-2009) n=266,109 Post-Expansion (2015-2018) n=303,550 p-value Age (SD) y - 67.13 (12.7) 65.55 (12.4) p< 0.001 Sex Male 134,445 (50.5) 159,973 (52.7) p< 0.001 Female 131,664 (49.5) 143,577 (47.3) Race NWH 211,311 (79.4) 226,924 (74.8) p< 0.001 NHB 30,526 (11.5) 37,611 (12.4) Hispanic 12,799 (4.8) 21,018 (6.9) Other 11,473 (4.3) 17,997 (5.9) Income Less than $40,227 49,766 (19.6) 49,676 (19.1) p< 0.001 $40,227 - $50,353 57,193 (22.5) 57,874 (22.3) $50,354 - $63,332 59,329 (23.5) 60,291 (23.2) $63,333 or more 87,568 (34.5) 92,041 (35.4) Percent Without High School Degree 17.6% or more 54,980 (21.6) 58,975 (22.6) p< 0.001 10.9% - 17.5% 67,951 (26.7) 69,392 (26.6) 6.3% - 10.8% 71,875 (28.3) 71,563 (27.5) Less than 6.3% 59,561 (23.4) 60,463 (23.2) Insurance Private 103,997 (39.1) 119,317 (39.3) p< 0.001 Medicaid 11,495 (4.3) 24,050 (8.0) Medicare 141,713 (53.3) 150,794 (49.7) Non-Insured 8,904 (3.3) 9,389 (3.0) Residence Location Metropolitan 218,379 (84.6) 251,012 (84.6) p< 0.001 Urban 34,764 (13.5) 40,309 (13.6) Rural 5,062 (2.0) 5,248 (1.8) Treatment Facility Community Cancer Program 25,022 (9.4) 26,467 (8.7) p< 0.001 Comprehensive Community Cancer Program 114,751 (43.1) 123,506 (40.7) Academic Program 69,335 (26.1) 91,285 (30.1) Integrated Network Cancer Program 57,001 (21.4) 62,292 (20.5) Charlson-Deyo Score 0 186,579 (70.1) 217,758 (71.7) p< 0.001 1 56,325 (21.2) 52,888 (17.4) 2 16,160 (6.1) 17,727 (5.8) >3 7,045 (2.6) 15,177 (5.0) Stage at Diagnosis 0 18,376 (6.9) 14,210 (4.7) p< 0.001 I 60,846 (22.9) 64,322 (22.2) II 66,828 (25.1) 72,303 (23.8) III 68,524 (25.8) 83,346 (27.5) IV 51,535 (19.4) 69,369 (21.9)

The Association Between Metabolic Syndrome and Colorectal Cancer Risk by Obesity Status in Korean Women: A Nationwide Cohort Study.

ObjectivesThis study aimed to determine the association between metabolic syndrome (MetS) and the incidence of colorectal cancer (CRC) in Korean women with obesity.MethodsCancer-free women (n=6 142 486) aged 40–79 years, who underwent National Health Insurance Service health examinations in 2009 and 2010 were included. The incidence of CRC was followed until 2018. The hazard ratio (HR) of MetS for the incidence of colon and rectal cancer was analyzed according to body mass index (BMI) categories, adjusting for confounders such as women’s reproductive factors. In addition, the heterogeneity of associations across BMI categories was assessed.ResultsWomen with MetS were at increased risk of colon and rectal cancer compared to women without MetS (HR, 1.20; 95% confidence interval [CI], 1.16 to 1.23 and HR,1.15; 95% CI, 1.11 to 1.20), respectively. The HR of MetS for colon cancer across BMI categories was 1.12 (95% CI, 1.06 to 1.19), 1.14 (95% CI, 1.08 to 1.20), and 1.16 (95% CI, 1.12 to 1.21) in women with BMIs <23.0 kg/m2, 23.0–24.9 kg/m2, and ≥25.0 kg/m2, respectively. The HR of MetS for rectal cancer across corresponding BMI categories was 1.16 (95% CI, 1.06 to 1.26), 1.14 (95% CI, 1.05 to 1.23), and 1.13 (95% CI, 1.06 to 1.20). The heterogeneity of associations across BMI categories was not significant in either colon or rectal cancer (p=0.587 for colon cancer and p=0.927 for rectal cancer).ConclusionsWomen with MetS were at increased risk of colon and rectal cancer. Clinical and public health strategies should be considered for primary CRC prevention with an emphasis on improving women’s metabolic health across all BMI groups.

Colorectal Cancer: Comparative Analysis Between Two Series of Patients Separated by More Than Three Decades

Abstract Aim This study characterizes Colorectal Cancer (CRC) incidence in the University Hospital Ramon and Cajal, Madrid, and analyzes variations over time. It establishes risk groups, aiming to discover whether diagnosis can be determined in less advanced stages of disease. Method Evolutionary epidemiological study of genetic and environmental factors contributing to the development of CRC in this district that enables the comparison of two cohorts of patients separated by 37 years: G1 (patients of current group) and G2 (patients of historical group). The main risk variables gleaned retrospectively were analyzed and the statistical association between cohorts was determined. Results The mean age of patients increased significantly from 64 to 71 along with the incidence of ascending colon cancer. G1 scored higher than G2 for: the incidence of colon cancer in men, detection of adenomatous polyps (48.1%), percentage of resectability with curative intent (80.4%), and Dukes A stage (34.1%) (p &lt; 0.001). Conclusion Biological aspects of CRC have been compared against its profile three decades earlier. We can confirm the existence of concrete changes in the manifestation and staging at the time of diagnosis or following earlier treatment.

Changes of gut microbiota in colorectal cancer patients with Pentatrichomonas hominis infection.

Pentatrichomonas hominis is a parasitic trichomonads protozoa that parasitizes in the colon and cecum of humans and other animals. Our previous studies have demonstrated that infection with P. hominis is associated with the incidence of colon cancer (37.93%). However, the mechanism by which P. hominis infections increase the incidence of colon cancer remains unclear. Previous studies have suggested that certain parasites promote colon cancer by regulating gut microbiota. This study aimed to elucidate whether the association between P. hominis infections and the increased incidence of colon cancer is related to changes in gut microbiota. Therefore, the gut microbiota patients with colon cancer who were infected with P. hominis and uninfected patients with colon cancer were analyzed by 16S rRNA high-throughput sequencing. The results demonstrated that patients with colon cancer who were not infected with P. hominis showed increased gut bacterial diversity, a higher relative abundance of Alcaligenes sp., Leucobacter sp., Paraprevotella sp., Ruminococcaceae UCG-002, and a significant reduction in the abundance of Veillonella sp., compared to individuals without colon cancer. Additionally, the relative abundance of the Ruminococcaceae UCG-002 and the Eubacterium eligens groups was reduced, while the relative abundance of bacteria associated with colon cancer, including Flavonifractor sp., Lachnoclostridium sp., and the Ruminococcus gnavus group, increased significantly in patients with colon cancer who were infected with P. hominis, compared to those of uninfected patients with colon cancer. In conclusion, these results suggested that P. hominis infections may aggravate the development of colon cancer and the findings provide new insights for subsequent in-depth studies on the pathogenesis, diagnosis, and prevention of colon cancer.

Diverticulitis does not increase the long-term risk of developing colon cancer: a systematic review and meta-analysis.

The aim of this review was to examine if diverticulitis increases the long-term risk (> 6months) of developing colon cancer. A systematic search was conducted in PubMed, Embase, and Cochrane CENTRAL. Google Scholar was also searched. We included studies with human adults of 18years of age and above. Studies that included only patients with diverticulitis as well as studies comparing groups with and without diverticulitis were included. The primary outcome was the incidence of colon cancer 6months or more after an episode of diverticulitis. Twelve records were included with 38,621 patients with diverticulitis. The crude rate of colon cancer among the prospectively followed populations with diverticulitis was by meta-analysis found to be 0.6% (95% CI 0.5-0.6%). The limitations of this review include heterogeneous reporting of outcomes across studies, specifically regarding population and outcome as well as variations in the design and reporting of the studies. We found that the long-term risk of colon cancer after diverticulitis is not increased. The results of our review support current practice on follow-up after an episode of diverticulitis with short-term follow-up being the primary focus.

The burden of colon cancer attributable to modifiable factors-The Norwegian Women and Cancer Study.

Colon cancer is the second most frequently diagnosed cancer in women in Norway, where incidence rates of colon cancer increased 3-fold between 1955 and 2014, for unknown reasons. We aimed to assess the burden of colon cancer attributable to modifiable risk factors in Norwegian women using the data from the Norwegian Women and Cancer (NOWAC) study. Self-reported information from 35 525 women from the NOWAC study were available. These included the following exposures: smoking status, alcohol consumption, body mass index, physical activity, intake of calcium, fibers, and red and processed meat. Colon cancer cases were identified from the Cancer Registry of Norway. A parametric piecewise constant hazards model was used to estimate the strength of exposure-cancer associations. Population attributable fractions with 95% confidence intervals (CIs) were calculated considering competing risk of death. The fraction of incident colon cancer attributable to ever smoking was 18.7% (95% CI 4.7%-30.6%), low physical activity 10.8% (95% CI -0.7% to 21.0%), alcohol consumption 14.5% (95% CI -2.8% to 28.9%), and low intake of calcium 10.0% (95% CI -7.8% to 24.8%). A small proportion of colon cancer cases was attributable to combined intake of red and processed meat over 500 g/week, overweight/obesity, and low intake of fibers. Jointly, these seven risk factors could explain 46.0% (95% CI 23.0%-62.4%) of the colon cancer incidence burden. Between 23% and 62% of the colon cancer burden among women in Norway was attributable to modifiable risk factors, indicating an important preventive potential of a healthy lifestyle.

Modeling age-specific incidence of colon cancer via niche competition.

Cancer development is a multistep process often starting with a single cell in which a number of epigenetic and genetic alterations have accumulated thus transforming it into a tumor cell. The progeny of such a single benign tumor cell expands in the tissue and can at some point progress to malignant tumor cells until a detectable tumor is formed. The dynamics from the early phase of a single cell to a detectable tumor with billions of tumor cells are complex and still not fully resolved, not even for the well-known prototype of multistage carcinogenesis, the adenoma-adenocarcinoma sequence of colorectal cancer. Mathematical models of such carcinogenesis are frequently tested and calibrated based on reported age-specific incidence rates of cancer, but they usually require calibration of four or more parameters due to the wide range of processes these models aim to reflect. We present a cell-based model, which focuses on the competition between wild-type and tumor cells in colonic crypts, with which we are able reproduce epidemiological incidence rates of colon cancer. Additionally, the fraction of cancerous tumors with precancerous lesions predicted by the model agree with clinical estimates. The correspondence between model and reported data suggests that the fate of tumor development is majorly determined by the early phase of tumor growth and progression long before a tumor becomes detectable. Due to the focus on the early phase of tumor development, the model has only a single fit parameter, the time scale set by an effective replacement rate of stem cells in the crypt. We find this effective rate to be considerable smaller than the actual replacement rate, which implies that the time scale is limited by the processes succeeding clonal conversion of crypts.

Effects of Anesthetics on Proliferation and Apoptosis of Drug-Resistant Human Colon Cancer Cells.

In recent years, people's living standards are getting higher and higher, and life pressure is also increasing, and there are also many problems in eating habits. This is also the direct cause of colon cancer. The aim of this paper was to investigate whether anesthetic drugs could positively affect the proliferation and apoptosis of colon cancer cells. In this paper, the significance of anesthetic drugs is proposed, and an artificial neural network algorithm based on artificial intelligence is proposed. It is well known that artificial neural networks play an important role in medicine. The experimental results of this paper show that the incidence of colon cancer in 2020 will be in the range of 5%-35%, and the incidence of colon cancer in 2021 will be in the range of 7%-30%. While colon cancer rates in 2021 do not appear to be as high as colon cancer rates in 2020, they are generally much higher than colon cancer rates in 2020. It can be seen that as the population ages, the number of colon cancer patients is increasing due to the lack of emphasis on health. This also means that the incidence of colon cancer is getting higher and higher, and traditional drug chemotherapy has been unable to play a good role in inhibiting the proliferation of colon cancer cells. Therefore, this paper investigated the effects of anesthetic drugs on the proliferation and apoptosis of human colon cancer cells.

The Prediction of Peritoneal Carcinomatosis in Patients with Colorectal Cancer Using Machine Learning.

The incidence of colon, rectal, and colorectal cancer is very high, and diagnosis is often made in the advanced stages of the disease. In cases where peritoneal carcinomatosis is limited, patients can benefit from newer treatment options if the disease is promptly identified, and they are referred to specialized centers. Therefore, an essential diagnostic benefit would be identifying those factors that could lead to early diagnosis. A retrospective study was performed using patient data gathered from 2010 to 2020. The collected data were represented by routine blood tests subjected to stringent inclusion and exclusion criteria. In order to determine the presence or absence of peritoneal carcinomatosis in colorectal cancer patients, three types of machine learning approaches were applied: a neuro-evolutive methodology based on artificial neural network (ANN), support vector machines (SVM), and random forests (RF), all combined with differential evolution (DE). The optimizer (DE in our case) determined the internal and structural parameters that defined the ANN, SVM, and RF in their optimal form. The RF strategy obtained the best accuracy in the testing phase (0.75). Using this RF model, a sensitivity analysis was applied to determine the influence of each parameter on the presence or absence of peritoneal carcinomatosis.