This is a phase II study to assess whether treatment with chemotherapy drugs FOLFOX (5-Fluorouracil (5FU), Oxaliplatin (Eloxatin) and Leucovorin (Folinic Acid)) or FOLFIRI (5-Fluorouracil (5FU), Irinotecan (Camptosar) and Leucovorin (Folinic Acid))and panitumumab before and after surgery can improve outcome in patients with liver metastases (the cancer has spread to other parts of the body such as the liver) that are resectable (can be surgically removed), from colorectal cancer that have a non mutant (wild-type) K-ras gene.. FOLFOX/FOLFIRI is an intravenous (given by vein) chemotherapy combination that is approved for colorectal cancer while panitumumab is also an intravenous drug and have been approved for treatment of refractory (not responding treatment) metastatic colorectal cancer whose cancers have the K-ras gene. These drugs are not approved for the treatment of colorectal cancer liver metastases (CRCLM) who can have surgery.. Patients will receive FOLFOX/FOLFIRI and panitumumab for four ...
Dysregulation of microRNAs has been confirmed to serve an important role in cancer development and progression. However, the role of microRNA (miR)‑544 in colorectal cancer progression remains unknown. In the present study, it was observed that the expression level of miR‑544 was increased in breast cancer cell lines and tissues using the quantitative polymerase chain reaction. Overexpression of miR‑544 promoted cell proliferation and invasion in colorectal cancer, whereas inhibition of miR‑544 suppressed colorectal cancer progression as determined using MTT, colony formation and Transwell assays. Furthermore, forkhead box O1 (FOXO1) was a direct target of miR‑544. FOXO1 mediated miR‑544‑regulated colorectal cancer progression and cell cycle distribution. In conclusion, the results of the present study revealed that miR‑544 serves an important role in promoting human colorectal cancer cell progression ...
Whether to perform primary tumor resection in patients with asymptomatic Stage IV colorectal cancer remains controversial; however, the more aggressively we perform radical resection and metastasectomy to selected patients, the more survival benefits the patients obtain.
We established an in vivo model of organ-specific colorectal cancer metastasis and demonstrated that the CD110+ tumor initiating cells contribute for colorectal liver metastasis. To gain a deeper understanding of its metastatic capacity, we performed a genome-wide transcriptome analysis on the CD110+ tumor cells derived from primary colon xenografts and their matched liver metastases. Results provide important information of the responses of the CD110+ cells during the process of liver colonization. Total RNA obtained from the CD110+ cells sorted from primary colorectal tumors (CRC102-PT and CRC108-PT) compared to those from the corresponding liver metastases (CRC102-LM and CRC108-LM).
The U.S. Food and Drug Administration (FDA) has approved panitumumab (Vectibix) for use in combination with FOLFOX (fluorouracil, leucovorin, oxaliplatin) as first-line treatment in patients with wild-type KRAS (exon 2) metastatic colorectal cancer.. This approval converts the accelerated monotherapy approval granted in 2006 to a full approval. Panitumumab was previously approved by the FDA as a monotherapy for patients with EGFR-expressing metastatic colorectal cancer after disease progression and prior treatment with fluoropyrimidine-, oxaliplatin-, and irinotecan-containing chemotherapy. The agent is not indicated for the treatment of patients with KRAS-mutant metastatic colorectal cancer or for whom KRAS mutation status is unknown.. The FDA has also approved the therascreen KRAS test as a companion diagnostic to guide use of panitumumab in the treatment of metastatic colorectal cancer.. Phase III Studies. The approval is based on results from the phase III PRIME and -ASPECCT trials. The ...
Although disease stage is the most relevant factor influencing treatment choice in locally advanced radically resected colorectal cancer, it is not uncommon to observe disease relapse in patients with apparent low risk stage that are usually excluded from an adjuvant therapy. On the contrary we also know that some patients with high risk stage are not likely to relapse independently from medical treatment received. Preclinical data suggested that cancer stem cells may influence the biological behaviour of many solid tumours including colorectal cancer. We tested a panel of genetic markers of stemness in resected Dukes stage B and C colorectal cancer and their impact on prognosis. We performed k-means unsupervised clustering (K = 2) using the mRNA expression data of 66 genes. The algorithm divided the patients into two groups (A and B) and most of the patients clustered in a manner consistent with relapse free survival, defined as the time between primary surgery and first radiological sign of ...
Metastatic Colorectal Cancer - Pipeline Review, H1 2014SummaryGlobal Markets Directs, Metastatic Colorectal Cancer - Pipeline Review, H1 2014, provides an overview of the Metastatic Colorectal Cancers therapeutic pipeline.This report provides comprehensive information on the therapeutic development for Metastatic Colorectal Cancer, complete with comparative analysis at various stages, therapeutics
Background Oxaliplatin is effective in adjuvant and first-line colorectal cancer chemotherapy. Oxaliplatin-induced severe chronic neurotoxicity is the main dose-limiting adverse event. No standard treatment for oxaliplatin-induced chronic neurotoxicity has been identified.. Materials and methods We conducted a prospective pilot clinical trial to explore whether neurotropin has neuroprotective effects on chronic neurotoxicity. From May 1 2010 to July 1 2011, 80 stage II and III colorectal cancer patients who were eligible to receive oxaliplatin-based chemotherapy voluntarily enrolled in the trial. The patients were randomly divided into 2 groups, one of which received neurotropin treatment.. Results The patients in the control group experienced significantly ≥ grade 2 and ≥ grade 3 neurotoxicity (by NCI CTCAE grading) than did those in the neurotropin group (60.9% vs. 38%, for at least grade 2 neurotoxicity, P = 0.001; 39% vs. 2.7%, for at least grade 3 neurotoxicity, P < 0.001). If ...
MedStar Montgomery Medical Center offers a wide array of advanced colorectal cancer treatments for both complex and common colorectal cancer types.
Colorectal cancer (CRC) is a heterogeneous and biologically poorly understood disease. To tailor CRC treatment, it is essential to first model this heterogeneity by defining subtypes of patients with homogeneous biological and clinical characteristics and second match these subtypes to cell lines for which extensive pharmacological data is available, thus linking targeted therapies to patients most likely to respond to treatment. We applied a new unsupervised, iterative approach to stratify CRC tumor samples into subtypes based on genome-wide mRNA expression data. By applying this stratification to several CRC cell line panels and integrating pharmacological response data, we generated hypotheses regarding the targeted treatment of different subtypes. In agreement with earlier studies, the two dominant CRC subtypes are highly correlated with a gene expression signature of epithelial-mesenchymal-transition (EMT). Notably, further dividing these two subtypes using iNMF (iterative Non-negative Matrix
Metastatic Colorectal Cancer Pipeline Review, H2 2012 Global Markets Directs, \Metastatic Colorectal Cancer Pipeline Review, H2 2012\, provides an overview of the Metastatic Colorectal Cancer therapeutic pipeline. This report provides information on the therapeutic development for Metastatic Colorectal Cancer, complete with latest updates, and special features on late-stage and discontinued p
FOLFIRI Combined with Bevacizumab as First-Line Treatment for Metastatic Colorectal Cancer Patients with Hyperbilirubinemia after UGT1A1 Genotyping. Yeh, Yung-Sung; Huang, Meng-Lin; Chang, Se-Fen; Chen, Chin-Fan; Hu, Huang-Ming; Wang, Jaw-Yuan // Medical Principles & Practice;Sep2014, Vol. 23 Issue 5, p478 Objective: To report a metastatic colorectal cancer patient with hyperbilirubinemia treated with a combination of bevacizumab and FOLFIRI (5-fluorouracil, leucovorin, and irinotecan) using uridine diphosphate glucuronosyl transferase (UGT1A1) genotyping. Clinical Presentation and Intervention: A... ...
OBJECTIVES: To assess the prior exposure to colorectal examinations between colorectal cancer (CRC) patients and matched control participants to estimate the effect of these examinations on the development of CRC and to obtain insight into the background incidence of colorectal examinations. METHODS: A population-based case-control study was conducted within the Dutch Integrated Primary Care Information database over the period 1996-2005. All incident CRC cases were matched with up to 18 controls (n=7,790) for age, sex, index date (date of CRC diagnosis) and follow-up before diagnosis. All colorectal examinations performed in symptomatic participants in the period 0.5-5 years before index date were considered in the analyses. RESULTS: Within the source population of 457 024 persons, we identified 594 incident cases of CRC. In the period 0.5-5 years before index date 2.9% (17 of 594) of the CRC cases had undergone colorectal examinations, compared with 4.4% (346 of 7790) in the control population ...
Colorectal Cancer Development Pathway from normal colorectal epithelium to cancer Colorectal cancer develops via an adenoma to carcinoma sequence with the accumulation of a number of genetic and epigenetic mutations (Figure 1‑3) (Morson 1968; Fearon and Vogelstein 1990). The mutations accumulated vary in hereditary cancer depending on the initiating mutation. In their normal…
Significant variability has been reported in the rates of proliferation of colorectal cancer tumors, and faster proliferation is associated with poor patient prognosis (9-12). In primary colorectal tumors, an association has been reported between high-grade (poorly differentiated; refs. 24, 25) or MSI (26) and faster proliferation rates. Here, we show that cell lines that form high-grade tumors when grown as xenografts or have microsatellite instability proliferate significantly faster than cell lines forming low-grade (differentiated) tumors or MSS lines. These results indicate that the proliferative profile of the cell line panel used here closely recapitulates the characteristics of primary colorectal tumors. This is consistent with our recent findings demonstrating that the mutational landscape of colorectal cancer cell lines closely resembles that of primary colorectal cancers (27), and collectively establish cell lines as suitable models for the investigation of this disease. ...
Results An optimal 13-gene expression classifier (PIGR, CXCL13, MMP3, TUBA1B, SESN1, AZGP1, KLK6, EPHA7, SEMA3A, DSC3, CXCL10, ENPP3, BNIP3) for prediction of relapse among patients with stage II CRC was developed using a consecutive Norwegian test series from patients treated according to current standard protocols (n=44, p,0.001, HR=18.2), and its predictive value was successfully validated for patients with stage II CRC in a second Norwegian CRC series collected two decades previously (n=52, p=0.02, HR=3.6). Further validation of the classifier was obtained in a recent external dataset of patients with stage II CRC from other populations (n=108, p=0.001, HR=6.5). Multivariate Cox regression analyses, including all three sample series and various clinicopathological variables, confirmed the independent prognostic value of the classifier (p≤0.004). The classifier was shown to be specific to stage II CRC and does not provide prognostic stratification of patients with stage III CRC. ...
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In a study reported in the Journal of the National Cancer Institute, Imperiale et al found that the National Cancer Institute (NCI) colorectal cancer risk assessment tool was able to estimate the current risk for advanced colorectal neoplasia.. Study Details. The study involved 4,457 persons aged 50 to 80 years undergoing first-time screening colonoscopy. The NCI tool was used to calculate the future risk of colorectal cancer on the basis of medical and family histories, lifestyle information, and physical measures. Advanced neoplasia was defined as a sessile serrated polyp or tubular adenoma ≥ 1 cm, a polyp with villous histology or high-grade dysplasia, or colorectal cancer. Subjects had a mean age of 57 years, and 52% were women.. Correlation of Risk. The overall prevalence of advanced neoplasia was 8.26%. Based on quintiles of increasing 5-year estimated absolute colorectal cancer risk, current risks of advanced neoplasia were 2.1%, 4.8%, 6.4%, 10.0%, and 17.6% (P , .001). For quintiles of ...
Etiology of the colorectal cancer is not completely understood. It is not possible to definitely clarify why some people catch the disease and why others do not. What we do know is colorectal cancer is not contagious. This disease is not transmitted from one person to the other.. Age: Risk of being caught by the colorectal cancer increases by aging. Ninety percent of people with final diagnosis of colorectal cancer are older than 50 years. Mean age at diagnosis is around 60 years.. Colorectal polyp: Polyps outgrow on interior wall of the colon. They are common in people older than 50. Polyps are mostly benign in nature or they do not transform into cancer. However, some polyps (i.e. adenomas) may progress into cancer. Diagnosis and excision of polyps substantially reduce the risk of colorectal cancer.. Familial history of colorectal cancer: Colorectal cancer is more likely for people who have a family member (parents, siblings or children) with personal history of colorectal cancer. The risk is ...
TY - JOUR. T1 - Changes of KRAS Exon 2 Codon 12/13 Mutation Status in Recurrent Colorectal Cancer. AU - Dócs, Ottó. AU - Fazakas, Ferenc. AU - Horváth, Nóra Lugosiné. AU - Tóth, L.. AU - András, C.. AU - Horváth, Z.. AU - Méhes, G.. PY - 2014/9/24. Y1 - 2014/9/24. N2 - Colorectal cancer (CRC) is a heterogeneous disease presenting with a wide spectrum of morphological and molecular characteristics sometimes even within the same patient. To understand the mechanisms of oscillations in the KRAS status we evaluated the collective of CRC patients tested using allele-specific PCR and Sanger-sequencing. Mutant KRAS allele was observed in 43.3 % of cases. Repeated analysis of KRAS status in recurrent tumors or metastases was performed in 18/665 cases and a total of 6 cases with different KRAS status was found. In three cases the histological pattern of the tumor was identical. In one patient different histology and molecular status was seen between the primary and the recurrent tumor samples. ...
Researchers from the University of Hawaiʻi Cancer Center and Office of Public Health Studies have found that patients who have type 2 diabetes in addition to other chronic diseases have a lower survival rate for colorectal cancer.. The study. Type 2 diabetes and colorectal cancer survival: The multiethnic cohort, published in the International Journal of Cancer, investigated the survival rates of colorectal cancer patients with or without type 2 diabetes, and with additional diseases such as heart disease or stroke. The findings showed type 2 diabetes alone does not significantly affect survival for colorectal cancer patients. However, patients with type 2 diabetes as well as other chronic diseases had a lower survival rate.. The researchers looked at 24 years of health data of more than 215,000 adults from California and Hawaiʻi who participated in the multi-ethnic cohort to identify predictors of survival. Among 3,913 new cases of colorectal cancer, the 707 participants with type 2 ...
In this study, modest correlations of AREG and EREG relative mRNA expression were observed between primary colorectal cancer and corresponding liver metastases. We have previously reported the correlation of VEGF [14], EGFR [15], and 5-FU metabolism-related genes [16] between primary colorectal tumor and liver metastases. Although EGFR mRNA expression showed a relatively strong correlation between the primary tumor and metastases [15], the correlations of AREG and EREG, which are the ligands of the EGFR family, between primary and metastases were weaker than that. The median values of AREG and EREG expression did not differ between primary cancer and metastases, which suggested that there was no up-regulation in the liver metastases. The strength of correlation was similar between synchronous and metachronous metastases, which suggested that expression levels were well preserved, even in relapse, for long time after primary tumor resection. Interestingly, the significance of EREG as a prognostic ...
We established an in vivo model of organ-specific colorectal cancer metastasis and demonstrated that the CD110+ tumor initiating cells contribute for colorectal liver metastasis. To gain a deeper understanding of its metastatic capacity, we performed a genome-wide transcriptome analysis on the CD110+ tumor cells derived from primary colon xenografts and their matched liver metastases. Results provide important information of the responses of the CD110+ cells during the process of liver colonization.
Your age. Getting older is a risk factor for colorectal cancer.. Your race and ethnicity. African Americans have a higher risk of getting colorectal cancer (and dying from it) than people of other races. And Ashkenazi Jews (Jewish people whose ancestors came from Eastern Europe) who have inherited certain genes are also at a higher risk for getting colorectal cancer.. Your familys medical history. You are more likely to get colorectal cancer if one of your parents, brothers, sisters, or children has had the disease. Your risk is higher if this family member had colorectal cancer younger than 45 years old, or if more than one family member had the disease.. Some common gene changes increase the chance of colorectal cancer. These changes are familial adenomatous polyposis (FAP) and Lynch syndrome, also called hereditary nonpolyposis colorectal cancer (HNPCC). Many people with these changed genes will get colorectal cancer if they arent carefully watched. Genetic testing can tell you if you carry ...
TY - JOUR. T1 - Genetic epidemiology of colorectal cancer. AU - Petersen, Gloria M. PY - 1995. Y1 - 1995. N2 - Genetic epidemiological methods have played an integral role in the characterisation of the genetic susceptibilities to colorectal cancer. Classic epidemiological approaches, such as case-control and prospective cohort studies, that utilise family history information have laid the foundation for the more specialised family-based genetic methods, segregation analysis and linkage analysis. The genetic epidemiology of colorectal cancer can be characterised by several themes: the consistently increased risk of colorectal cancer in first-degree relatives of patients with colorectal cancer; genetic predisposition to some, if not the majority of colorectal neoplasms; and genetic heterogeneity of the inherited colorectal cancer syndromes. With the rapid development of molecular genetic techniques, new opportunities for further research include studies to estimate the proportion of colorectal ...
OBJECTIVES:. I. Compare overall survival in patients with locally advanced, metastatic, or recurrent colorectal cancer treated with fluorouracil, leucovorin calcium, oxaliplatin, and bevacizumab vs capecitabine, oxaliplatin, and bevacizumab.. II. Compare progression-free survival and time to treatment failure in patients treated with these regimens.. III. Compare the response of patients with measurable disease treated with these regimens.. IV.Compare toxicity rates of these regimens in these patients. V. Compare patient-reported functional status and convenience of therapy in patients treated with these regimens.. VI. Correlate germline polymorphisms of DNA repair (e.g., ERCC-1, XRCC1, GST-P1, XPD, and ribonucleotide reductase), target enzymes (e.g., thymidylate synthase, dihydropyrimidine dehydrogenase, and thymidine phosphorylase), angiogenesis (e.g., vascular endothelial growth factor), and growth factors (e.g., epithelial growth factor receptor) with survival, progression-free survival, and ...
The purpose of this study is to determine the activity of SCH 717454 in patients with relapsed or recurrent colorectal cancer.
At present, a full understanding of the mechanisms by which colorectal cancer (CRC) distant metastases form is still beyond our reach because of the intricate regulation of gene expression. MicroRNAs (miRNAs) are shown to be involved in various human diseases including cancers through negative regulation of target gene expression at the post-transcriptional level. However, there are only a few studies on the roles of miRNA aberrations in liver metastasis of human colorectal cancer. To identify miRNA expression patterns associated with liver metastasis in human colorectal cancer, the miRNA expression profiles of colorectal cancer tissues with liver metastasis and their non-metastatic counterparts were studied using microRNA microarrays and further confirmed by quantitative RT-PCR. We show that 28 miRNAs are differentially expressed in the colorectal carcinomas with liver metastasis compared to the non-metastatic counterparts. Of these, 4 miRNAs including miR-150*, miR-125b-2*, miR-1179 and ...
Colorectal cancer causes significant morbidity and mortality in the United States. The incidence of colorectal cancer can be reduced with increasing efforts directed at mass screening of average-risk adults 50 years and older. Currently, fecal occult blood test and flexible sigmoidoscopy have the highest levels of evidence to support their use for colorectal cancer screening. Colonoscopy does not have a proven colorectal cancer mortality benefit, but it does have the greatest single-test accuracy, and it is the final test in the pathway to evaluate and treat patients with other abnormal screening tests. Double-contrast barium enema has sparse data of effectiveness. Computed tomographic colonography, fecal DNA testing, and Pillcam Colon are promising tests that need further study before they can be recommended for widespread screening. Routine screening should continue until 75 years of age. There is good evidence that fiber and antioxidants are not effective for primary prevention of colorectal cancer;
Epidemiological characteristics of colorectal cancer may differ by particular anatomical subsite, suggesting that the subsite-specific colorectal cancers may represent different disease entities. This study explored the time trends over a 23-year period in colorectal cancer incidence at various subsites by sex and age group. Data on the incidence of colorectal cancer were obtained from a population-based cancer registry in Shanghai, Peoples Republic of China. Between 1972 and 1994, 30,693 patients with colorectal cancer were registered at the Shanghai Cancer Registry. The overall age-adjusted colorectal cancer incidence rates increased , 50%, or 2% per year from 1972-1977 to 1990-1994, from 14 to 22 per 100,000 among men and from 12 to 19 per 100,000 among women. The increases in rates were considerably more rapid for colon cancer, with rates approximately doubling, than they were for rectal cancer. Proximal colon cancer was more common than distal colon cancer over the whole study period, ...
This systematic review with meta-analyses has shown that tumor PTGS2 expression is associated with an increased risk of colorectal cancer recurrence and poorer colorectal cancer-specific survival. However, it was not possible to conduct a meta-analysis of estimates for risk of cancer recurrence and cancer-specific survival that adjusted for other prognostic factors such as tumor stage. Adjustment for potential publication bias also meant the association with colorectal cancer-specific survival was no longer observed. In addition, PTGS2 expression was not associated with overall survival in patients with colorectal cancer, especially after adjustment for age, sex, and other tumor characteristics. Therefore, from summation of the existing literature, it remains unclear whether there is any independent association between tumor PTGS2 expression and colorectal cancer progression.. Patients with tumors that express PTGS2 were at an increased risk of colorectal cancer recurrence and colorectal ...
Simplicity is enormously complex in the treatment of metastatic colorectal cancer. In terms of survival, life expectancy of patients with metastatic colorectal cancer improved substantially from 3 to 6 months in the 1980s when only 5-fluorouracil was available, to more than 20 months today with the availability of various new chemotherapeutic and targeted agents. The use of chemotherapeutic agents - including fluoropyrimidines, irinotecan, and oxaliplatin - has been refined through decades of clinical experience. Maximal exposure, irrespective of sequence, is simply the principle of treating patients through progression with chemotherapy. Targeted therapy has emerged in the past decade, and adds complexity to the treatment principle: survival benefit has been shown with both anti-vascular endothelial growth factor and anti-epidermal growth factor receptor antibodies in individual lines of treatment, but controversy exists as to the best sequence of application. Adding to this complexity, ...
Anticancer Effect of COX-2 Inhibitor DuP-697 Alone and in Combination with Tyrosine Kinase Inhibitor (E7080) on Colon Cancer Cell Lines Colon cancer;DuP-697;COX-2 inhibition;tyrosine kinase inhibitor; Colorectal cancer remains one of the most common types of cancer and a leading cause of cancer death worldwide. In this study, we aimed to investigate effects of DuP-697, an irreversible selective inhibitor of COX-2 on colorectal cancer cells alone and in combination with a promising new multi-targeted kinase inhibitor E7080. The HT29 colorectal cancer cell line was used. Real time cell analysis (xCELLigence system) was conducted to determine effects on colorectal cell proliferation, angiogenesis was assessed with a chorioallantoic membrane model and apoptosis was determined with annexin V staining. We found that DuP-697 alone exerted antiproliferative, antiangiogenic and apoptotic effects on HT29 colorectal cancer cells. For the antiproliferative effect the half maximum inhibition concentration ($IC_{50
TY - JOUR. T1 - FOLFOX4 in advanced colorectal cancer. T2 - A monoinstitutional experience. AU - Boscolo, Giorgia. AU - Pasetto, Lara Maria. AU - Jirillo, Antonio. AU - Monfardini, Silvio. PY - 2006/5. Y1 - 2006/5. N2 - Aims and background: Patients included in clinical trials are "selected", and they usually differ from those commonly treated. Methods: From 1999 to 2004, in the Medical Oncology Department of Padua (Italy), 70 metastatic colorectal cancers were treated with FOLFOX4. Results: Our results, compared with those of the registration trial (response rate, duration of response and progression-free survival) appeared lower; overall survival was improved. Conclusions: The number of therapeutic regimens more than their type influenced the results.. AB - Aims and background: Patients included in clinical trials are "selected", and they usually differ from those commonly treated. Methods: From 1999 to 2004, in the Medical Oncology Department of Padua (Italy), 70 metastatic colorectal cancers ...
The WNT signaling pathway is commonly altered during colorectal cancer development. The E3 ubiquitin ligase, RNF43, negatively regulates the WNT signal through increased ubiquitination and subsequent degradation of the Frizzled receptor. RNF43 has recently been reported to harbor frequent truncating frameshift mutations in sporadic microsatellite unstable (MSI) colorectal cancers. This study assesses the relative frequency of RNF43 mutations in hereditary colorectal cancers arising in the setting of Lynch syndrome. The entire coding region of RNF43 was Sanger sequenced in 24 colorectal cancers from 23 patients who either (i) carried a germline mutation in one of the DNA mismatch repair genes (MLH1, MSH6, MSH2, PMS2), or (ii) showed immunohistochemical loss of expression of one or more of the DNA mismatch repair proteins, was BRAF wild type at V600E, were under 60 years of age at diagnosis, and demonstrated no promoter region methylation for MLH1 in tumor DNA. A validation cohort of 44 colorectal ...
BACKGROUND: Pre-existing non-cancer conditions may complicate and delay colorectal cancer diagnosis. METHOD: Incident cases (aged ⩾40 years, 2007-2009) with colorectal cancer were identified in the Clinical Practice Research Datalink, UK. Diagnostic interval was defined as time from first symptomatic presentation of colorectal cancer to diagnosis. Comorbid conditions were classified as competing demands (unrelated to colorectal cancer) or alternative explanations (sharing symptoms with colorectal cancer). The association between diagnostic interval (log-transformed) and age, gender, consultation rate and number of comorbid conditions was investigated using linear regressions, reported using geometric means. RESULTS: Out of the 4512 patients included, 72.9% had ⩾1 competing demand and 31.3% had ⩾1 alternative explanation. In the regression model, the numbers of both types of comorbid conditions were independently associated with longer diagnostic interval: a single competing demand ...
MiR-629-5p has been shown to function as a tumor promoter in some types of cancer. However, the role of miR-629-5p in colorectal cancer remains unclear. Here, the significant up-regulation of miR-629-5p in colorectal cancer tissues and cell lines was observed. Overexpression of miR-629-5p showed a positive effect on cell proliferation and migration. The enhanced miR-629-5p level also suppressed cell apoptosis and resulted in a low Bax level and a high Bcl-2 level. Further down-regulating miR-629-5p demonstrated opposite effects. CXXC finger protein 4 (CXXC4) was predicted as a direct target of miR-629-5p. Dual-luciferase reporter and Western blotting assays exhibited miR-629-5p directly bound to the 3′UTR of CXXC4 and then down-regulated its expression at post-transcriptional level. CXXC4 knockdown rescued the decreased cell proliferation and migration and the enhanced cell apoptosis induced by inhibiting miR-629-5p expression. Notably, overexpression of miR-629-5p also conferred ...
TY - JOUR. T1 - Impact of circulating tumor DNA mutant allele fraction on prognosis in RAS-mutant metastatic colorectal cancer. AU - Elez, Elena. AU - Chianese, Chiara. AU - Sanz-García, Enrique. AU - Martinelli, Erica. AU - Noguerido, Alba. AU - Mancuso, Francesco Mattia. AU - Caratù, Ginevra. AU - Matito, Judit. AU - Grasselli, Julieta. AU - Cardone, Claudia. AU - Esposito Abate, Riziero. AU - Martini, Giulia. AU - Santos, Cristina. AU - Macarulla, Teresa. AU - Argilés, Guillem. AU - Capdevila, Jaume. AU - Garcia, Ariadna. AU - Mulet, Nuria. AU - Maiello, Evaristo. AU - Normanno, Nicola. AU - Jones, Frederick. AU - Tabernero, Josep. AU - Ciardello, Fortunato. AU - Salazar, Ramon. AU - Vivancos, Ana. PY - 2019/1/1. Y1 - 2019/1/1. N2 - Despite major advances in the treatment of metastatic colorectal cancer (mCRC), the survival rate remains very poor. This study aims at exploring the prognostic value of RAS-mutant allele fraction (MAF) in plasma in mCRC. Forty-seven plasma samples from 37 ...
Pan-Asian adapted ESMO consensus guidelines for the management of patients with metastatic colorectal cancer; A JSMO - ESMO initiative. The most recent version of the European Society for Medical Oncology (ESMO) consensus guidelines for the treatment of patients with metastatic colorectal cancer (mCRC) was published in 2016, identifying both a more strategic approach to the administration of the available systemic therapy choices, and a greater emphasis on the use of ablative techniques, including surgery.. At the 2016 ESMO Asia Meeting, in December 2016, it was decided by both ESMO and the Japanese Society of Medical Oncology (JSMO) to convene a special guidelines meeting, endorsed by both ESMO and JSMO, immediately after the JSMO 2017 Annual Meeting. The aim was to adapt the ESMO consensus guidelines to take into account the ethnic differences relating to the toxicity as well as other aspects of certain systemic treatments in patients of Asian ethnicity.. These guidelines represent the ...
Colorectal cancer is the third most common type cancer and represents 9.7% of total cancer cases across the globe. According to American Cancer Society col
Telomeres of some young-onset colorectal cancer patients showed accelerated aging.. • Other patients had telomeres longer than those of young healthy people.. PHILADELPHIA - For the first time, researchers have found a link between long telomeres and an increased risk for colorectal cancer, according to research presented at the American Association for Cancer Research special conference on Colorectal Cancer: Biology to Therapy, held here Oct. 27-30, 2010.. Telomeres are small strips of DNA that cover the ends of chromosomes - they are similar to the plastic coverings on shoelace tips. They prevent chromosome tips from fraying during cell division. If the telomeres shorten, then cells age. Shortened telomeres have been associated with an increased risk of cancer development, said Lisa A. Boardman, M.D., associate professor of medicine, Mayo Clinic, Rochester, Minn.. Boardman and colleagues sought evidence of biological aging in people who develop colorectal cancer at a young age. The ...
Grant Support: By grants from the National Institutes of Health (CA75123, CA79663) and Targeted Diagnostics and Therapeutics, Inc. Dr. Gelmann and Mr. Park were supported by training grants from the National Institutes of Health (5T32 GM08562 and T32 DK07705, respectively). Dr. Waldman is the Samuel M.V. Hamilton Professor of Medicine at Jefferson Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania.. Requests for Reprints: Scott A. Waldman, MD, PhD, Division of Clinical Pharmacology, Department of Medicine, Jefferson Medical College, Thomas Jefferson University, 132 South 10th Street, 1170 Main, Philadelphia, PA 19107; e-mail, [email protected] For reprint orders in quantities exceeding 100, please contact the Reprints Coordinator; phone, 215-351-2657; e-mail, [email protected] Current Author Addresses: Drs. Cagir, Bittner, and Fry: Division of Colorectal Surgery, Department of Surgery, Thomas Jefferson University, 1100 Walnut Street, Philadelphia, PA ...
Colorectal cancer patients with liver metastases and severe hyperbilirubinemia: A consecutive series that explores the benefits and risks of chemotherapy Tamana Walia, J Fernando Quevedo, Timothy J Hobday, Gary Croghan, Aminah JatoiDivision of Medical Oncology, Rochester, MN, USABackground: Do colorectal cancer patients with hyperbilirubinemia and liver metastases benefit from chemotherapy?Methods/Results: This study entailed a review of 3,019 consecutive patients with colorectal cancer. Within this cohort, 20 met the studyâ s a priori selection criteria, which included a new diagnosis of colorectal cancer, no prior therapy, and a total bilirubin of â ¥3.0 mg/dL. All 20 patients had liver metastases, and as a whole the group had a median serum bilirubin of 6.4 mg/dL (range 3.1, 28 mg/dL). Six patients received chemotherapy with an oxaliplatin-containing regimen, and four subsequently sustained a drop in their bilirubin. In one instance, a drop from 27.2 to 2.5 mg/dL occurred. These six patients
The No. 2 cancer killer in the United States, colorectal cancer, could get bumped down from its ranking if more people get screened. The rate of adults developing and dying from colorectal cancer has decreased, according to a new Vital Signs report released today by the Centers for Disease Control and Prevention.. The rate of new cases of colorectal cancer fell from 52.3 per 100,000 in 2003 to 45.4 per 100,000 in 2007, representing nearly 66,000 fewer cancers. The colorectal cancer death rate fell from 19.0 per 100,000 in 2003 to 16.7 per 100,000 in 2007, representing nearly 32,000 fewer deaths, the report says. The estimated direct medical cost of colorectal cancer was $14 billion in 2010; for each person who died of colorectal cancer in 2006, the lost productivity costs were $15.3 billion, or about $288,468 per person, the report says.. The report finds that colorectal cancer screening increased overall from 52 percent in 2002 to 65 percent in 2010. Still, about 1 in 3 people between the ages ...
In vitro and in vivo studies have associated iron with both the initiation and promotional stages of carcinogenesis. We investigated whether iron was associated with colorectal cancer in a nested case-control study within the α-tocopherol, β-carotene cancer prevention study cohort. Exposure was assessed at baseline, using a 276-item food frequency questionnaire and a fasting serum sample. The study included 130 colorectal cancer cases (73 colon cancers and 57 rectal cancers) and 260 controls. Conditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs). Supplemental iron intake was only reported for 4 cases and 18 controls; therefore, we were unable to obtain meaningful results for this variable. Comparing the highest to the lowest quartiles, there was an inverse association between serum ferritin and colorectal cancer risk (OR = 0.4, 95% CI = 0.2-0.9) and a suggestion of an inverse association between dietary iron and colorectal cancer risk (OR = ...
Colorectal cancer is malignant cells found in the colon or rectum. The colon and the rectum are parts of the large intestine, which is part of the digestive system. Because colon cancer and rectal cancers have many features in common, they are sometimes referred to together as colorectal cancer. Cancerous tumors found in the colon or rectum also may spread to other parts of the body.. Excluding skin cancers, colorectal cancer is the third most common cancer in both men and women. The American Cancer Society estimates that about 140,000 colorectal cancer cases and about 50,000 deaths from colorectal cancer occur each year. The number of deaths due to colorectal cancer has decreased, which is attributed to increased screening and polyp removal and to improvements in cancer treatment.. ...
Colorectal cancer is malignant cells found in the colon or rectum. The colon and the rectum are parts of the large intestine, which is part of the digestive system. Because colon cancer and rectal cancers have many features in common, they are sometimes referred to together as colorectal cancer. Cancerous tumors found in the colon or rectum also may spread to other parts of the body.. Excluding skin cancers, colorectal cancer is the third most common cancer in both men and women. The American Cancer Society estimates that about 140,000 colorectal cancer cases and about 50,000 deaths from colorectal cancer occur each year. The number of deaths due to colorectal cancer has decreased, which is attributed to increased screening and polyp removal and to improvements in cancer treatment.. ...
Cysteine-rich 61 (Cyr61), a member of the CCN protein family, possesses diverse functionality in cellular processes such as adhesion, migration, proliferation, and survival. Cyr61 can also function as an oncogene or a tumour suppressor, depending on the origin of the cancer. Only a few studies have reported Cyr61 expression in colorectal cancer. In this study, we assessed the Cyr61 expression in 251 colorectal cancers with clinical follow up. We examined Cyr61 expression in 6 colorectal cancer cell lines (HT29, Colo205, Lovo, HCT116, SW480, SW620) and 20 sets of paired normal and colorectal cancer tissues by western blot. To validate the association of Cyr61 expression with clinicopathological parameters, we assessed Cyr61 expression using tissue microarray analysis of primary colorectal cancer by immunohistochemical analysis. We verified that all of the cancer cell lines expressed Cyr61; 2 cell lines (HT29 and Colo205) demonstrated Cyr61 expression to a slight extent, while 4 cell lines (Lovo, HCT116,
Trends in Colorectal Cancer. Colorectal cancer incidence rates between 1983 and 2000 were relatively stable in men and declined slightly in females. In both sexes, the incidence rate has declined significantly (0.8% per year) since 2000. Between 2001 and 2007 for males and between 1998 and 2007 for females, overall mortality rates declined significantly. The rates declined, on average, by at least 2% per year since 2003 in males. In men and women combined, colorectal cancer is the third most common cancer at 13%. Mortality rates continue to decline in both sexes-by 2.6% per year in males since 2003 and 1.8% per year in females since 1998. Colorectal cancer has a significant impact on mortality for men and women combined, with 12% of all cancer deaths expected.. Screening for colorectal cancer can reduce both incidence (by identifying and removing precancerous polyps) and mortality. Screening has already been occurring in several provinces, which may partly account for the decline in mortality, ...
The main objective of the current investigation was to study the efficacy of EPA as an inhibitor of recurrent colorectal cancer growth and to determine whether EPA in combination with FuOx would be more effective than either agent/regimen alone.. The preventive and therapeutic efficacy of a combination of EPA and DHA or each PUFA alone has been demonstrated in multiple preclinical studies using a variety of rodent models of early-stage colorectal cancer (37). These studies have consistently demonstrated reduction in colorectal cancer incidence (reviewed in ref. 37). Our data demonstrate for the first time that EPA acts synergistically with FuOx to markedly inhibit the growth of chemoresistant colon cancer cells that form bulk of the recurrent tumor. Although the underlying cause for tumor recurrence is not fully understood, one of the reasons is thought to be the presence of CSCs/CSLCs that are resistant to conventional chemotherapy and retain limitless potential to regenerate (1-3, 38). The ...