Hepatocellular carcinoma (HCC) is the most common type of liver cancer, occurring primarily in patients with chronic liver damage, such as that caused by hepatitis B, hepatitis C, or long-term alcohol use. It is the third-highest cause of cancer mortality worldwide. Unfortunately, because HCC develops slowly and can be asymptomatic for years, patients are often diagnosed at an advanced stage.

Follicular lymphoma is a slow-growing cancer that occurs when the body produces abnormal B cells that form clumps, or “follicles,” in the lymph nodes. Like T cells, B cells are a type of white blood cell integral to the immune system. Unlike T cells, which attack the body’s own cells when they become infected or cancerous, B cells produce antibodies that target invading bacteria, viruses, and other pathogens.

As we know well by now, vaccines must be updated periodically because viruses constantly evolve new strains that may or may not bind to our existing antibodies. The influenza vaccine, for example, is updated every year; it seems likely that the SARS-CoV-2 vaccine will follow the same cadence. To develop and update these vaccines, researchers must test how panels of antibodies respond to panels of viruses. The number of possible antibody-virus combinations makes testing every interaction impractical, so even the most laborious studies have to settle for non-exhaustive data.

The proteins CDK4 and CDK6 are well-known regulators of the cell cycle, driving cells into the DNA replication phase that occurs before cell division. Since their discovery in the 1990s, scientists have understood that mutations in these regulatory proteins can lead to uncontrolled cell division, or cancer.  Thanks to persistent research efforts over the past thirty years, CDK4/6 inhibitors have been approved for the treatment of breast cancer, but given the disruptive power of these oncoproteins, it is likely that such inhibitors could be effective for other types of cancer as well. When it comes to targeted therapies, more specific means less toxic, so understanding which proteins to target in each cancer is a crucial first step.

The outermost layer of the human brain, known as the cerebral cortex, is responsible for our highest mental capacities—language, memory, emotion, decision-making, and much more. It contains an immense diversity of cells, between 14 and 16 billion neurons, organized in patterns complex enough to elude the farthest reaches of neuroscience.

As anyone who has undergone chemotherapy or radiation therapy knows, nausea is a frequent and distressing side effect and anti-nausea medications do not always work. Effective remedies for nausea are critical for cancer patients’ quality of life and ability to continue with treatment. But as with many types of pain, such remedies require a better understanding of the neural pathways that produce the sensation.

Head and neck squamous cell carcinoma, or HNSCC, is a cancer that develops in the mucous membranes of the mouth, nose, and throat, most often affecting men in their 50s and 60s. HNSCC is generally treated with surgery, followed by chemotherapy and/or radiation, but given the functional importance of the affected area, less severe treatment options could vastly improve patients’ quality of life. Additionally, the prognosis for patients with human papillomavirus (HPV)-positive head and neck cancer is much better than that of HPV-negative patients, highlighting the need for expanded treatment options.

Despite the best efforts of cancer researchers and clinicians, pancreatic cancer remains a highly lethal disease, with only 5% of patients surviving 5 years after their diagnosis. This is in part because pancreatic cancer cells have relatively few mutations, meaning fewer strange-looking proteins, or neoantigens, on their surface to attract the attention of cancer-killing immune T cells. This makes most pancreatic tumors “immune cold,” safe from detection by the body’s defense system.

Ras proteins, present in all mammalian cells, are molecular switches that control the processes of cell survival and proliferation. Unsurprisingly, mutations in any of the three RAS genes (KRAS, NRAS, or HRAS) can lead to uncontrolled cell growth, or cancer. Since these cancer drivers were first identified in the 1980s, it has been clear that different types of cancer are coupled with specific RAS mutants. For example, nearly 90% of pancreatic tumors display KRAS mutations, while NRAS mutations are more likely to appear in blood cancers. Why these associations exist, however, is not well understood.

Colorectal cancer is among the leading causes of cancer deaths worldwide, second only to lung cancer. As with many cancers, the primary cause of death in this type of cancer is metastasis, or when the cancer spreads from its original tissue to another organ in the body. In colorectal cancer, the liver is most common site of metastasis—more than half of all colorectal cancer patients will develop tumors in their liver during the course of their disease. Targeting the genes and pathways that promote liver metastasis may be key to developing better treatments for colorectal cancer, but until recently, these genetic mechanisms were not well defined.