-A curious adult from California
May 13, 2010
The short answer is usually not. Most cervical cancers happen because of a virus.
So it isn't your parents' DNA that is to blame. It is the DNA of a little virus called HPV.
In fact, this is why there is a vaccine available for this cancer. Vaccines are used for viruses all the time. You can get vaccinated against chicken pox, flu, and the measles because they are all caused by viruses. Same thing with cervical cancer.
One way a mom might pass an increased risk of cervical cancer to her child is by passing on HPV. There are certainly cases where a baby can get a virus from an infected mother. A scary example of this is the virus that causes AIDS, HIV.
So can a mother who has HPV pass it on to her baby during delivery? Yes, but the risk is tiny. And even if babies do get the HPV virus from mom, their bodies usually get rid of the virus on their own.
Having said all of this, I don't want to imply that there aren't any cases where cervical cancer isn't inherited. It does happen occasionally. Sometimes cervical cancer can be passed on as part of a syndrome.
Peutz-Jeghers syndrome is one such example. People with this syndrome can have differently colored spots on their skin, on their lips, around their mouths, inside their mouths, their hands, and their feet. These spots are sort of like freckles.
These people also have many benign growths along their stomachs, intestines, and colon. These growths may become malignant, or cancerous, with time.
Sometimes these bumps can appear on a woman's cervix. If they turn cancerous, then this woman will have developed cervical cancer because of her Peutz-Jeghers syndrome.
Peutz-Jeghers syndrome is a rare condition that can be passed from affected parents to their children. So it can be inherited. Which means that sometimes cervical cancer is inherited this way too.
There are other rare conditions like this as well but they aren't involved in most cases of cervical cancer. Like I said, most of these come from that virus, HPV. And for the rest of the answer, I thought I'd focus on how HPV can cause cancer.
Not all HPV is Created Equal
HPV is the most common sexually transmitted infection. About 75-80% of people will get HPV before the age of 50 and over 20 million women in the U.S. alone are infected. Luckily though, most of these cases won't go on to cause the cancer.
See, there are tons of HPVs and not all of them cause cervical cancer. In fact, most people with HPV do not develop any symptoms or health problems at all. In 90% of cases, the body's immune system fights off HPV naturally within two years.
Sometimes though, the virus can survive in a woman for years. If it can do so for 15 or 20 years, then it can sometimes convert normal cells on the surface of the cervix into cancerous ones.
This is why some types of HPV viruses are called high-risk, oncogenic, or carcinogenic. These include HPV types 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 56, 58, 59, 66, 68, and 73. That's a whole lot of numbers. What's the different between these and the low-risk group?
The answer is in the HPV genome
. A genome is almost always made of DNA and contains all the genetic information necessary to make a living thing. So a viral genome contains all the instructions needed to make new viruses.
Just like individual people can have slightly different genomes, so too can different HPVs. In virology, these different types are called strains.
A viral genome is much simpler than a human one. A virus really just needs to make copies of itself that can go on to infect more people. This takes very few instructions.
The genome of an HPV has six early (E) genes that help control the virus genes and how they behave in cells. They also have two late (L) genes with the instructions for the shell of the virus. And part of the genome helps control when these various genes are turned on as well.
The two most important HPV genes in the development of cancer are E6 and E7. Both of these genes need to be on all the time in order for cancer to develop.
E6 and E7 Can Let Damaged Cells Live On
New DNA changes
To understand how E6 and E7 can cause cancer, we need to step back and talk about what cancer is. And how it forms.
Cancer is caused by changes in the DNA of our genome. These changes can sometimes affect how our genes work. If the change happens in the wrong gene (called an oncogene), then you might get cancer.
These changes can be caused by UV light from the sun or chemicals in the environment. Sometimes our cells cause changes in our own DNA on accident. This can happen whenever a cell copies its DNA and divides.
Luckily our cells have ways to protect against DNA damage. Most of the time a cell can repair the damage. And if it can't, then the cell commits suicide (called apoptosis). This helps prevent damaged cells from multiplying and possibly leading to cancer.
Some forms of E6 and E7 keep these damaged cells from committing suicide. So these cells keep building up mutations until they grow uncontrollably and will not die. This is the definition of a cancer cell.
This is why E6 and E7 have to always be on for a long time. It takes years for the DNA changes or mutations to build up. And if E6 and/or E7 ever do turn off, the suicide machinery turns back on and the cell kills itself. Cancer averted.
Fortunately most forms of E6 and E7 can't do this. Only high risk strains of HPV have the risky versions of E6 and E7.
How E6 and E7 Can Cause Cancer
To understand how E6 and E7 can cause cancer, we need to know a couple of more things about genes. Each gene has the instructions for a specific protein. And each protein has a specific job it does.
Genes can also come in different versions and each version can have the instructions for a slightly different protein. So different versions of E6 make different E6 proteins. Same thing with the E7 gene.
So it is actually certain versions of the E6 and E7 proteins that can lead to cancer and not the E6 and E7 genes. These proteins can cause cancer by gumming up our cell's suicide machinery.
The E6 and E7 proteins work with each other to transform a normal cell into a cancerous one. But not all versions of E6 and E7 can do this. That's because their ability to transform cells depends on how well they can work with some of the cell's own proteins, p53 and retinoblastoma (Rb). Versions of E6 and E7 that can cause cancer have stronger interactions with Rb and p53 -- they stick better to these proteins.
In a typical cell, the p53 protein stops cells from growing if they have damage in their DNA. When E6 binds to p53, p53 is broken down and can't do its job. This means cells with DNA damage will keep growing.
The cell with the DNA damage can continue to grow and make new cells with the same DNA damage. We don't know for sure yet, but it is possible that the binding of E6 with p53 also helps stimulate infected cells to divide and multiply.
E7 has a different role. Its job seems to be to make cells that have working p53 kill themselves. This means E7 helps get rid of working cells and helps non-working cells continue to grow and make copies of themselves.
Let's add the Rb protein to the mix. Like p53, the Rb protein slows the growth of cells when they have DNA damage. It also leads to cell death if necessary. When E7 binds to Rb protein, instead of interrupting cell growth, cells with damaged DNA may be allowed to continue to grow and replicate.
Together, these processes allow cells with DNA damage to grow. This may lead to malignant change, or cancer.
HPV's E6 and E7 proteins prevent human p53 and Rb from stopping the growth of damaged cells.