Tumor markers, also called biomarkers, are substances that are produced by the cancer, or by other cells of the body, in response to cancer. Tumor markers for colorectal cancer can be found in the blood, which are measured using a blood test, or are found in the tumor tissue itself. Having a high level of a tumor marker suggests that cancer may be present in the body, but by itself, a high tumor marker level is not enough to make a diagnosis.
Tumor markers may be used in conjunction with other tests (scans, biopsies, etc.) to help diagnose a patient who has symptoms suspicious for cancer, to predict prognosis after diagnosis, and assist in making treatment decisions. In colorectal cancer, tumor markers are most often used to evaluate the patient's response to cancer treatment or to monitor for a recurrence (return of the cancer after treatment). A decrease in a tumor marker may indicate that the cancer is responding to treatment. If there is no change, or the tumor marker increases, this may indicate that the treatment is not working or that the cancer has returned. These results must be evaluated in combination with radiology tests, physical exam and the increase or decrease in any symptoms the patient may be experiencing.
There are some limits to the use of tumor markers. There are non-cancerous conditions that can cause tumor markers to be elevated, so these must also be considered when interpreting the test results. In addition, not everyone with colorectal cancer will have an elevated tumor marker. Your doctor will recommend testing for tumor markers only if you need them.
Markers found in the blood:
Carcinoembryonic antigen (CEA) level is the tumor marker most often used in colorectal cancer. This level can be checked prior to surgery to predict prognosis, can be used during therapy to assess response to treatment or after completion of therapy to monitor for recurrence.
CA 19-9 is a blood marker that may be elevated in colorectal cancer.
Markers found in tumor tissue:
MSI (microsatellite instability): MSI is a way to measure a deficiency of mismatch repair (MMR) in tumor DNA. A deficiency of MMR results in an increase in mutations within the colon cells, which partly contributes to the development of colon cancer.MSI can be used to identify early stage colon cancer that may require more aggressive treatment or to identify patients who should have further genetic testing due to the risk for a familial syndrome related to several cancer types.
MSI identifies tumors as MSI-high (MSI-H) or MSI-Stable and MSI-low.
K-RAS mutations: specific mutations in the K-RAS gene can predict whether or not a patient is likely to benefit from treatment with several biologic therapies.
References & Further Reading
The American Society of Clinical Oncology (ASCO)
Understanding Your Pathology Report: Colon Cancer
OncoLink Patient Guide to Tumor Markers
Duffy MJ, Lamerz R, Haglund C, Nicolini A, Kalousova M, Holubec L, et al. Tumor markers in colorectal cancer, gastric cancer and gastrointestinal stromal cancers: European group on tumor markers 2014 guidelines update. International journal of cancer Journal international du cancer. 2014;134(11):2513-22.
Febbo PG, Ladanyi M, Aldape KD, De Marzo AM, Hammond ME, Hayes DF, et al. NCCN Task Force report: Evaluating the clinical utility of tumor markers in oncology. Journal of the National Comprehensive Cancer Network : JNCCN. 2011;9 Suppl 5:S1-32; quiz S3.
Winder T, Lenz HJ. Molecular predictive and prognostic markers in colon cancer. Cancer treatment reviews. 2010;36(7):550-6.
Carcinoembryonic antigen (CEA) level is the tumor marker most often used in colorectal cancer. This level can be checked prior to surgery to predict prognosis, can be used during therapy to assess response to treatment or after completion of therapy to monitor for recurrence. CA 19-9 is a blood marker that may be elevated in colorectal cancer.
Markers found in tumor tissue:
MSI (microsatellite instability): MSI is a way to measure a deficiency of mismatch repair (MMR) in tumor DNA. A deficiency of MMR results in an increase in mutations within the colon cells, which partly contributes to the development of colon cancer.MSI can be used to identify early stage colon cancer that may require more aggressive treatment or to identify patients who should have further genetic testing due to the risk for a familial syndrome related to several cancer types.
MSI identifies tumors as MSI-high (MSI-H) or MSI-Stable and MSI-low.
K-RAS mutations: specific mutations in the K-RAS gene can predict whether or not a patient is likely to benefit from treatment with several biologic therapies.
Do you mean how to follow it clinically? Because CEA would be best for that...but is also not very good. Or do you mean to test if something is indeed cancer? That would be MMR, BRAF, KRAS, etc.
@Dear Nicole> I am trying to find out the best clinical biomarker and also new approaches to this field of study. and after that it's mechanism and problems and how we can improve it to have more sure answers.
CEA can be used as a tool to follow up cases post colorectal surgery.
Carcinoembryonic antigen (CEA) level is the tumor marker most often used in colorectal cancer. This level can be checked prior to surgery to predict prognosis, can be used during therapy to assess response to treatment or after completion of therapy to monitor for recurrence.
CA 19-9 is a blood marker that may be elevated in colorectal cancer.
Markers found in tumor tissue:
What is the best biomarker/tumor marker for colorectal cancer? - ResearchGate. Available from: https://www.researchgate.net/post/what_is_the_best_biomarker_tumor_marker_for_colorectal_cancer [accessed Dec 4, 2015].
For some reason my response from last night did not get added, so I will try again. In 1996, our team of 4 learnt of Vascular Endothelial Growth Factor which is considered the main growth factor involved in neovascularisation. We be gain our research into breast and colorectal cancer simultaneously, on the basis that every cell needs oxygen to survive, and new vessels supply oxygen to new cells, till cell multiplication is balanced by apoptosis, such that there is no further mitosis or meiosis of the last cancer cell. Thus, although the cell remains viable, it cannot divide any further, It is thus gratifying to see that 20 years later, anti-VEGF antibodies are being used as third line chemotherapy, to control various cancers including breast, colorectal lung and renal. The studies we performed are all in peer-reviewed journals with high impact factors, and include: largest collection of normal human serum, to define normal range of serum VEGF, including stability of frozen serum versus blood with time frames. Then, we demonstrated variability of normal serum VEGF with oestrogen levels in normal menstrual cycles, using males, post-menopausal women and pre-menopausal on combined OCP as comparators. Then we studied serum VEGF in a large cohort of breast cancer (200 patients) and colorectal cancer (120 patients); and showed that pre operative and pre neoadjuvant serum VEGF correlated to stage of colorectal cancer but type of breast cancer, I.e. To oestrogen receptor status. We compared serum VEGF to CEA and CA 15.3 in breast cancer, and found VEGF predicted presence of cancer better. In CRC we showed that postoperative and post adjuvant chemo-radiotherapy serum VEGF predicted curative resections versus those in patients with liver metastasis. In breast cancer cell culture we showed that supernatant VEGF reduced quantitatively in response to hormone-, chemo- and radio-therapy. Finally, we developed an in-house ELISA that detected the VEGF receptor, flt-1, and this could be stained in both breast and colorectal cancer patient's histology slides, such that the level could be quantified. The last part of this data remains incomplete and currently soluble flt-1 and the tissue-fixed VEGF receptor KDR have been further defined into VEGF-R (receptors). 1 to 4. As the four people involved with this research are all consultant surgeons of whom two are professors and the other two clinical, we could not take the research further. A professor of vascular surgery coordinated with us to investigate VEGF as treatment of ischaemic vascular disease, with success. I would thus recommend taking the study of VEGF receptors further, with the aim of understanding the relevance of tissue to serum VEGF. If you do, please quote the work of the following: Dr Ms Kamal Heer; Dr Harish Kumar, Professor Michael Kerin, Professor John R T Monson. We all researched together at the Academic Surgical Unit, Castle Hill Hospital, UK, in association with the University of Hull. The vascular professor is professor Ms Shivanti Homer, at Leeds University Hospitals, UK. Look in the following journals for starters: Clinical Cancer Research, Anti Cancer Research and the British Journal of Cancer. I do not know where Prof Homer published her work.
There are a lot of biological markers but none is very good. It is better to make a complete follow-up using images techniques and other clinical and biochemical parameters
Though in the Western world most of us use extensive imaging, blood indices including tumour markers for diagnosis, planning therapy and intensive follow up, I believe the question pertains to better methods of diagnosis, where all have failed. For example, in the best scenario, most tumour markers are elevated above the normal range in approx. two third cases; and preop staging although good, is not 100% in either its positive or negative predictive value. Tests for screening rely on a very high unacceptable rates of false positivity as well as false negativity, when one considers pre-malignant lesions. Thus, what we are all looking for are markers that directly correlate to the actual viable tumour load. This is why growth factors are more useful in determining the viability of cancer tissues. It is thus not surprising that after many years of chemo and radiotherapy alone, anti-tumour and anti-growth factor antibodies have provided a newer and more promising group of drugs in treatment. It depends on whether one talks about day-to-day diagnosis in a clinical scenario, or whether the question was more geared towards areas of current research. I would find it hard to believe if any discussion on cancer didnot take current imaging and blood investigations for granted.