Editors: Whit Froehlich, John Charpentier, and Scott Barolo
Cervical cancer has been getting much more attention as of late, partly due to the HBO adaptation of Rebecca Skloot’s book The Immortal life of Henrietta Lacks. As a survivor of the same type of cancer that took Henrietta’s life and led to the development of the HeLa cell line, I found that Skloot’s book resonated deeply with me. My diagnosis compelled me to learn more about cervical cancer, which is one of the most preventable forms of cancer.
What Is Cervical Cancer?
Cervical cancer is an abnormal and uncontrolled growth of the cells lining the cervix, which acts like the doorway to the uterus. The cervix lining is mostly made up of two different cell types. Lining the outer cervix that faces the vagina are squamous cells, which are flat in shape, while the open passage of the cervix which leads into the uterus is lined by glandular cells, which are blockier in shape and produce mucus. Cancer can arise from either of these cell types; however, squamous cell cancers are the more frequent.
Most cervical cancers are caused by Human Papilloma Virus (HPV). HPV is commonly known as the virus that causes genital warts, but what many don’t realize is that there are over a dozen types of sexually transmitted HPVs, and only a few of them result in genital warts. The National Institutes of Health (NIH) highlight that persistent infection with certain HPV strains, especially types 16 and 18, is the major cause of most cervical cancer cases.
My mom was diagnosed with cancer two years ago. She had early-stage breast cancer: tumor size of less than five centimeters, fewer than three cancer-positive lymph nodes in the armpit region, and no cancer-positive lymph nodes nearby. But hers was also an aggressive type of cancer. At the time, I was a graduate student in the States and my parents lived in China, so we talked on the phone every two days about the progress of her treatment. She received surgery, radiation, a tailored drug treatment, and chemotherapy. My mom is tough and stubborn. Most of the time she just mentioned the good news that the cancer had been eliminated. Occasionally, she would say that her life was changed by the cancer treatment: for example, she had to quit her job.
I was shocked by my mom’s diagnosis. She is always physically active and mostly eats vegetables. I barely recognized her after the chemotherapy. She had lost 30 pounds and all of her hair, her skin was pale, and her nails were purple. Her face was unrecognizable because of the weight and hair loss, and she looked almost 20 years older.
My mom is cancer-free now, but she is not the same person that she was. Her appetite is half of what it was before, and she cannot lift heavy things. As a graduate student studying cancer biology, I had learned that chemotherapy would cause side effects like the ones I saw in my mom, including hair loss, vomiting, and nail loss. However, until my mom’s physical appearance and life were transformed by chemotherapy, I didn’t realize the magnitude of its impact on patients. Looking at my mom, I wish that we had better options for patients with early-stage breast cancer so they don’t have to suffer these devastating side effects.
We have known tobacco to be a cause of many cancers for decades now. It is associated with it least 14 types of cancers (see Figure 1). Less understood is how tobacco causes cancer. The short answer—it causes mutations. Tobacco smoke is a mixture of many chemicals, including at least 60 carcinogens (cancer-causing chemicals).
A trans-national team of researchers has begun unearthing the distinct types of mutations caused by tobacco smoke to better understand the biological pathways leading to tobacco-induced cancer. They found that tobacco causes specific types of DNA damage in organs directly exposed to smoke (like the lungs) and that smoking tobacco generally leads to higher rates of mutation in all tissues. Understanding how the chemicals in tobacco smoke cause mutations can help scientists identify new and emerging mutagens and design better treatment strategies.
The assassins have a description of their targets, who are hiding in plain sight among the non-combatants. The targets are guerillas who’ve infiltrated the neighborhood, overwhelming the local authorities and fomenting chaos. After only minutes on patrol, the assassins go on the attack, quickly identifying and eliminating the enemy without harming a single bystander.
This scenario may sound like the plot of a Hollywood blockbuster, but it’s also a good metaphor to describe the activity of engineered immune cells against cancer cells. The assassins are called CAR-T (Chimeric Antigen Receptor-T) cells, and they receive their elite training at the hands of physicians and scientists, who teach them to recognize particular molecules on the surface of tumors.
At first glance, aging and cancer are polar opposites. Many people will think of aging as growing old and dying. Cancer, on the other hand, is tumors and abnormal, uncontrolled cell growth.
But aging and cancer have more in common than we might think. Both cancerous and aged cells show genome instability– an increased tendency of mutations to occur in your genome. There are multiple factors that lead to genome instability, but we will focus on how gene mutation arise, which is a permanent error in genes.