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The medical treatment of metastatic colorectal cancer (mCRC) has advanced significantly over the last 10 years as the result of the introduction of several active cytotoxic and biologic agents into standard clinical practice. The current standard of care for metastatic colorectal cancer (mCRC) commonly combines cytotoxic chemotherapy with biologic agents. Another agent that targets the VEGF system is aflibercept, which is currently approved in the United States for use in combination with FOLFIRI for the treatment of patients with mCRC that has progressed following an oxaliplatin-containing regimen.[7] It is a recombinant fusion molecule of the extracellular domain of human VEGFR-1 and VEGFR-2 fused to the fragment crystallizable (Fc) portion of human immunoglobulin G (IgG)-1.
Evidence exists that prolonged inhibition of the VEGF-mediated proangiogenic system is required to maximize treatment benefit for patients receiving anti-VEGF therapy, in particular because the mechanism and onset of secondary resistance could differ between chemotherapy and bevacizumab.[8] The efficacy of prolonged VEGF inhibition with bevacizumab added to chemotherapy has been highlighted by several randomized trials. In recent years, a lot of our research efforts have focused on identifying potential predictive biologic markers that might provide information regarding tumor response to anti-VEGF therapy.
At this point, no predictive biomarker for anti-VEGF therapy is available that could guide clinical practice. In addition to targeting VEGF alone, small-molecule inhibitors are being developed that target angiogenesis in other ways. EGFR (also known as ErB1 or HER1) is a member of the ERbB transmembrane tyrosine kinase receptor family.
Both antibodies have been tested as components of first-line therapy in combination with modern chemotherapy regimens, such as FOLFOX and FOLFIRI.[26-29] In clinical practice, cetuximab and panitumumab are currently used either in combination with standard combination chemotherapy regimens, with irinotecan alone, or as single agents. The search for predictive biomarkers for EGFR-targeting agents is one of the most promising and exciting areas of clinically relevant translational research in colorectal cancer at this time.
The search for other potential predictive markers of response to EGFR inhibitors eventually focused on downstream targets in the EGFR signaling pathway, including KRAS, NRAS, BRAF, and PIK3CA (the gene encoding the PI3K protein).
In 2008, the first convincing evidence from an analysis of biospecimens obtained from a large, randomized phase III trial emerged showing that KRAS mutations rendered panitumumab single-agent therapy ineffective.[33] A plethora of subsequent trials have confirmed these findings for cetuximab and panitumumab, used either as single agents or in combination with chemotherapy.
KRAS is a phosphorylated signal transducer that self-inactivates via intrinsic guanosine triphosphatase (GTP)-ase activity.[34] Studies consistently demonstrate that KRAS wild-type status is necessary but not sufficient for response to EGFR inhibitors. Seven specific mutations in exon 2 (codons 12 and 13) make up more than 90% of all KRAS mutations, and these are the mutations currently assessed in standard tests. The significance of potentially missing patients with RAS mutations and subjecting them to EGFR antibody therapy was highlighted by the results of the Dutch CAIRO-2 phase III trial. Successful Cancer surgery at We Care India partner hospital allows Henry Stolz to live a normal life despite a microendoscopic Decompression. Colon and rectal cancers begin in the digestive system, also called the GI (gastrointestinal) system (see the picture below). This information is not designed to replace a physician's independent judgment about the appropriateness or risks of a procedure for a given patient.
We Care Health Services - India a€“ Mumbai (Bombay), Chennai (Madras), Hyderabad, Kolkata, Delhi, Bangalore. If you have colon cancer, the next step for your doctor is to find an appropriate treatment option for the colon cancer cure according to your condition.
Chemotherapy is the process of treatment with drugs that kill cancer cells and is often used when there is a risk that the colon cancer will come back.
Radiotherapy (treatment with x-rays that kill cancer cells) may be used either before or after surgery for rectal cancer.
The stage depends on how deep the cancer is in the wall of the colon and how much the cancer has spread to the lymph nodes or other organs. Stage I cancer of the colon means that the tumor is only in the inner layer of your colon and has not spread further through the wall of your colon. Now you want to know what are the complementary & colon cancer alternative treatments available apart the above mentioned common treatment methods for colon cancer cure.
This function may be safe for some people, but not for others just like prescription drugs, and in some dosages may have serious side effects. There are various foundations, support groups and organizations giving a supporting hand for the needful with respect to funds for treatments, moral support, giving suggestions to overcome the disease and much more. They offer you with clear explanations and offer you choices regarding your treatment options and do everything they can to help you reach your goal of adding your name to the list of colon cancer survivors. Although all of their journeys were different, the colon cancer survivors have one thing in common.
The ultimate aim of these survivors is to find a better approach for colon cancer cure either by the common methods or by the colon cancer alternative treatments.
Angiogenesis inhibitors, or antiangiogenic drugs, are designed to target tumor blood vessels and interfere with the tumor blood supply. Antiangiogenic therapy neutralizes growth factor signaling which normally causes new blood vessels to form through the process of angiogenesis.
Anti-EGFR therapy is an additional treatment with antiangiogenic properties that targets the epidermal growth factor receptor (EGFR), a molecule identified on cancer cells that contributes to tumor development and growth, and cancer cell proliferation. Anti-EGFR treatment is ineffective in tumors that carry mutations of the KRAS gene, so it is important to identify KRAS mutation status before considering anti-EGFR therapy.
If you are diagnosed with metastatic colorectal cancer, a number of treatment options are available for you. You will work with your doctor to identify the right dosage and duration of your treatment, so it is important that you stay informed of all the options in order to have a productive discussion with your doctor. SurgerySurgery is standard for Stage I-through-III CRC, where the tumor is considered local. It’s normal to interact with multiple doctors at different stages of treatment for colorectal cancer, including but not limited to medical oncologists, radiation oncologists, and colorectal surgeons. There is a limit to the amount of radiation a body can receive without causing irreversible damage to health tissues.
ChemotherapyChemotherapy (commonly referred to as ‘chemo’) is the treatment of cancer through medicines or drugs that attack and kill cancer cells.111 It differs from surgery and radiation therapy112 in that it is a systemic therapy, which is a treatment that goes throughout the entire body. The development of new chemotherapies has been successful in that a larger percentage of patients are responding to these new therapies.114 There are many different types of chemotherapy drugs, and often, the drugs are used in combination to attack the cancer more aggressively. Table 2 outlines systemic drugs used for colorectal cancer,116 which includes chemotherapy and targeted therapy.
CapeOX+ Bevacizumab is a combination of Oxaliplatin and Capecitabine that is taken orally for 14 days, along with IV infusion of Bevacizumab for 1 day.
FOLFIRI + Ziv-aflibercept is a combination of Irinotecan, Leucovorin, 5-FU and Ziv-aflibercept. Capecitabine + Bevacizumab is a combination of taking Capecitabine orally for 14 days and Bevacizumab IV infusion for 1 day.
Chemotherapy can also be used for neoadjuvant therapy in order to shrink the tumor before surgery, facilitating the procedure, and it can be used after surgery to attack any cancer cells that might remain.
Chemotherapy is accompanied by side effects because, as the drugs kill cancer cells, they can also affect healthy cells. Patients may differ in the type, number and extent of side effects they experience during chemotherapy. 111  “Learning about Chemotherapy Treatment: What is chemotherapy and how does it work?” American Cancer Society. 114  “Learning about Chemotherapy Treatment: What is chemotherapy and how does it work?” American Cancer Society.
Introduction to Targeted TherapiesBeginning in 2004, new treatments were developed called “Targeted Therapies,” which are designed to attack specific cell pathways used by cancers to survive and grow. Tissue around the cancer, known as the tumor microenvironment, can maintain a more normal structure. Together, these new types of therapies represent a revolution in cancer treatment that offers new options and new hope for patients with mCRC. If you have mCRC, the type of targeted cancer therapy you may receive depends on many factors, including the specific targets identified in your tumor.
Targeted cancer therapies are being studied for use alone, in combination with other targeted therapies, or with different forms of chemotherapy to treat mCRC. BevacizumabBevacizumab (Avastin®) is an antibody drug that binds to and neutralizes a protein called VEGF-A.
Bevacizumab was approved in 2004 as first-line therapy for mCRC, based on the results of the randomized, placebo-controlled, double blind clinical trial called AVF 2107. In 2006, bevacizumab was approved for treatment in the second-line setting of mCRC, in combination with FOLFOX chemotherapy, based on the results of the 829 patient clinical trial called E3200. Ziv-afliberceptZiv-aflibercept (Zaltrap®) is a type of targeted drug known as a fusion protein.
The approval of ziv-aflibercept in 2012 was based on the results of a randomized, double-blind, placebo-controlled clinical trial called VELOUR. RegorafenibRegorafenib (Stivarga®), a targeted therapy that comes in pill form, is a tyrosine kinase inhibitor (TKI).
Regorafenib was approved in 2012 based on the results of the randomized, double-blind, placebo-controlled CORRECT trial, which enrolled 760 patients with mCRC previously treated with multiple lines of therapies.
Anti-EGFR TreatmentsThe epidermal growth factor receptor (EGFR) is a molecule identified on cancer cells that contributes to tumor development and growth. There are two anti-EGFR targeted agents approved for mCRC: cetuximab (Erbitux®) and panitumumab (Vectibix®). Cetuximab is a targeted therapy used with chemotherapy for first line treatment of patients who have KRAS mutation-negative (wild-type), EGFR-expressing mCRC.120 It is also used as a single agent in patients who have failed previous chemotherapies. KRAS (pronounced kay-rass) is a gene that helps doctors customize therapy for patients with mCRC.
Side EffectsMost targeted therapies have side effects that are generally milder and better tolerated than chemotherapy.
Because there are many treatment options for mCRC, you and your doctor will work together to select the proper treatment that will give you the most benefit.
There are many ongoing clinical studies to find predictive biomarkers (molecular characteristics of a tumor that can help inform decisions about a patient’s treatment148) that will identify the colorectal patients who will best respond to antiangiogenic therapies.
There are ongoing studies investigating the optimum sequence combinations and duration of the various chemotherapies and targeted treatments. Such developments hold significant promise for providing each patient with the most effective treatment, greatly improving patient outcomes. This site has been determined by HON in Geneva, Switzerland to comply with standards for trustworthy health information. Slideshare uses cookies to improve functionality and performance, and to provide you with relevant advertising. This information represents the views of the doctors and nurses serving on the American Cancer Society's Cancer Information Database Editorial Board. Clipping is a handy way to collect and organize the most important slides from a presentation. Although certain cancers remain difficult to treat and are still associated with early mortality, the 5-year survival rate (considered complete remission) among people of all ages treated for colorectal cancer (CRC) now approximates 62%.1,2 For many patients, CRC and its treatment's aftermath resemble chronic diseases--patients may die with the cancer, rather than from the cancer, or remain cancer-free until death from another cause. When Treatment EndsOnce chemotherapy ends, oncologists generally wait several months before ordering surveillance testing for CRC patients (Table). Late EffectsLate effects (toxicities that are absent or subclinical at the end of therapy but apparent later) and long-term effects (toxicities that start during treatment and continue) are concerns.3,11 Surgery, radiation, and chemotherapy cause several expected adverse effects.
Bowel cramping and intestinal blockage are common; they diminish or resolve for some people, but for others, they become chronic.
Mental Health IssuesWhen oncology treatment ends, CRC patients report a range of feelings--from relief, to numbness, to paralyzingfear. Some people expect to function exactly as they did before their cancer diagnosis and are disappointed if they cannot.
Months to Years LaterUntil about 20 years ago, cancer survivors treated with surgery, chemotherapy, and radiation did not survive longenough to characterize lingering problems.


Radiation therapy has been associated with development of second solid tumors, usually in or very near previously irradiated sites, called radiation ports. End NotePharmacists can expect to see increasing numbers of people with cancer progressing through and remaining inthe health care system. There are three main types of treatment for bowel cancer – surgery, chemotherapy and radiotherapy. Surgery is performed to remove the segment of the large intestine, which contains the cancer.
Chemotherapy, or drug treatment for cancer, is commonly recommended following surgery if the cancer has spread to the adjacent lymph glands. If areas of bowel cancer are visible outside the bowel on x-rays or scans [bowel cancer secondaries or metastases] this is a more serious situation and chemotherapy or monoclonal antibodytherapy are used to control the cancer rather than cure.
Radiotherapy is a powerful X-ray beam, which can also be used to control bowel cancer secondaries and relieve symptoms. There are a combination of treatments given to treat bowel cancer, depending on where the cancer is in your body.
You may wish to have your doctor’s proposed course of action confirmed by another consultant or to explore the possibility of alternative treatments. Talk to your consultant or your GP and explain why you would like another opinion; this can then be arranged if required. Several recent phase III trials reported median overall survival data exceeding 30 months, an achievement inconceivable only 5 years ago.
At present, there are six different classes of drugs (three classes of cytotoxic agents, three classes of biologic agents) available for the treatment of mCRC.
In the VELOUR trial, patients whose disease had progressed within 6 months of receiving oxaliplatin-containing chemotherapy (with or without bevacizumab) were randomly assigned to receive either FOLFIRI with aflibercept or FOLFIRI with placebo.[7] Patients who received aflibercept had a longer median OS and PFS regardless of prior bevacizumab exposure.
A prespecified analysis of a large phase III trial (NO16966) in which bevacizumab was added to an oxaliplatin-based first-line regimen demonstrated that improvements in PFS were much more profound in patients who received treatment until progression than in those who stopped therapy for other reasons.[9] Since the treatment-limiting toxicity of oxali-platin-based first-line therapy is cumulative neurotoxicity, proactive strategies have to be employed to maximize treatment duration for patients who start palliative therapy with FOLFOX + bevacizumab, the most commonly used first-line regimen in the United States.
Unfortunately, thus far, the isolation of predictive markers for anti-VEGF therapy has proven elusive.
Regorafenib is an orally active small-molecule inhibitor of angiogenic, stromal, and oncogenic receptor serine-threonine and tyrosine kinase. Initially, protein expression levels of the drug target, EGFR, were thought to correlate with the efficacy of EGFR antibodies, similar to the findings for trastuzumab in human epidermal growth factor receptor 2 (HER2)-positive breast cancer. In accordance with FDA guidelines, a test for KRAS mutational status needs to be performed before the use of EGFR monoclonal antibodies, since cetuximab and panitumumab are only indicated for mCRC tumors that are KRAS wild-type. However, while mutations in KRAS exon 2 comprise the most commonly seen mutations, there are still subsets of KRAS and other NRAS or RAS family “mutants” that are being missed with current testing. In this trial, 755 patients with chemo-naive mCRC were treated with capecitabine, oxaliplatin, and bevacizumab, and randomly assigned to additionally receive either cetuximab or only the three-drug combination. This is where food is processed to create energy and rid the body of solid waste matter (stool). The small intestine leads to the large intestine (also called the large bowel or colon), a muscular tube about 5 feet long.
Colorectal cancer starts in the inner layer and can grow through some or all of the other layers.
The treatment option selection for colon cancer cure is based on the staging of the disease. The lymph nodes are the small structures in the body that produce and store cells that fight infection. Finally one needs to remember that the safety of herbal medicines in pregnancy is largely unknown. They all reached out to various centers and found what they were looking for in a treatment facility. All material provided on this website is provided for informational or educational purposes only.
Resistance or relapse: Tumors may continue to grow despite treatment, or respond to treatment and then begin to grow again. Antiangiogenic treatments are offered in three lines of therapy to address reoccurrence of the cancer or unresponsiveness. It may be used alone or in combination with other therapies to shrink tumors before surgery or to destroy any remaining cancer cells after chemotherapy.108 Radiation can also be used to reduce tumor size to make a patient more comfortable, even when the cancer cannot be removed. Most chemotherapeutic drugs are taken as a liquid injection into a vein, while others are taken as a pill. This is known as combination therapy, which can also reduce the likelihood that the cancer would become resistant to any single chemotherapeutic drug.115 Combination therapy may use non-chemo drugs such as targeted therapy, which is also a systemic therapy and consists of anti-EGFR and antiangiogenic therapies. Your doctor will work with you in deciding which drug, or combination of drugs, would be best for you depending on the type and stage of your cancer, and whether surgery will be involved.
These new treatments capitalize on advances in our understanding of the molecular basis of cancer and are improving our ability to treat metastatic colorectal cancer. Food and Drug Administration (FDA) began to approve antiangiogenic therapies for the treatment of cancer.
It is effective as first-line treatment for mCRC and is used in combination with chemotherapy.
This trial enrolled more than 800 patients and found that bevacizumab plus chemotherapy improved median overall survival compared to those treated with chemotherapy alone. Bevacizumab was approved in 2013, based on the results of the ML18147 clinical trial which enrolled 820 patients, as a treatment in second-line use in combination with fluoropyrimidine-irinotecan or fluoropyrimidine-oxaliplatin based chemotherapies, depending on prior treatment. This drug is designed to target multiple growth factors involved in cancer and angiogenesis, specifically proteins called VEGF-A, VEGF-B and a related protein called placental growth factor (PlGF).
This trial studied 1226 patients with mCRC whose disease progressed during or within 6 months of receiving chemotherapy or chemotherapy plus bevacizumab.
The results showed a significant improvement in median overall survival among patients treated with regorafenib versus those who received placebo. In about 80% of malignant CRC tumors, EGFR signaling plays a role in the progression of the disease.
Discharged from specialtycare, patients must learn to address health concerns--many of which are related to cancer--in primary practicesettings as "routine" health concerns. In general, treatment's lingering and delayed effects fade in the months following treatment, but certain adverse effects may regress slowly. Platinum-based antineoplastics often cause acute or chronic pain, burning, weakness, or numbness in the hands or feet. Disease recurrence is always possible, even if survival odds are promising; fear of relapse is normal.
Multiagent chemotherapy and combined chemotherapy and radiationhave increased survival and revealed a pattern of late effects.
Environments or genetic aberrationsthat triggered the first tumor may cause a second primary cancer (a tumor distinct from a recurrence or metastasis).
The incidence of radiation-induced tumors begins to rise about 15 yearsafter treatment.17 Certain antineoplastic classes-alkylating agents, anthracyclines, nitrosoureas, steroids, and topoisomerase inhibitors--are also linked to second cancers. They will need to anticipate patients' concerns, both physical and psychological, and askabout lingering and late effects.
Depending on the stage and location of your cancer, you will usually receive one, or a combination of these treatments. At the same time the surgeon removes 10 to 20 lymph glands, which lie close to the cancer in order to examine these under the microscope and determine whether the cancer has started to spread beyond the bowel.
Spread to the lymph glands indicates that there is also a possibility that the cancer may a have spread through the blood system to other parts of the body and chemotherapy is given to help to kill any small but invisible areas of remaining cancer. Not all of the effective systemic therapies are funded by PHARMAC or by insurance companies, often due to their cost. However, radiotherapy is also used as part of the initial, curative treatment for rectal cancer.
The table below is a summary of what they might be, according to your own individual diagnosis.
Most doctors are willing to refer you for a second opinion; however they will be honest if they do not feel you will gain anything from seeing another consultant. The first major step forward in the medical management of mCRC was provided by the addition of irinotecan and oxaliplatin to fluorouracil-based therapy; this increased survival from about 12 months to about 20 months.
The Table provides an overview of all agents that have been approved by the US Food and Drug Administration (FDA) for the treatment of mCRC, and gives the approved indications for the use of each.
The intracellular domain of VEGFR contains catalytic tyrosine kinase domains that, when activated, initiate a signaling cascade that results in endothelial cell survival, proliferation, migration, differentiation, and increased vascular permeability.
Therefore, induction-maintenance approaches that include a limited number of oxaliplatin-containing treatment cycles upfront and maintenance therapy with a fluoropyrimidine-bevacizumab combination can be considered a standard of care. Activation of these pathways will ultimately result in inhibition of apoptosis, as well as in cell differentiation and cell proliferation.
Of 1,183 patients included in this randomization, 93% had been previously evaluated for a KRAS exon 2 mutation, and 40% were found to have tumors with this mutation. They are discussed together here except for the section about treatment, where they are discussed separately.
In order to understand colorectal cancer, it helps to know something about the structure of the digestive system and how it works. The colon absorbs water and nutrients from the food and also serves as a storage place for waste matter. The stage (extent of spread) of a cancer depends to a great degree on how deep the cancer goes into these layers. There are some other, more rare, types of tumors of the colon and rectum, but the facts given here refer only to adenocarcinomas.
Huge numbers of people take herbs and vitamins, but very little is known scientifically about either their effectiveness or their safety.
If a tumor is resistant or relapses after therapy, other subsequent therapies are often effective. For cancer that has metastasized, targeted therapy has been an additional option since 2004.
These treatments work by targeting the growth of abnormal blood vessels that feed tumors and have revolutionized cancer treatment. The drug is also approved as part of second line treatment in combination with chemotherapy.
Ziv-aflibercept is approved for use as treatment in second-line therapy in combination with chemotherapy (FOLFIRI) for mCRC. The study found a significant improvement in median overall survival if patients were treated with ziv-aflibercept combined with the FOLFIRI chemotherapy, compared to those who received chemotherapy alone. The drugs cetuximab and panitumumab are ineffective in tumors that carry mutations of the KRAS gene. 10 Printer-friendly version Compass, a quarterly supplement to OncoLog, discusses cancer types for which no standard treatment exists or more than one standard treatment is available. Many patients find their eyes drier or more watery after treatment and may need supportive care.
Many patients with CRC have a temporary or permanent ostomy, which is rarely welcome.13 These changes can lead to anxiety or depression that is frequently responsive to anxiolytics or antidepressants. Surgery for CRC is tailored to the patient's specific circumstances, and its late effects vary tremendously. This risk is especially pronounced for those with hereditary nonpolyposis colon cancer, the Lynch syndromes, and multiple primary malignant neoplasia.


People with bowel cancer can also receive monoclonal antibody treatments if the bowel cancer has spread to other parts of the body. Most bowel cancers can be removed without the need for a permanent colostomy bag but if the cancer is low in the rectum a colostomy may be required. If areas of bowel cancer are visible outside the bowel on x-rays or scans [bowel cancer secondaries or metastases] this is a more serious situation and chemotherapy or monoclonal antibody therapy are used to control the cancer rather than cure.
You can ask your Oncologist whether these treatments may have any additional benefit in your personal situation.
Cancers in the rectum can spread in small quantities to the walls of the pelvis and radiotherapy is given to the pelvic area to kill any areas of cancer that have spread to the pelvis. It is important that you recognise that this process may take time and may delay starting your treatment. The introduction of biologic agents such as vascular endothelial growth factor inhibitors and epidermal groTawth factor inhibitors further increased survival—to more than 2 years in prospective trials. The approved conventional cytotoxic agents fall into three classes: fluoropyrimidines (fluorouracil [5-FU] and the oral fluoropyrimidine analogue capecitabine), topoisomerase I inhibitors (irinotecan), and platinum-containing compounds (oxaliplatin).
Bevacizumab is a humanized monoclonal antibody that binds to VEGF-A, preventing VEGF-A from binding to its target receptor.
The PFS curve demonstrates that about 50% of patients enrolled in CORRECT did not derive benefit from regorafenib. Both of the monoclonal antibodies against EGFR—cetuximab, a chimeric IgG1 antibody, and panitumumab, a fully human IgG2 antibody—have single-agent efficacy in advanced colorectal cancer. As part of this study, an expanded RAS mutation status was determined in 1,060 of the 1,183 patients in the study (Figure 2). The waste matter (stool) moves from the colon into the rectum, the last 6 inches of the digestive system.
We now know that most of these cancers begin as a polyp--a growth of tissue that starts in the lining and grows into the center of the colon or rectum. Initially, antiangiogenic therapies targeted the specific proteins vascular endothelial growth factor (VEGF), but now the latest therapies target multiple growth factors and pathways.
Patients receive bevacizumab as an intravenous infusion every two weeks and can be scheduled on the same day that chemotherapy is given.
Patients typically receive ziv-aflibercept every two weeks through an intravenous infusion with chemotherapy. Anti-EGFR treatment targets this receptor to interrupt its signaling and, thus, hinder tumor development. Roughly 40% of colorectal cancers have KRAS mutations while the non-mutated KRAS gene (also known as “wild type”) is found in the remaining 60%. Our goal is to help readers better understand the nuances of management for such diseases and the variables that MD Anderson specialists consider when counseling patients about treatment alternatives. Support groups can be very helpful.14,15 If insomnia, nightmares, or fear interferes with activities of daily living, referral to a counselor who specializes in cancer survivorship is warranted. Recently, an expanding array of molecular prognostic and predictive biomarkers have been developed that are being integrated into clinical practice. At this point in time, however, no predictive biomarker exists to identify patients who might benefit from this novel multikinase inhibitor. This finding suggests that the use of EGFR inhibitors is not only ineffective in patients with KRAS-mutated mCRC, but may also be potentially harmful. Of the 1,060 patients, 48% were identified as having wild-type RAS (no KRAS or NRAS mutations in exons 2, 3, or 4). Of the 620 patients who were originally classified as not having a mutation in KRAS (exon 2), 17% had mutations in other RAS exons. Today, there are three types of antiangiogenic therapies for treating metastatic colorectal cancer—antibody, fusion protein, and tyrosine kinase inhibitor—that are available in three lines of therapy.
Patients may continue bevacizumab even after stopping chemotherapy, as long as the disease is controlled and side effects are manageable.
Treatment continues as long as the disease does not progress and side effects are manageable. Identifying KRAS mutation status avoids unnecessary expenses and toxicities from anti-EGFR inhibitors, which are ineffective in KRAS mutated colorectal cancers.
Occasionally, these tests reveal suspicious hepatic or pulmonary lesions, especially the latter if the patient had radiation. Fatigue, a serious problem of unclear etiologyfor many patients, may persist for years after treatment. In this review we discuss the current treatment options in metastatic colon cancer, with a special focus on biologic agents and how molecular understanding guides treatment decisions. Single-agent panitumumab showed benefit compared with BSC in a large, international phase III trial in an extensively pretreated population, demonstrating significant improvement in PFS.[23] OS was not increased, presumably because 75% of patients crossed over from BSC to the panitumumab arm. In this subgroup of patients, PFS and OS in the primary and exploratory analysis were decreased in the panitumamab + FOLFOX4 group compared with the FOLFOX4 group. There is agreement that surgery alone is adequate for American Joint Committee on Cancer stage I disease, in which the tumor is confined within the submucosa or muscularis propria, and that additional therapy is needed for stage III disease, which by definition has invaded regional lymph nodes. Based on these data, panitumumab was approved as a single-agent salvage therapy option in the United States in 2006.
Of note, previously specified mutations in KRAS and NRAS at codon 59 were identified in seven patients, and exclusion of these mutated alleles slightly improved PFS and OS. Resolution of alopecia (a condition often considered minor by clinicians but terribly traumatic to many patients) usually resolves in stages. The findings in this study demonstrate that RAS mutations as well as KRAS exon 2 mutations predict a lack of response to EGFR inhibitors in patients with mCRC.
Current standard guidelines give clinicians the options of adjuvant chemotherapy or observation only following surgery for this intermediate category of disease, which represents a quarter of all cases of colon cancer. Initial hair may be a different color, a different texture, thicker, thinner, curlier, or straighter than pretreatment hair, but eventually it returns to normal. Radiotherapy to the pelvis for rectal cancer may cause permanent pubic or perineal alopecia.
In fact, the use of EGFR antibodies in the patient population with RAS mutations not identified with standard KRAS exon 2 analysis might be associated with a detrimental effect on patient outcomes.
Because chemotherapy itself is not without risk and adjuvant therapy typically requires 6 months of treatment, physicians wish to avoid giving adjuvant chemotherapy to patients who would derive no significant benefit from it.
However, trials of adjuvant therapies large enough to produce significant results have seldom focused specifically on patients with stage II disease. The majority of these phase III trials compared observation following surgery to adjuvant 5-FU (the longtime standard) and often included patients with stage III disease. Kopetz, although several statistically underpowered studies have not shown significant evidence of prolonged survival with adjuvant chemotherapy for patients with stage II colon cancer, a reduced risk of recurrence was seen retrospectively in the MOSAIC trial of adjuvant FOLFOX therapy for patients with high-risk stage II disease.
Indeed, expert panels from both the National Cooperative Cancer Network and the American Society of Clinical Oncology have recommended that adjuvant therapy for stage II disease be considered and discussed with patients. Both panels strongly recommended that such treatment be given within clinical trials, when possible.
For stage II colon cancer, several well-known pathological and clinical factors are associated with a higher risk of recurrence.
Tumors are classified as high-frequency MSI (MSI-H) if two or more markers are unstable, low-frequency MSI (MSI-L) if only one is unstable, and microsatellite stable (MSS) if no instability is found in any of the five markers. Immunohistochemistry is now routinely performed to check for loss of key components of the DNA mismatch repair mechanism, which can also indicate the presence of an MSI-H phenotype. Although only about 15% of colon cancer patients are found to have MSI-H tumors, it is important to identify these patients because they have a better overall prognosis regardless of stage. Prior trials indicated that patients with MSI-H tumors do not benefit from single-agent 5-FU. In fact, an updated pooled analysis of several studies showed that patients with MSI-H stage II tumors who received adjuvant 5-FU actually fared worse in both disease-free and overall survival compared with those who received no adjuvant therapy. Eng pointed out that these results apply only to single-agent 5-FU; the role of FOLFOX in patients with MSI-H is currently unknown. By definition, stage II colon cancers are T3 or T4, and T4 tumors are associated with an increased risk of recurrence.
T4 tumors are those that extend into adjacent structures (T4a) and those that perforate into the visceral peritoneum (T4b). Gross perforation is associated with substantial morbidity and even death from the immediate event, as well as a high risk of colon cancer recurrence; but microperforations noted pathologically are also associated with poor outcomes. Eng said that 16 of 17 studies included in a recent systematic review found that increased survival in patients with stage II colon cancer was associated with increased numbers of lymph nodes evaluated.
One study found that 8-year overall survival increased from 56% when 10 or fewer nodes were sampled to 90% when more than 40 nodes were evaluated.
Current guidelines from the American Society of Clinical Oncology, American College of Surgeons, and National Quality Forum recommend examination of at least 12 lymph nodes to achieve proper evaluation—examination of fewer nodes constitutes a risk factor for recurrence, even when the nodes examined are negative. For two patients with identical tumor characteristics, the treatment decision might differ for the patient in otherwise good health and the one who has significant comorbidities because each patient’s tolerance for chemotherapy must be considered. The latter combination proved superior and has been the standard adjuvant treatment for stage III colon cancer since 1998. FOLFOX was accepted as an approved standard adjuvant therapy regimen for stage III colon cancer after showing a dramatic (23%) reduction in the risk of recurrence and an improvement in the 6-year overall survival rate. Capecitabine, an oral prodrug of 5-FU, has been shown to be equivalent to intravenous bolus 5-FU in treating stage III colon cancer.
The effects of 5-FU are well documented—in general, 5-FU therapy is well tolerated, although return to baseline quality of life can take as much as a year after the end of therapy, according to one study. Oxaliplatin is associated with increased toxicity and increased potential for unremitting neurotoxicity that will last for several weeks to months following discontinuation of the drug. Oxaliplatin would therefore not be appropriate for patients with baseline neuropathy and would be considered more cautiously for patients whose tolerance for chemotherapy is in question.
The longterm effects are the same, but during treatment, side effects are more pronounced and concentrated within the few days following infusion of 5-FU. If the patient’s tumor were MSI-H, the choice would be doubly clear, as MSI-H not only confers a better prognosis but also is known to reduce the response to the least toxic chemotherapy. But in cancer care, the ideal and the clear-cut are seldom the reality, and most patients present with a combination of prognostic factors that must be assessed to determine the risk-benefit ratio for the individual.
Kopetz said, “Occasionally, patients with MSI-H, and therefore a good prognosis, present with other pathological features consistent with high risk, such as perforation and a very low number of retrieved lymph nodes. For example, two patients might have a potential 30% risk reduction, but if one person’s initial risk is 50%, the reduction by 30% results in an absolute reduction of about 15%. But a person whose initial risk is only 10% would derive an absolute reduction of only about 3%,” he explained. Although several gene profile tests are in development and one, OncoType DX Colon, has been approved by the U.S. Kopetz said these tests have prognostic value but are not predictive of which patients are most likely to benefit from chemotherapy. It is the first clinical trial to stratify patients with stage II colon cancer as having low or high risk of recurrence depending on their molecular marker analysis.
Participants are considered to have a high risk of recurrence if their tumors are MSS or MSI-L with loss of heterozygosity at chromosome 18q (LOH 18q, indicated as a risk factor for recurrence in prior studies in patients with stage III colon cancer).



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