President John F. Kennedy pledged in 1961 to put a man on the moon by the end of the decade. It took less than nine years to accomplish.
In 1971, President Richard Nixon promised there would be a cure for cancer in 10 years. It’s been 41 — and researchers are just starting to figure out what’s taking so long.
“We got to the moon in nine years because we had 400 years of physics behind us, from Galileo on,” says Charles Saxe, director of the Cancer Cell Biology and Metastasis program at the American Cancer Society.
“When Richard Nixon said we’ll cure cancer, we had nowhere near that kind of knowledge base.”
Scientists feeling the push from Nixon’s National Cancer Act, and armed with the federal funding it brought, stepped up their lab work and organized extensive clinical trials in an attempt to figure out exactly what causes cancer, and to find a cure. What they found was they didn’t have a clue.
“When we started to dig in, we realized it was more complicated than we even believed,” Saxe says. “We didn’t have the tools to understand how cancer happens. Things we thought we had simple answers for, we tested — and it didn’t work. A lot of humility came into play.”
And a lot of attention has gone on to focus on breast cancer. In the last 41 years, the American Cancer Society — the largest non-governmental funder of cancer research — has given out over $450 million in grants for breast cancer research alone. That money hasn’t gone to waste; the five-year survival rate for breast cancer patients has gone from around 45 percent to 90 percent.
But there’s still no cure.
Significant advances in understanding breast cancer didn’t start until the 1990s, with the genetic revolution.
“It took the whole genetic revolution before we could make rapid progress. Before we could begin to reach the equivalent of the 400 years of knowledge available to the physicists,” says Saxe. “We’re able to look at it from a genetic level now — what the cells are thinking, what the cells are trying to do.
“The cells are trying to grow in an environment where they’re being told to stop. That’s all driven by the genes,” he says. “The more we understand the individual genes, the more we can attack the growing cells.”
Genes are made up of DNA. They hold the information to build and maintain the body’s cells.
Through the Human Genome Project, which kicked off in October 1990, scientists set out to identify the 25,000 genes in the human body and map out the sequence of the 3 billion DNA subunits. By identifying the genes and understanding how they’re supposed to work, scientists hoped to be able to recognize when something went wrong.
They found that certain genes regulate cell growth. An error in the gene — a mutation — can cause cell growth to spiral out of control.
Cancer is characterized by abnormal cell growth. It appears when cells divide too quickly, or forget how to die.
A woman living in the United States has a one in eight lifetime risk of being diagnosed with breast cancer, according to the National Cancer Institute at the National Institutes of Health, with women of Ashkenazi Jewish descent more likely than the general population to carry certain genetic mutations that have been linked to the development of the disease.
The prevalence in Ashkenazi women can be explained by “simple genetics,” says Saxe. It’s known as the founder affect.
“You have a small community not breeding with the outside population, a mutation spontaneously occurs among a few people, and then it spreads. It’s really predictable at this point,” he says.
The mutation an Ashkenazi woman might carry is in the BRCA1 or BRCA2 genes, or “breast cancer susceptibility” genes. Compared to a woman who hasn’t inherited a mutation in one of those genes, someone who has is about five times more likely to develop breast cancer, according to the National Cancer Institute.
Advancements in early detection of breast cancer have played a role in increasing survival rates. The disease is much easier to treat when “you’re looking at a smaller population of cells you’re trying to kill,” Saxe explains.
With that in mind, the U.S. Preventive Services Task Force recommends that Ashkenazi women should have genetic testing for BRCA mutations if they have a first-degree relative with breast or ovarian cancer or two second-degree relatives on the same side of the family with breast or ovarian cancer.
“There is a range of different types of breast cancers, with different molecular signatures. Part of the problem is that, historically, we’ve grouped them all together,” says Lawrence Solin, chair of radiation oncology at Einstein Healthcare Network in Philadelphia. “The good news is we’re beginning to learn how to treat these different types, rather than thinking of breast cancer as a single disease. This approach is going to accelerate progress tremendously.”
Solin was the lead researcher for the Oncotype DX test, a “molecular tool” that lets doctors predict the risk of recurrence in patients with ductal carcinoma in situ, the most common type of early, or non-invasive, breast cancer.
Most breast cancer patients start with some type of surgery to remove the tumor. The idea behind Oncotype DX, Solin explains, is to determine which patients also require more aggressive treatment in the form of radiation, chemotherapy or hormonal therapy or a combination — and will have to endure the effects those treatments bring — and which patients just need the surgery.
“Now that we are beginning to see how these sorts of molecular profiles can determine treatment, there’s going to be an explosion over the next five to 10 years of being able to really tailor therapies to individual tumors in individual women,” Solin says. “There is a huge amount of excitement in the research community.”
Rachel Vigoda is an award-winning writer and editor in Philadelphia. Her work has appeared in several online and print publications.
This article originally appeared in a “Fighting Cancer” special section of the Exponent.