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PubMed2004

[An early diagnosis of colorectal cancer].

Colorectal cancer is still a huge challenge for modern oncology due to a number of patients. The malignant disease is associated with industrial countries and mostly occurs in Europe and United States. Despite screening programs there are a constant number of 30% patients who have advanced colorectal cancer that is clinically relevant. On the other hand, a body of evidence is accumulating on the molecular mechanisms that play a pivotal role in development of sporadic and hereditary kind of colorectal cancers. In this review we presented molecular mechanisms involved in development of colorectal cancer. Moreover, we described the results of screening programs used to detect an early stage of colorectal cancer and modern molecular techniques useful at the time of detection micrometastatic disease involving lymph nodes and bone marrow.

Biopsy↗

PubMed2005

Review article: Population screening for colorectal cancer.

Colorectal cancer is a common cancer and common cause of death. The mortality rate from colorectal cancer can be reduced by identification and removal of cancer precursors, adenomas, or by detection of cancer at an earlier stage. Pilot screening programmes have demonstrated decreased colorectal cancer mortality; as a result many countries are developing colorectal cancer screening programmes. The most common modalities being evaluated are faecal occult blood testing, flexible sigmoidoscopy and colonoscopy. Implementation of screening tests has been hampered by cost, invasiveness, availability of resources and patient acceptance. New technologies such at computed tomographic colonography and stool screening for molecular markers of neoplasia are in development as potential minimally invasive tools. This review considers who should be screened, which test to use and how often to screen.

Colorectal Neoplasms↗

PubMed1999

Genome-wide allelotyping indicates increased loss of heterozygosity on 9p and 14q in early age of onset colorectal cancer.

Colorectal cancer remains a significant public health challenge, despite our increased understanding of the genetic mechanisms involved in the initiation and progression of this disorder. It has become clear that multiple mechanisms lead to the tumorigenic phenotype, with familial predisposition syndromes accounting for less than 15% of all colorectal cancers. A genome-wide scan for loss of heterozygosity (LOH) was carried out with 150 highly polymorphic markers in an effort to identify additional loci involved in colorectal tumorigenesis in DNA samples from 42 colorectal cancer patients. The results confirm earlier observations that tumor DNAs from patients with hereditary nonpolyposis colon cancer (HNPCC) either maintain heterozygosity or exhibit altered or additional alleles. DNAs from patients with early onset colorectal carcinomas (diagnosed prior to age 50) revealed a higher overall degree of LOH than DNAs from patients with sporadic colorectal cancers diagnosed later in life (after age 50). While regions on 1p, 10q and 14q are suggestive, statistical analysis of LOH at these regions failed to reach significance. However, LOH at 9p did reveal a statistically significant increase in the early onset patient group, compared to the greater than age 50 group. LOH on 9p may involve inactivation of p16/CDKN2 through aberrant DNA methylation on the remaining chromosome, resulting in a situation analogous to a homozygous deletion of p16 and providing a selective growth advantage to these cells. This marker may prove to be a useful prognostic indicator for patient stratification in the design of therapy for early onset colorectal cancer patients.

Age of Onset↗

PubMed2003

Role of APC and DNA mismatch repair genes in the development of colorectal cancers.

Colorectal cancer is the third most common cause of cancer-related death in both men and women in the western hemisphere. According to the American Cancer Society, an estimated 105,500 new cases of colon cancer with 57,100 deaths will occur in the U.S. in 2003, accounting for about 10% of cancer deaths. Among the colon cancer patients, hereditary risk contributes approximately 20%. The main inherited colorectal cancers are the familial adenomatous polyposis (FAP) and the hereditary nonpolyposis colorectal cancers (HNPCC). The FAP and HNPCC are caused due to mutations in the adenomatous polyposis coli (APC) and DNA mismatch repair (MMR) genes. The focus of this review is to summarize the functions of APC and MMR gene products in the development of colorectal cancers.

Adenomatous Polyposis Coli Protein↗

PubMed2003

Hereditary polyposis syndromes and hereditary non-polyposis colorectal cancer.

Colorectal cancer due to hereditary syndromes comprises approximately 5% of the overall colorectal cancer burden. Conditions fall into two distinct categories, the polyposis syndromes and hereditary non-polyposis colorectal cancer. It is important for the clinician to have a working knowledge of both as screening and surveillance recommendations differ significantly from those applicable to the general population. The polyposis syndromes include familial adenomatous polyposis, Peutz-Jeghers syndrome, juvenile polyposis, and Cowden syndrome. For each condition, a review of both the intestinal and extra-intestinal clinical findings is presented as well as the genetic basis, genetic testing, screening, surveillance and treatment options. As genetic testing for several of these conditions has recently become both commercially available and standard practice, special attention is given to indications and strategies for genetic testing in hereditary colorectal cancer syndromes.

Adenomatous Polyposis Coli↗

PubMed2002

Chemotherapeutic potential of curcumin for colorectal cancer.

Colorectal cancer is one of the leading causes of cancer deaths in the Western world. More than 56,000 newly diagnosed colorectal cancer patients die each year in the United States. Available therapies are either not effective or have unwanted side effects. Epidemiological data suggest that dietary manipulations play an important role in the prevention of many human cancers. Curcumin the yellow pigment in turmeric has been widely used for centuries in the Asian countries without any toxic effects. Epidemiological data also suggest that curcumin may be responsible for the lower rate of colorectal cancer in these countries. Curcumin is a naturally occurring powerful anti-inflammatory medicine. The anticancer properties of curcumin have been shown in cultured cells and animal studies. Curcumin inhibits lipooxygenase activity and is a specific inhibitor of cyclooxygenase-2 expression. Curcumin inhibits the initiation of carcinogenesis by inhibiting the cytochrome P-450 enzyme activity and increasing the levels of glutathione-S-transferase. Curcumin inhibits the promotion/progression stages of carcinogenesis. The anti-tumor effect of curcumin has been attributed in part to the arrest of cancer cells in S, G2/M cell cycle phase and induction of apoptosis. Curcumin inhibits the growth of DNA mismatch repair defective colon cancer cells. Therefore, curcumin may have value as a safe chemotherapeutic agent for the treatment of tumors exhibiting DNA mismatch repair deficient and microsatellite instable phenotype. Curcumin should be considered as a safe, non-toxic and easy to use chemotherapeutic agent for colorectal cancers arise in the setting of chromosomal instability as well as microsatellite instability.

Anti-Inflammatory Agents↗

PubMed2004

Epidermal growth factor receptor as a therapeutic target for the treatment of colorectal cancer.

Colorectal carcinoma is the third most common malignancy worldwide. The use of currently available therapies results in only a modest impact on overall survival of patients with advanced-stage disease. New approaches for the treatment of colorectal cancer are urgently needed. The epidermal growth factor receptor (EGFR) is frequently dysregulated in colorectal carcinoma, and overexpression of the receptor confers a poor prognosis. Targeting the EGFR has become a rational approach for the treatment of colorectal carcinoma. Several strategies to inhibit the EGFR and its downstream signaling pathways are currently being investigated in preclinical and clinical studies, including monoclonal antibodies directed against the extracellular domain of the receptor and small-molecule inhibitors of its tyrosine kinase activity. Some of these drugs have already been tested in colorectal cancer and have shown preliminary evidence of antitumor efficacy. Important issues to elucidate in the future include the definition of the biologic context in which these drugs are more likely to be effective and the integration of the different agents in current therapeutic strategies for colorectal cancer. This article will provide a comprehensive review of the current available preclinical and clinical data on EGFR-targeted therapies in colorectal cancer.

Antibodies, Monoclonal↗

PubMed2002

Epidemiology of colorectal cancer.

Colorectal cancer is a important public health problem: there are nearly one million new cases of colorectal cancer diagnosed world-wide each year and half a million deaths. Recent reports show that, in the US, it was the most frequent form of cancer among persons aged 75 years and older. Given that the majority of cancers occur in elder people and with the ageing of the population in mind, this observation gives further impetus to investigating prevention and treatment strategies among this subgroup of the population. Screening research, recommendations and implementation is an obvious priority. While there are many questions to be resolved, it is apparent that many facets of colorectal cancer are becoming increasingly understood and prospects for prevention are becoming apparent. Achieving colorectal cancer control is the immediate challenge.

Adult↗

PubMed1999

Colorectal cancer.

Colorectal cancer is a leading cause of morbidity and mortality with about 300,000 new cases and 200,000 deaths in Europe and the USA each year. Published trials have established a role for chemotherapy in colorectal cancer, in the adjuvant setting for Dukes C colon cancer, with an absolute survival benefit of about 5% and in advanced colorectal cancer, for which it improves quality of life and increases survival by 6-12 months. For rectal cancer, radiotherapy decreases rates of local recurrence and, in locally advanced disease, successfully palliates pain, tenesmus, and bleeding. The evolving understanding of colorectal carcinogenesis, in particular recognition of vital genes that may be mutated or lost during tumour development, has been translated into innovative gene therapy techniques. Finally it is increasingly apparent that surgical site specialisation and a multidisciplinary approach (including surgeons, pathologists, and oncologists) may lead to optimum outcomes for patients with colorectal cancer.

Colorectal Neoplasms↗

PubMed1998

Colorectal cancer.

Colorectal cancer is the leading cause, after lung cancer, of death from cancer in Australia. About 50% of colorectal cancers are attributed to dietary factors and about 15%-20% to genetic factors, including high risk familial syndromes. The most common presenting symptoms are rectal bleeding (left-sided cancers) and iron-deficiency anaemia (right-sided cancers). Patients with suggestive symptoms should have a digital rectal examination, followed by sigmoidoscopy and biopsy if a rectal lesion is suspected, or colonoscopy if colon cancer is suspected. Treatment of most colorectal cancers is segmental resection with a wide resection margin; the role of adjuvant therapy is still being refined. Screening with annual (or biennial) faecal occult blood tests is recommended for people over 50 years without symptoms and with average or slightly above average risk; more intensive, earlier screening is recommended for those with greater risk.

Colectomy↗

PubMed2003

Development of ZD1839 in colorectal cancer.

Colorectal cancer is one of the most frequent human malignancies. Therapeutic options are mainly limited to chemotherapy with 5-fluorouracil in various schedules or in combination with irinotecan and oxaliplatin; however, novel approaches are also in development. These new agents specifically attack molecular targets involved in tumor biology. One such target is the epidermal growth factor receptor (EGFR), which is highly expressed in many tumors and is associated with a poor prognosis. The EGFR plays a key role in cell proliferation and has been implicated in several processes that mediate cancer progression. ZD1839 is an orally active, selective EGFR tyrosine kinase inhibitor that has shown extensive preclinical activity and favorable tolerability in advanced clinical trials in a variety of tumors. In colorectal cancer cells, ZD1839 has shown both in vitro and in vivo antitumor activity as monotherapy or in combination with cytotoxic agents such as paclitaxel and irinotecan. Preclinical data have also shown that ZD1839 reverses resistance to irinotecan and enhances its efficacy by improving oral bioavailability. These studies indicate that EGFR inhibition by ZD1839 may have a valuable role in the treatment of colorectal cancer, and clinical studies in patients with colorectal cancer are ongoing.

Animals↗

PubMed2002

Recent and ongoing clinical trials for treating colorectal cancer.

Colorectal cancer is one of the most common cancers worldwide. Through well-designed clinical trials, advances have been made in the treatment of localised and advanced colorectal cancer. It has been established that 6 months of 5-fluorouracil-based chemotherapy will improve overall survival in patients with stage III colon cancer. The role of adjuvant chemotherapy in stage II colon cancer remains an unresolved issue. Recent studies have demonstrated an improved survival with the addition of irinotecan to 5-fluorouracil and leucovorin for the treatment of advanced colorectal cancer. Immunotherapy, molecular targeted therapy and liver-directed therapy, in addition to new chemotherapy combinations, are all being evaluated for the treatment of localised and advanced colorectal cancer. Ongoing and proposed studies are incorporating the identification of genetic and molecular abnormalities, which may provide prognostic information as well as direct treatment decisions.

Antineoplastic Agents↗

PubMed2003

Gene therapy for colorectal cancer.

Colorectal cancer is an important public health problem worldwide. Gene therapy has therapeutic potential for patients with advanced or recurrent colorectal cancer, incurable by conventional treatments. To date, many strategies of gene therapy have been explored, including mutant gene correction, prodrug activation, immune stimulation and genetically-modified oncolytic viruses. Although the preclinical results of gene therapy for colorectal cancer have shown promise, gene therapy is still at an early stage of clinical development and has not yet shown a significant therapeutic benefit for patients. The main obstacles for introduction of gene therapy to patients are poor targeting selectivity of the vectors and inefficient gene transfer. As the science supporting tumour-selective vectors evolves, gene therapy may expand rapidly in the clinical practice of colorectal cancer treatment.

Animals↗

PubMed1996

Prophylaxis against colorectal cancer.

Colorectal cancer is diagnosed in more than 3000 people every year in Denmark, with a population of 5 million, and 2000 die from this disease every year. The aetiology of the disease is complex, but an increasing number of cancers have been related to genetics and Denmark is contributing with a well-established register of familial adenomatous polyposis and a recently founded register for hereditary nonpolyposis colorectal cancer, both with major international relationships. The Danish tradition of epidemiology and clinical trials has also been demonstrated in population screening trials for colorectal cancer in average-risk persons as well as high-risk groups with precursors of the disease. The present review places Danish contributions within the prophylaxis of colorectal cancer during the last decade in an international context.

Adenomatous Polyposis Coli↗

PubMed2000

Screening for colorectal cancer.

Colorectal cancer is the third most commonly diagnosed cancer and the second leading cause of cancer deaths in the United States. Fortunately, both the incidence and mortality associated with the disease have declined during the past 2 decades. This is likely due, at least in part, to improved efforts at screening and more aggressive removal of adenomatous polyps. However, colorectal cancer screening is still generally underutilized. This article reviews the current status and future outlook for colorectal cancer screening, including a discussion of risk factors for the disease, its anatomic distribution, proposed mechanisms of development from adenomatous polyps, rationale for screening, and screening options. Published literature concerning the cost-effectiveness of colorectal cancer screening is also summarized. The article concludes with a discussion of the emerging consensus regarding the importance of and approaches to screening.

Adenomatous Polyps↗

PubMed1998

Use and safety of aspirin in the chemoprevention of colorectal cancer.

Colorectal cancer is the third leading cause of cancer-related mortality and a significant public health problem in the United States. Aspirin and other nonsteroidal anti-inflammatory drugs reduced the incidence of colorectal cancers and related mortality by 30% to 60% as well as the incidence of colonic adenomas. This effect is presumably due to an inhibition of cyclooxygenase 2, an inducible enzyme involved in the synthesis of prostaglandins. Prostaglandins are increased in colorectal neoplasms. Aspirin's effect appears to be dose related and enhanced by long-term exposure. Two prospective studies, however, failed to show a protective benefit of aspirin in colorectal cancer. When used long term, aspirin has significant adverse effects and is poorly tolerated. The gastrointestinal toxicity of aspirin is dose related, but even low doses of aspirin (75 mg per day) when used regularly result in significantly higher gastrointestinal toxicity, manifested by melena, hematemesis, and peptic ulcer disease, in aspirin users compared with nonusers. Furthermore, some studies indicate an increased risk of hemorrhagic strokes in aspirin users. Presently, aspirin should not be recommended for the primary chemoprevention of colorectal cancer in the general population due to significant risks of serious cerebrovascular and gastrointestinal adverse effects associated with long-term aspirin use.

Aspirin↗

PubMed2005

[Fluorine-18-2-deoxy-2-fluoro-D-glucose positron emission tomography in colorectal cancer].

Colorectal cancer is a leading cancer in many countries. The glucose metabolic activities of the tumor cells are higher than that of the normal cells. They could uptake much more 2-[18F] Fluoro-2-Deoxy-d-Glucose (18F-FDG), an analogue of glucose, than normal cells do. The physicians can search the lesions via 18F-FDG positron emission tomography (PET). 18F-FDG-PET has higher sensitivity and accuracy in diagnosing the primary lesion, recurrence, liver metastasis and extrahepatic metastasis of the colorectal cancer, compared with the conventional technique. The results of the 18F-FDG-PET often restage the colorectal cancer and even change the treatment plan as 18F-FDG-PET provides more information than traditional technique does. Also, it could be used to follow up the case of the colorectal cancer after operation, systematic chemotherapy and radiotherapy. The current review addresses the metabolism, the clinical application, the shortcomings and the future prospect.

Colorectal Neoplasms↗

PubMed2006

Chemotherapy for colorectal cancer.

Colorectal cancer is the most commonly diagnosed cancer in the EU. Various randomised studies have shown a survival benefit with chemotherapy in the adjuvant setting. Adjuvant chemotherapy with 5-fluorouracil/folinic acid (5FU/FA) for 6 months after curatively resected node-positive colon cancer has become the standard practice. However, controversy still exists regarding the optimal regimen and whether to treat node-negative patients. The latest QUASAR trial results seem to strengthen the argument in favour of adjuvant treatment of Dukes B cancer. Patients with Dukes B tumours and any adverse prognostic indicator should be given the benefit of adjuvant therapy. A number of novel agents (oxaliplatin, irinotecan) showing activity in advanced disease are currently being evaluated in the adjuvant setting. A patient with metastatic colorectal cancer should today be expected to have a median survival of 18-20 months compared to that of 11-14 months only a few years ago. 5FU/FA has been the mainstay of therapy for metastatic colorectal cancer for over 40 years and confers a survival benefit over supportive care. The response rate of 5FU is improved by modulation with FA or by continuous infusional regimens (currently the best expected response rate is around 20-25%). As per the recent National Institute for Clinical Excellence guidelines, the oral agents capecitabine or tegafur with uracil (in combination with FA) can be used as first-line treatment in metastatic colorectal cancer and, although their response rate has not been directly compared to infusional 5FU, survival is unlikely to be inferior. Newer chemotherapeutic agents like irinotecan and oxaliplatin are now entering regular usage due to improved response rates (around 50% in 5FU/FA-containing doublets) and survival. Irinotecan monotherapy is second-line treatment approved by the National Institute for Clinical Excellence, although sequential infusional 5FU/FA irinotecan to infusional 5FU/FA oxaliplatin may convey the best survival with the least side effects. The position of combination chemotherapy before (to downstage) or after metastasectomy (usually from the liver) is still a topic of heated debate. Other routes (intrahepatic, intraperitoneal) are still to be proven and not recommendable outside the trial setting. The latest results of chemotherapy combinations with biological treatments (bevacuzimab and cetuximab) have been very promising indeed. Further improvements in survival, response and quality of life are expected. .

Antimetabolites, Antineoplastic↗