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CEA (Carcinoembryonic Antigen): 
Its Role as a Marker in the Management of Cancer

National Institutes of Health
Consensus Development Conference Statement
September 29-October 1, 1980

Conference artwork, a number of grey and white discs on a black background with a red geometric shape in the middle.

This statement is more than five years old and is provided solely for historical purposes. Due to the cumulative nature of medical research, new knowledge has inevitably accumulated in this subject area in the time since the statement was initially prepared. Thus some of the material is likely to be out of date, and at worst simply wrong. For reliable, current information on this and other health topics, we recommend consulting the National Institutes of Health's MedlinePlus

This statement was originally published as: CEA (Carcinoembryonic Antigen): Its Role as a Marker in the Management of Cancer. NIH Consens Statement 1980 Sep 29-Oct 1; 3(7):1-4.

For making bibliographic reference to the statement in the electronic form displayed here, it is recommended that the following format be used: CEA (Carcinoembryonic Antigen): Its Role as a Marker in the Management of Cancer. NIH Consens Statement Online 1980 Sep 29-Oct 1 [cited year month day]; 3(7):1-4.


A Consensus Development Conference was held at the National Institutes of Health on September 29 - October 1, 1980, to address issues concerning the role of the carcinoembryonic antigen (CEA) as a marker in the management of cancer.

At NIH, Consensus Development Conferences bring together biomedical research scientists, practicing physicians, consumers, and others with special interest or knowledge, in an effort to reach general agreement on the scientific evaluation of a medical technology. That technology may be a drug, device, or laboratory, medical, or surgical procedure.

For this Consensus Conference, the members of the Panel were limited to biomedical and clinical investigators actively working in the field, clinically involved in patient care, and familiar with the technology under assessment. The Panel met following formal presentations and discussions to assess the issues based on the evidence presented. This summary is the result of the Panel's deliberations.

Human neoplasms may produce and release into the circulation a variety of substances collectively referred to as tumor markers. The oncofetal antigens comprise one particular group of markers, of which the carcinoembryonic antigen (CEA) has been the most widely studied.

CEA is a glycoprotein of about 200,000 molecular size. It is expressed in significant amounts during embryonic life, especially by the large intestine, and postnatally by carcinomas arising from this site. CEA can be released by these tumors into the circulation to cause raised levels which may be measured by sensitive radioimmunoassay and related techniques. Such methods have, however, demonstrated that small amounts of CEA are also present in the normal adult large intestine and in the circulation of healthy subjects.

Subsequent investigations have revealed that many epithelial-derived tumors at other sites may also express CEA and be associated with elevated circulating blood levels. Thus, it may be that the assay of plasma CEA has protean applications in oncology.

The Consensus Development Panel and members of the audience considered evidence to address the following questions:

  1. Should CEA be used in cancer screening?
  2. Is CEA helpful in cancer diagnosis?
  3. What does CEA tell about the extent and outcome of cancer?
  4. Is CEA helpful in monitoring cancer treatment?

Plasma CEA Levels in Health and Disease

Using the presently available radioimmunoassay, 2.5 ng/ml is stated to be the upper limit of normal for plasma CEA levels. Values in excess of 2.5 ng/ml may be found in association with cancers, in particular those of the gastrointestinal tract, pancreas, ovary, lung, and breast. Similarly raised CEA levels may, however, be detected in cigarette smokers, in patients with benign neoplasms, and in 15 to 20 percent of subjects with inflammatory disorders such as ulcerative colitis, Crohn's disease, pancreatitis, liver disease, and pulmonary infections. Thus, raised plasma CEA values are not specific for cancer, although very high levels (for example, above 20 ng/ml) are highly suggestive of malignancy. It is important that serial assays of CEA be used in reaching a clinical judgement, and not any single determination. The panel believes that each laboratory performing CEA assays should establish its own "normal" range. The recommended upper level of "normal" (2.5 ng/ml) in the population requires additional evaluation. Values cited in this document are based on the only radioimmunoassy commercially available at the time of the conference, the Hoffman-La Roche assay. Other assay systems may give different results.  

Conclusions and Recommendations

After listening to and discussing the evidence, the Panel reached the following conclusions:

Should CEA Be Used in Cancer Screening?

As indicated above, studies to date have revealed a major overlap in the distribution of plasma CEA values in subjects with inflammatory diseases and benign and malignant tumors of the gastrointestinal tract and of other sites, including breast, bronchus, urothelium, ovary, uterus, and cervix. Therefore, the plasma CEA assay does not possess the sensitivity (true-positive rate) or the specificity (true-negative rate) required to discriminate between localized malignant tumors and benign disorders.

Consequently, these data, together with the fact that raised CEA levels occur in smokers, vitiate the use of plasma CEA assays in the screening of an asymptomatic population to detect neoplastic disease. The use of CEA to assist with the surveillance of so-called high-risk groups, in whom CEA-producing tumors may develop, remains to be established.  

Is CEA Helpful in Cancer Diagnosis?

Few prospective studies have been effected with the aim of determining whether the availability to clinicians of a plasma CEA result would help in confirming a suspected malignancy in symptomatic patients. In addition, the caveats with respect to cancer specificity which limit the CEA test's applicability for screening (namely, that raised levels occur with smoking, non-neoplastic diseases, and benign tumors) are also pertinent with respect to assisting in reaching a diagnosis in a symptomatic population.

Therefore, we cannot recommend, based on the presently available data, that CEA be used independently to establish a diagnosis of cancer. However, in a patient with symptoms, a grossly elevated value, greater than 5-10 times the upper limit of the reference normal range for that particular laboratory, should be considered strongly suggestive for the presence of cancer in the particular patient. In this situation further diagnostic efforts to establish the presence or absence of cancer are indicated.  

What Does CEA Tell About the Extent and Outcome of Cancer?

Many workers have shown that preoperative plasma CEA levels correlate with the clinical stage of disease in several tumor types. Patients with colorectal, or possibly, bronchial carcinomas whose preoperative CEA levels are at the lower end of the spectrum have better survival rates than patients whose levels are in excess of 10 ng/ml.

It should be remembered, moreover, that the correlation between increasing plasma CEA levels and progressive cancer is not always perfect and that a normal CEA cannot be taken as evidence of localized disease or remission. About 15 to 20 percent of patients with proved malignancies never have elevated plasma levels. Such false negatives may be related to the degree of tumor differentiation. Poorly differentiated colorectal carcinomas, for example, tend to be associated with a reduced proclivity for CEA expression and release.

On the basis of the available data, we recommend that a preoperative plasma CEA value be obtained in patients with either colorectal or bronchial carcinomas and be used as an adjunct to clinical and pathological staging methods.  

Is CEA Helpful in Monitoring Cancer Treatment?

The regular and sequential assay of plasma CEA is the best presently available noninvasive technique for postoperative surveillance of patients to detect disseminated recurrence of colorectal cancer. As a monitor of colorectal cancer, CEA has been found to be elevated when residual disease is present or is clinically progressing. Following complete surgical removal of a colorectal malignancy, an elevated plasma CEA value should usually return to a normal value by 6 weeks. The failure to observe a reduction of a previously elevated preoperative CEA titer strongly indicates the presence of residual tumor. It is also possible to demonstrate in a substantial number of patients that CEA becomes significantly elevated before metastatic disease can be detected by clinical or other diagnostic measures. This information can be achieved by obtaining plasma samples for CEA assay preoperatively, 4 to 6 weeks postoperatively, and thereafter at regular intervals as an integral component of overall patient followup. While slowly rising levels may be more indicative of local recurrence, rapidly rising values reaching very high levels, usually in excess of 20 ng/ml, are found most often with hepatic and osseous metastases.

For patients with metastatic tumor, the CEA assay may complement standard clinical measurements of tumor response to therapy. However, as in the case of other clinical laboratory tests, there are examples of discordance between the observed change in tumor mass and the corresponding CEA values. In patients with advanced unmeasurable tumor, especially colorectal carcinoma, CEA assays may offer the only index to measure changes in tumor burden. Although definite criteria to aid in deciding whether to continue or alter therapy in patients with unmeasurable tumor, based on serial CEA determinations, are not established, it appears that a steadily, markedly rising titer is indicative of a poor therapeutic response. In such circumstances, each physician should make an individual decision whether CEA monitoring will be of clinical value in the management of a particular patient.

It is important to remember that raised values, due to various causes such as smoking, intercurrent infection, etc., can be seen in patients where the tumor is clinically stable and that decreasing CEA values are not invariably a sign of successful therapy. Furthermore, a proportion of patients with recurrent or advanced colorectal cancer may not show elevated plasma CEA values.

The role of CEA in the postoperative and therapeutic monitoring of patients with other types of cancer, such as pancreatic, gastric, and gynecological neoplasms, is less convincing than it is for colorectal cancer. In patients with metastatic breast cancer or lung cancer, especially small cell carcinoma, and significant CEA elevations, changes in CEA titers may be of value in reflecting response to chemotherapy. More studies are required to evaluate the role of CEA determinations for initiating or changing therapy in tumor types other than colorectal cancer.

The Panel would like to stress the view that the clinical utility of a tumor marker may be related to the efficacy of a therapeutic regimen. Where earlier recognition of disease progression is not accompanied by appropriate therapy, no benefit is gained. On the other hand, as more successful treatments for the major tumor types become available, CEA and other tumor markers will be more useful in the management of cancer.

Additional Needs

The Panel has identified several areas for future study which should improve the clinical utility of the CEA assay: the improvement of assay methodology; the evaluation of monoclonal antibodies to CEA for improving assay specificity; the establishment of a laboratory quality control system using a CEA standard preparation; the clinical study of CEA in combination with other markers; the diagnostic role of CEA in biological fluids other than plasma; the individual and collective comparison of CEA with other specific diagnostic modalities; the estimation of tumor CEA content in relation to plasma CEA values; and the study of the pathophysiology and metabolism of CEA.

This Consensus Conference on CEA (Carcinoembryonic Antigen): Its Role as a Marker in the Management of Cancer was sponsored by the National Cancer Institute, assisted by the Office of Medical Applications of Research, Office of the Director, NIH.  

Consensus Development Panel

David M. Goldenberg, Sc.D., M.D.
(Panel Chairman)
University of Kentucky Medical Center
Lexington, Kentucky
A. Munro Neville, M.D., Ph.D.
(Panel Rapporteur)
Ludwig Institute for Cancer Research
Sutton, Surrey
Anne C. Carter, M.D.
State University of New York School of Medicine
Downstate Medical Center
Brooklyn, New York
Vay Liang W. Go, M.D.
Mayo Clinic
Rochester, Minnesota
Edward Douglas Holyoke, M.D.
Roswell Park Memorial Institute
Department of Health
State of New York
Buffalo, New York
Kurt J. Isselbacher, M.D.
Massachusetts General Hospital
Harvard Medical School
Boston, Massachusetts
Philip S. Schein, M.D.
Vincent T. Lombardi Cancer Research Center
Georgetown University Medical Center
Washington, D.C.
Morton Schwartz, Ph.D.
Memorial Sloan-Kettering Cancer Center
New York, New York


Dr. Muhyi Al-Sarraf
Associate Professor in Oncology
Wayne State University School of Medicine
Detroit, Michigan
Dr. T. Ming Chu
Director of Cancer Research
Roswell Park Memorial Institute
Buffalo, New York
Dr. Milton Dalbow
Division of Radiation Oncology
Allegheny General Hospital
Pittsburgh, Pennsylvania
Dr. Thomas S. Edgington
Department of Molecular Immunology
Scripps Clinic and Research Foundation
La Jolla, California
Dr. James T. Evans
Department of Surgery
Erie County Medical Center
Buffalo, New York
Dr. Herbert Fritsche
Laboratory of Medicine
M.D. Anderson Hospital and Tumor Institute
Houston, Texas
Dr. Phil Gold
Director, Division of Clinical Immunology
Montreal General Hospital
Montreal, Quebec
Dr. Darrow Haagensen
Mallory Institute of Pathology Foundation
Boston, Massachusetts
Dr. Hans J. Hansen
Director, Department of Immunology
Head, Cancer Diagnostic Research Laboratory
Hoffmann-LaRoche Inc.
Nutley, New Jersey
Dr. Ronald B. Herberman
National Cancer Institute
National Institutes of Health
Bethesda, Maryland
Dr. Jakob Lokich
Cancer Research Institute
New England Deaconess Hospital
Boston, Massachusetts
Dr. Henry Lynch
Professor and Chairman
Department of Preventive Medicine
Creighton University School of Medicine
Omaha, Nebraska
Dr. Aaron Malkin
Sunnybrook Medical Center
Department of Biochemistry
Toronto, Ontario
Dr. Edward Martin
Ohio State University
College of Medicine
University Hospital
Columbus, Ohio
Dr. K. Robert McIntire
Chief, Diagnosis Branch
Division of Cancer Biology and Diagnosis
National Cancer Institute
National Institutes of Health
Bethesda, Maryland
Dr. A. R. Moossa
Professor of Surgery
University of Chicago
Chicago, Illinois
Dr. Michael O'Connell
Department of Medical Oncology,
Mayo Clinic
Rochester, Minnesota
Dr. Michael Perkel
Emory University Clinic
Atlanta, Georgia
Dr. Gustavo Reynoso
Chief of Pathology
Charles S. Wilson Hospital
Johnson City, New York
Dr. Morton Schwartz
Memorial Sloan-Kettering Institute
New York, New York
Dr. Markku Seppala
Professor of Obstetrics and Gynecology
Department of Obstetrics and Gynecology
University Central Hospital
Dr. H. J. Staab
Friedrich-Miescher Laboratory
Max Planck Institute
Dr. Paul Sugarbaker
National Cancer Institute
National Institutes of Health
Bethesda, Maryland
Dr. Charles Todd
Chairman, Division of Immunology
City of Hope Medical Center
Duarte, California
Dr. Joseph T. Tomita
Head, Cancer Research Laboratory
Abbott Laboratories
North Chicago, Illinois
Dr. John R. Van Nagell, Jr.
Director, Gynecology Oncology Department
University of Kentucky
University Hospital
Lexington, Kentucky
Dr. Ronald Vincent
Department of Thoracic Surgery
Roswell Park Memorial Institute
Buffalo, New York
Dr. Harry Wanebo
Department of Surgery
University of Virginia Medical Center
Charlottesville, Virginia
Dr. Noel Warner
Immunobiology Laboratory
Departments of Pathology and Medicine
University of New Mexico School of Medicine
Albuquerque, New Mexico
Dr. Samuel A. Wells, Jr.
Director of Clinical Research
Duke University Medical Center
Durham, North Carolina
Dr. Norman Zamcheck
Gastrointestinal Research Laboratory
Mallory Institute of Pathology Foundation
Boston City Hospital
Boston, Massachusetts

Conference Organizers

K. Robert McIntire, M.D.
National Cancer Institute
Bethesda, Maryland
Louis P. Greenberg, M.S.
National Cancer Institute
Bethesda, Maryland

Conference Sponsors

National Cancer Institute

Office of Medical Applications of Research

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