Updated June 3, 2019

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MYC genes are often associated with cancer and the growth of cancerous tumors, most specifically the c-MYC gene, which is also commonly referred to as MYCC. In fact, mutated c-MYC genes are overexpressed in at least 40% of tumors and the majority of human cancers 1.

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What Is MYC?

MYC is a family of regulator genes and proto-oncogenes that consist of three human genes: c-MYC, l-MYC, and n-MYC.

The official MYC medical term is MYC proto-oncogene, bHLH transcription factor, and MYC gene abbreviation is simply MYC.

The c-MYC gene was the first of these genes to be discovered, and because of that, it’s often referred to simply as the MYC gene. It’s also known as MRTL, MYCC, and bHLHe39.

MYC genes are classified as protein-coding genes. This means they are genes that translate the genetic code in your body that specifies the correspondence between codons and amino acids.

MYC genes specifically control various aspects of cell growth in your body and regulate your cellular metabolism.

They are considered proto-oncogenes, which are normal genes that have the potential of becoming oncogenes due to gene mutations or increased expression.

Oncogenes are genes with the potential to cause cancer. They are often found in tumor cells, where they are typically mutated or expressed at high levels.

While mutated MYC genes aren’t present in all forms of human cancer, they are present in many forms. Typically, mutated MYC genes, most commonly a mutation of the c-MYC gene, are found in forms of lymphoma, breast cancer, melanoma, and leukemia.

Is MYC a Tumor Suppressor Gene?

The MYC gene isn’t a tumor suppressor, but it works to control one. The c-MYC gene is considered a “master regulator” because it controls many aspects of both cellular growth regulation and cellular metabolism.

Regulating these things are extremely important because when cellular growth isn’t controlled, cancer cells can develop and spread quickly.

In normal cells, the c-MYC gene activates the PTEN tumor suppressor, which helps prevent cancerous tumors from growing in the body. But an MYC gene mutation speeds up cell growth and metabolism and suppresses PTEN activity, which often leads to cancer.

Basically, the loss of tumor suppressors and the activation of oncogenes is what drives growth in cancerous tumors 2.

The Structure of MYC

All MYC-family genes are protein products containing basic helix-loop-helix (bHLH) and leucine zipper (LZ) structural motifs.

Each of these motifs has specific functions. The bHLH works to bind MYC proteins to your DNA, and the LZ motif reacts with the bHLH to create factor MAX, a gene that encodes the MAX transcription factor, which helps regulate cell expression.

When the MYC genes aren’t working properly, your body’s cell growth speeds up, which can cause some types of cancer to form and spread.

MYC-Related Proteins

Your MYC genes are considered protein-coding genes. They encode nuclear phosphoproteins, called myc1 and myc2, that play a role in your body’s cell cycle progression, apoptosis, and cellular transformation.

Myc1 and myc2 are considered MYC isoforms because these proteins have a similar, but not identical amino acid sequence. However, when it comes to the MYC gene, Uniprot, which is known in the scientific community as a comprehensive, high-quality protein sequence resource, shows eight more potential isoforms in the MYC gene.

Once the MYC genes encode these proteins, the protein merges with the factor MAX transcription, forming a heterodimer that binds to your E box DNA consensus sequence to regulate the way several targeted genes work together.

Abnormal c-MYC genes don’t encode the nuclear phosphoprotein properly, which in turn, increases your body’s cell expression. When your body’s cells grow rapidly, without any regulation, cancer cells can form.

Cancer feeds off of the growth of normal cells. So as your body continues to increase cell production, the cancer can spread or tumors can grow.

The Role of MYC

Your MYC genes are multifunctional transcription factors that drive several different synthetic functions necessary for rapid cell division.

At the same time, the MYC genes inhibit the expression of genes that allow rapid, unnecessary cell growth, specifically in regards to tumors. Basically, while promoting cell growth and regulating cellular metabolism, the MYC genes regulate several gene families that contribute to producing abnormal cell growth.

Scientists have also been researching the role MYC genes play in the production of induced pluripotent stem cells (iPSCs) since the discovery that mature cells can be reprogrammed to become pluripotent, which means they give rise to all the cells in the body. Eventually, MYC could play a major role in producing iPSCs to use in the field of regenerative medicine.

These iPSCs could represent a single source of cells used to replace those lost to damage or disease, including cells in the heart, liver, and pancreas. Unfortunately, as of May 2019, scientists haven’t found a way to produce effective iPSCs without deregulating the c-MYC gene, and because that can cause cancer, the procedure has been deemed too dangerous to perform on humans.

MYC and Cancer

MYC genes, specifically the c-MYC gene, contribute to the growth of many human cancers. MYC genes are classified as either oncogene and proto-oncogene — oncogenes are abnormal or mutated genes, and proto-oncogenes are normal genes.

Some people have both oncogenes and proto-oncogenes, while other, cancer-free, people only have normal (proto-oncogene) MYC genes.

When you have mutated c-MYC genes, your cellular growth rate and cellular metabolism aren’t properly regulated. This typically results in increased cell expression and decreased function of your body’s tumor suppressors.

Because your body’s tumor suppressors aren’t functioning properly, tumors — sometimes cancerous ones — can start growing in your body.

While many cancers are considered to be c-MYC driven cancers, such as breast cancer, some forms of cancer are attributed to v-MYC, which is a viral homolog of the c-MYC gene. The v-MYC oncogene forms when several acute transforming retroviruses interact with mutated c-MYC genes.

Leukemia and sarcoma are cancers that form from v-MYC oncogenes instead of mutated c-MYC genes 3.

B-cell lymphoma is considered a c-MYC cancer. However, it’s caused by a b-MYC mutation, which only happens in part of the c-MYC gene.

Other forms of cancer that are known to show an increased expression of MYC including lung cancer, melanoma, colon cancer, multiple myeloma, and neuroblastoma.

Alterations of the C-MYC Gene In Human Cancers

Altered c-MYC genes are found in many forms of human cancer. That’s because these alterations cause MYC overexpression.

Cancer feeds on the overgrowth of cells, eventually generating invasive and destructive tumors to form.

While mutated c-MYC genes are found in several different types of cancer, different alterations of the gene are possible. When mutated c-MYC genes interact with some rotaviruses, v-MYC cells are formed.

These are basically c-MYC cells with a virus, and they are most commonly found in sarcomas and leukemias.

Another alteration of the c-MYC gene is b-MYC. This is an N-terminal homolog of the c-MYC gene that lacks the C-terminal DNA binding protein of the c-MYC gene. This type of alteration is typically found in B-cell lymphoma.

How Does the MYC Gene Cause Cancer?

Normal MYC genes don’t cause cancer. However, mutated c-MYC genes are often found in human cancers, including breast cancer, leukemias, and lymphomas.

MYC gene rearrangement causes the c-MYC gene to malfunction. This causes MYC proliferation, as well as a decrease in your body’s natural tumor suppressors.

When cell growth is unregulated and your tumor suppressors aren’t working properly, cancer and/or cancerous tumors can develop.

Different forms of cancer are caused by different types of MYC gene alterations. For example, MYC breast cancer is caused by a mutation of the b-MYC gene, which is part of the c-MYC gene.

However, leukemia and sarcoma are often caused by v-MYC, which is caused when rotaviruses interact with mutated c-MYC genes.

While some forms of cancer contain mutated c-MYC genes, not all do. For example, c-MYC lymphoma refers specifically to B-cell lymphomas. This is because abnormal c-MYC genes are an essential pathogenesis of B-cell lymphomas, but they are rarely found in T-cell lymphomas 4.

However, B-cell lymphoma makes up about 85% of all non-Hodgkin lymphomas in the United States, so mutated c-MYC genes are present in the majority of people with non-Hodgkin lymphomas 5.

When and How to Test for MYC

You can’t simply order a DNA test to determine if you have mutated MYC genes. These tests are typically ordered by a hematologist or oncologist to confirm or rule out a cancer diagnosis.

Unlike DNA tests that are completed using a saliva sample, DNA testing for MYC mutations is completed using fluorescent in situ hybridization (FISH) test. This test uses probes to identify fusion of the MYC genes with numerous partner genes.

To conduct the test, the lab needs either a blood sample in a lithium heparin tube or a bone marrow sample in transport media. Ideally, the sample should be dedicated specifically to MYC testing instead of a sample that needs to be used for multiple tests.

Of course, DNA testing processes continually improve. And because researchers are starting to use the data they’ve compiled to target c-MYC genes as part of regular cancer treatment, you might be able to have your MYC genes tested in the future.

However, such tests will probably only be available when prescribed by doctors and to people who have a family history of human c-MYC cancers.

Targeting Oncogenic MYC for Cancer Therapeutic Purposes

The MYC gene is deregulated in over 50% of human cancers. It’s also associated with a poor prognosis and unfavorable patient survival rates.

This is because MYC has a central role in the majority of the oncogenic process. Because of this, many experts believe and continue to study cancer treatment involving MYC inhibitors. Cancer therapy options continually evolve.

However, direct targeting of MYC has proved to be a challenge because MYC genes have an “undruggable” protein structure.

MYC is mostly located in the cell’s nucleus. This makes it hard to target specifically, but also, when targeting nuclear MYC, antibodies don’t have a way to attach themselves to the gene.

This means that treating mutated MYC genes with monoclonal antibodies, which are typically used as a cancer treatment, is impractical.

Because directly targeting MYC genes during cancer treatments hasn’t been successful so far, researchers have begun testing different ways to indirectly target the mutated MYC genes. To indirectly treat mutated MYC genes, scientists are testing ways to alter or treat essential targets involved in the deregulation of the MYC genes.

As of May 2019, one treatment has shown great promise.

Instead of targeting the MYC genes directly, the treatment targets MYC transcription by interfering with chromatin-dependent signal transduction to RNA polymerase. The idea behind the treatment is that because MYC strictly depends on factor MAX to regulate gene transcription, interrupting the body’s MYC-MAX complex in patients with MYC cancer inhibits the signaling process, which in turn, stabilizes the body’s MYC.

Treatments that indirectly target the MYC gene are aimed at stabilizing the gene so that it regulates cell growth properly. When rapid cell division and increased cell growth stops, cancer cells are also affected.

This makes it easier for current treatments to kill active cancer cells before they spread throughout the body further.

Ultimately, while the idea of targeting mutated MYC genes directly as a form of cancer treatment is powerful, it’s not something a feasible option yet. Treatments targeting the body’s MYC-MAX complex or those that target the stability of the MYC genes directly have shown much more promise.

Scientists are also researching different methods of targeting the MYC-mRNA translation and the MYC transcription in hopes of finding a good treatment option for MYC-driven cancers. They are even experimenting with synthetic lethal interaction and MYC in an effort to develop a lethal interaction that only kills cancerous cells.

Unfortunately, while some methods have shown promise, none of the options are considered safe forms of cancer treatment currently.

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Referenced Sources

  1. c-Myc and Cancer Metabolism.
    Donald M. Miller, Shelia D. Thomas, Ashraful Islam, David Muench, and Kara Sedoris. 15 Oct 2013.
  2. MYC Acts via the PTEN Tumor Suppressor to Elicit Autoregulation and Genome-Wide Gene Repression by Activation of the Ezh2 Methyltransferase.
    Mandeep Kaur and Michael D. Cole. January 2013.
  3. MYC on the Path to Cancer.
    Chi V. Dang. 30 Mar 2013.
  4. The Role of c-MYC in B-Cell Lymphomas: Diagnostic and Molecular Aspects.
    Lynh Nguyen, Peter Papenhausen, and Haipeng Shao. 08 Apr 2017.
  5. WebMD - American Cancer Society.
    Last Revised: 29 January 2019.