A summary of the latest medical developments in breast cancer from Google Alerts, for the week ending 8 November 2013.
It’s a strange mix this week, with the usual search for the causes of cancer in DNA and food and cholesterol, and drug therapy mixed with robots!
1. Diet rich in bread after the menopause can raise risk of breast cancer
OK, I know this is not the most earth-shaking news, but I’ve always been interested in nutrition and cancer. When I was first diagnosed I was told to avoid anything with gluten. Fortunately, I don’t need bread to survive, so I was able to tolerate the diet. But it was just one of these blanket dietary bans, with no rationale behind it except that it caused inflammation in the body and gummed up the digestive system. As for pasta – well, that was carbohydrate which would convert to sugar and fuel the cancer cells.
If we’re going to use GI to measure whether or not a food is appropriate, surely pasta (which is refined carbohydrates) is as bad as bread?
- A simple switch from sandwiches to pasta could help cut the risk of breast cancer.
- A diet rich in bread after the menopause can raise the risk of developing the disease by 60 per cent, warned researchers.
- However, the chances dropped among older women who relied more on pasta.
- The study in the Annals of Oncology suggests that bread promotes high levels of the female hormone oestrogen – a known risk factor for breast cancer – because of its high GI (Glycaemic Index) rating.
- Pasta is at the opposite end of the scale measuring the effect of carbohydrate-rich foods on blood-sugar levels.
2A Cholesterol – new driver of breast cancer
(There seem to be two separate groups who’ve been conducting research into related substances.)
What I want to know is what kind of cholesterol stimulates breast cancer? Low density lipid (LDL) “bad” cholesterol or high-density lipid (HDL) “good” cholesterol or triglycerides or all three? And what is a safe level?
- A team of researchers at UT Southwestern has found that as cholesterol is metabolised, a potent stimulant of breast cancer is created
- The metabolised cholestrol fuels estrogen-receptor positive breast cancers, and that may also defeat a common treatment strategy for those cancers.
- The discovery of a cholesterol metabolite called 27-hydroxycholesterol, or 27HC as another driver of breast cancer may explain why endocrine-based therapy is often unsuccessful, providing a new target for therapy, the researchers say.
2B Study Identifies New DNA Trigger for Breast Cancer Metastasis
- University of Pennsylvania researchers have revealed how a reduction in mitochondrial DNA content leads human breast cancer cells to take on aggressive, metastatic properties.
- The work, published in the journal Oncogene, breaks new ground in understanding why some cancers progress and spread faster than others
- It may offer clinicians a biomarker that would distinguish patients with particularly aggressive forms of disease, helping personalize treatment approaches.
- An enzyme called CYP7B1, metabolizes 27HC
- CYP7B1 is diminished in breast tumors compared with normal breast tissue.
- There is a more than 7-fold poorer overall survival in women whose tumors display low CYP7B1, compared with women with high tumor CYP7B1.
- Studies have shown that estrogen upregulates the 27HC metabolizing enzyme CYP7B1. Therefore, the commonly-used therapies that block estrogen synthesis or action may actually increase the abundance of this newly discovered promoter of breast cancer, the researchers also concluded.
3. Mutations linked to breast cancer treatment resistance
- Two groups independently report the identification of ESR1 mutations in hormone-resistant metastatic breast cancer.
- Researchers have identified a type of mutation that develops after breast cancer patients take anti-estrogen therapies.
- The analysis found that patients had mutations in the estrogen receptor.
- All of them had been treated with an aromatase inhibitor, a type of drug that blocks estrogen production.
- The researchers found that the mutations were not present before the patients started their treatment, which means it was the therapy itself that caused the mutations to develop or be selected.
- The mutations explain one reason why patients often become resistant to this therapy.
- The researchers also suggest that blood tests could be used to monitor patients and detect these mutations to potentially shift treatment before resistance develops. It’s not yet known how frequently these mutations in the estrogen receptor occur.
- The mutations did not prevent current estrogen therapies from working, but instead made it so that more of it was needed to stop the tumors from growing or metastasizing—in some cases so much so that using such therapies became impractical.
- Currently, no treatment exists to target the mutations.
- The two studies appear online in Nature Genetics:
They say no treatment exists that target the mutations, but wait … all is not lost!
4A Read about an osteoporosis drug that stops growth of breast cancer cells, even in resistant tumors by degrading estrogen receptors (study presented on 15 June 2013):
Osteoporosis drug stops growth of breast cancer cells, even in resistant tumors
“We found bazedoxifene binds to the estrogen receptor and interferes with its activity, but the surprising thing we then found was that it also degrades the receptor; it gets rid of it,” said senior author Donald McDonnell, PhD, chair of Duke’s Department of Pharmacology and Cancer Biology.
4B. And read also about androgen therapy for breast cancers that have developed resistance to treatments that target estrogen dependence (presented at the AACR in 2013):
Studies show increasing evidence that androgen drives breast cancer
– I find this very interesting. The current hormonal therapy protocol is aimed at blocking the action of estrogen, whether through drugs like Tamoxifen or aromatase inhibitors, or through surgery by removing the ovaries that produce estrogen. I’ve had friends who’ve had their ovaries removed, and the cancer has continued to gallop. Perhaps this is one of the answers. It would be wonderful if this was found to be more effective than removal of the ovaries which of course triggers menopause.
Remarkably, the anti-androgen drug enzalutamide had effects comparable to the anti-estrogen drug tamoxifen in breast cancer cells that expressed both ER and AR. HER2 cell lines that were also AR+ showed promising responses as well.
5. Levels of Hormones Help Better Predict Breast Cancer
A research team, led by Harvard Medical School professor Shelley S. Tworoger, found that higher blood concentrations of certain hormones led to a greater chance of developing breast cancer.
The findings indicate that a simple blood test could prove useful for predicting whether women will develop the disease.
6. Robot Detects Breast Cancer With Space-Grade Tech
- The Image-Guided Autonomous Robot, or IGAR, aims to make breast biopsies more precise and automated.
- The robot works with enough precision to insert the needle within about 0.3 inches (8 millimeters), of the suspicious lesion with a high degree of accuracy.
- IGAR will improve sampling, reduce the pain of the procedure, save time and, as a result, save money.
- It will allow all radiologists to perform this procedure equally well, regardless of the number of cases per year and move the site of treatment from operation room to radiology suite for a significant number of patients.
7. Machines learn to detect breast cancer
- Software that can recognize patterns in data is commonly used by scientists and economics.
- Researchers in the US have applied similar algorithms to help them more accurately diagnose breast cancer.
- The researchers outline details in the International Journal of Medical Engineering and Informatics.
8. Early onset of puberty in girls linked to obesity and breast cancer
Breast development at younger ages is a concern among physicians and parents because early menstruation, which can accompany it, has been linked to higher risk of breast cancer.
9. Drug-resistant melanoma and breast cancer treated with potential new drug
- LEE011, a small-molecule inhibitor of cyclin-dependent kinases (CDK) 4/6 showed promising results in drug-resistant melanoma and drug-resistant breast cancer
- In many cancers, retinoblastoma, a tumor suppressor protein, is deactivated because of an increase in the activity of the proteins CDK 4 and 6.
- LEE011 is the most selective CDK4/6 inhibitor to date
- The drug is developed by Novartis Oncology
10. New method for breast cancer drug delivery using hydrogel
- Scientists have developed a novel synthetic hydrogel made up of over 96% water and a degradable polymer.
- The gel is capable of using a range of different drug molecules.
- Because the gel dissolves slowly, it can release the drugs relatively slowly, meaning that the process of providing anti-cancer drugs to the target site is more efficient.
- The device was developed by IBM and Singapore’s Institute of Bioengineering and Nanotechnology.
11. Treating chest lymph nodes in early breast cancer patients improves survival
- Giving radiation therapy to the lymph nodes located behind the breast bone and above the collar bone to patients with early breast cancer improves overall survival without increasing side effects.
- This new finding ends the uncertainty about whether the beneficial effect of radiation therapy in such patients was simply the result of irradiation of the breast area, or whether it treated cancer cells in the local lymph nodes as well, the 2013 European Cancer Congress on Saturday 2 November, 2013.