Carcinoembryonic antigen (CEA) is a blood biomarker that can signify several different types of cancer, including colorectal, thyroid, and breast cancers. Freedman and Gold discovered CEA first in colon cancer cells, but it was later found in the stomach, tongue, oesophagus, cervix, and prostate epithelial cells. Fetal oncogenes help control the production of a 200 kDa glycoprotein, usually made by the fetus’ embryonic endodermal epithelium, which is found in the fetal body. CEA is generally removed from the bloodstream after birth, but a small amount of it may stay in the colon tissue. The CEA gene family is on chromosome 19q13.2. It has 29 genes, but only 18 of them are usually active. Table 1 shows that high serum CEA is linked to a wide range of both malignant and nonmalignant medical problems, so it can’t be used as a sure way to tell if you have cancer. As a result, routine screening or diagnosis of malignancies with this test alone is not advised. Right now, CEA cell is being studied as a cancer treatment target. The paper will look at CEA cells as they significantly impact cancer prevention.
Review of the Literature
MedlinePlus states that CEA cells are carcinoembryonic antigen cells. These cells make up most of the proteins in a baby’s body. After birth, the number of cells decreases, or they all die. Adults with more CEA cells may be more likely to get cancer, but this isn’t a sure thing (MedlinePlus). Because CEA cells are tumors that are linked to certain types of cancer, this is why it’s essential to know about them. CEA cell is now being studied as a cancer potential treatment. The article will look into the role of CEA cells in cancer prevention. Most people now know how to use the CEA cells to look for other diseases. Unfortunately, unlike other cancer websites, this one doesn’t consider factors that aren’t related to genetics.
Gou et al. claim that the transcription factor NF-B has a high activity level in cancer cells. Toxicology-limiting toxicity due to a lack of selectivity for malignant cells is a severe problem for cancer treatment. One of the most significant drawbacks of gene-directed enzyme prodrug treatment (GDEPT) is the lack of cancer-specific promoters that can be used to enhance the therapeutic index of anticancer medicines (Gou 747). Normal epithelial cells don’t express carcinoembryonic antigen (CEA), but cancerous epithelial cells express it. Within 300 bp of the start of the CEA translation process, four cis-acting DNA-binding elements are needed for particular CEA transcription. Using an adenovirus vector with the CEA promoter can make it easier for 5-DFCR/5-FU conversion to be selective in cancerous tissues that have CEA (Gou 752).
Because CEA has a transcriptional activity 10- to 300-fold lower than that of CMV and RSV virus genes in most cancer cell lines, it doesn’t have as much power as those viral genes to make cells grow. There are very few anti-tumor effects when adenoviruses are used to deliver the CEA promoter-driven suicide gene into the body. If you want to give your genes a little extra boost, you might consider using a 2.1-kilo CEA enhancer (Gou 753). In cells that don’t have a lot of CEA, this prodrug strategy based on a CEA enhancer-promoter can’t get enough CD activity. Using CEA promoter-based gene therapy in vivo and in clinical trials is problematic because it doesn’t work well. This is true for other cancer-specific promoters, too. As Guo et al. write in their paper, cells that make enzymes guided by genes might use the DNA-binding site of NF-B as a “cancer promoter.”
According to Gonzalez-Exposito, T cells that detect MHC molecules on target cells as non-self can hinder allogeneic systems. Autologous systems are more sensitive and specific than non-autologous systems due to lower background killing activity. For comparison, we ran our tests on cancer cells alone and in combination with T cells but without antibodies as a control (Gonzalez-Exposito). The tiny number of experiments in which alloreactivity inhibited the proliferation of cancer cells could be identified and eliminated because of this. When autologous T cells are scarce, allogeneic T cells can be used in PDO co-culture models. People taking part in clinical trials can speed up the process of finding immuno-oncology candidate resistance mechanisms by using PDO T cell co-culture systems (Gonzalez-Exposito). Pre-clinical drug development must use PDOs because they can represent intra-tumor heterogeneity. They can be created from tumors that match the stage and treatment history of patients who are testing new medications.
In contrast to cell lines, CEA expression in PDO populations is usually diverse, yielding the most extreme bimodal CEA expression patterns (Gonzalez-Exposito). As a result, it has been shown that CRC cells can transition between high and low CEA levels. In vitro results show that all four of the eight PDOs with heterogeneous CEA expression profiles are incredibly and somehow partially resistant to Cibisatamab therapy. This means that immunotherapies that target CEA could benefit from the findings, as explained by Gonzalez-Exposito.
According to Chau, unique molecular subgroups in gastrointestinal malignancies have been found by applying modern integrative genomic technology. A better clinical outcome is achievable by finding special genetic groups and highlighting the different types of cancers affecting other body parts (Chau). Many things could affect the development of combination therapy, including immunotherapy, such as the tumors’ molecular properties and the interactions between tumors and their surroundings. Current research focuses on immune checkpoint blockade to successfully integrate these new drugs into GI cancer therapy paradigms. This demands an in-depth understanding of the unique immune milieu in these tumors (Chau). An observed high mortality ratio -to-incidence ratio is related to gastrointestinal (GI) tract cancers (Chau). More than 2,894,000 people die each year from oesophagus, gastric, pancreas, liver, and colorectal malignancies.
A particular success has been reached with cytotoxic chemotherapy for metastatic oesophagal, gastric, and colorectal malignancies, despite numerous incremental improvements in survival. The use of cutting-edge, integrative genomics has led to the discovery of the subtypes of Separate molecular subtypes. Identifying unique genetic subgroups and highlighting the heterogeneity in cancers of each primary anatomical site may improve clinical outcomes (Chau). Furthermore, tumors’ molecular characteristics and how they interact with their microenvironment may influence the development of therapeutic strategies. Immunotherapy is among the therapeutic approach that may be affected.
Furthermore, tumor molecular characteristics and interactions with the tumor microenvironment may have impacts. This may impact the development of combination treatments, such as immunotherapy. In CRC PDOs from metastatic CRCs that are resistant to treatment, there is a lot of CEA expression heterogeneity. This makes Cibisatamab less effective in vitro. People who took part in clinical trials should look at their samples to see if CEA expression heterogeneity has links to Cibisatamab resistance. It is possible to raise CEA expression by blocking the WNT/-catenin pathway, suggesting the potential for combination therapies to improve the clinical efficacy of Cibisatamab sensitivity activity.
CEA Test: MedlinePlus Medical Test; Available at; https://medlineplus.gov/lab-tests/cea-test.\
Chau I. Clinical development of PD-1/PD-L1 immunotherapy for gastrointestinal cancers: facts and hopes. Available at; Clin Cancer Res. 2017; 23(20):6002–11
Gonzalez-Exposito, R., Semiannikova, M., Griffiths, B. et al. CEA expression heterogeneity and plasticity confer resistance to the CEA-targeting bispecific immunotherapy antibody Cibisatamab (CEA-TCB) in patient-derived colorectal cancer organoids. . Immunotherapy cancer 7, 101 (2019).
Guo, X., Evans, T., Somanath, S. et al. In vitro evaluation of cancer-specific NF-κB-CEA enhancer-promoter system for 5-fluorouracil prodrug gene therapy in colon cancer cell lines. Br J Cancer 97, 745–754 (2007). Available at; https://doi.org/10.1038/sj.bjc.6603930