A summary of the latest medical developments in breast cancer, culled from Google Alerts, for the week ending Friday 10 January 2014.
I realise that some of the developments I’m posting have been published earlier in 2013 which means they’re not exactly new or germane to 2014; however, they have just recently been released by some news-sites in Google Alerts, so I have chosen to include them.
I’m conscious that Best of Breast is beginning to resemble a sci-fic novel with a formulaic plot and one-dimensional characters:
- there’s always the mwah-ha-ha VILLAIN (one, if not more) like a MUTANT gene (with unpronounceable acronym) that causes cancer,
- the HERO (new drug or improvement in treatments or group of scientists that promise to curb cancer),
- the WAR – sadly, it’s still classed as a “war against cancer” with victors and losers,
- the VICTIMS (the long-suffering and heroic cancer patients who are waiting patiently for a cure that doesn’t involve the death rays of radiotherapy and chemotherapy),
- the WEAPONS (immunotherapies, vaccines, targeted treatments, magic bullet cures, death rays, chemical warfare)
- DEATH (like in Terry Pratchett novels) who lurks too close for comfort. (Also has bit part as RECURRENCE),
- the REVELATION/MOUSE CONSPIRACY (new drug only works on mice/rats, or is in a trial and will take years before it’s available for commercial use).
- All that’s missing is a really good save-the-world ending – some ALIEN species or OBI-WAN character descending down on earth with the Cure for Cancer … .
So Roll-On 2014, and please bring me the cure for cancer!
1. Scientists discover how to destroy cancer cells in the blood stream before they infect other parts of the body
- Specially selected proteins can be attached to white blood cells so that as they travel through the blood, they also destroy cancerous cells
- Biomedical engineers at Cornell University made the breakthrough, which prevents the disease from infecting other organs
- Human blood samples and later mice, were injected with two proteins in laboratory tests.
- One protein was an adhesive called E-selectin and the other was Tumour Necrosis Factor Related Apoptosis-Inducing Ligand (TRAIL).
- The TRAIL protein joined with the E-selectin protein stick to leukocytes, otherwise known as white blood cells, which are abundant in the bloodstream.
- When a cancer cell comes into contact with TRAIL, which is nearly unavoidable in the frenzied flow of blood, the cancer cell essentially kills itself, the researchers explained in the study, which is published online in the journal Proceedings of the National Academy of Sciences.
For more information:
There’s a sense of deja vu this week with research on cholesterol and cancer. I was sure I’d read this somewhere and yes … in 2013 there was research into cancer and … cholesterol.
2. Does good cholesterol increase breast cancer risk?
- High levels of high density lipoprotein (HDL), also known as the “good cholesterol,” are thought to protect against heart disease.
- However, high levels of HDL have also been linked to increased breast cancer risks and to enhanced cancer aggressiveness in animal experiments.
- A team of researchers led by Philippe Frank, Ph.D., a cancer biologist in the Department of Biochemistry and Molecular Biology at Thomas Jefferson University, has shown that an HDL receptor found on breast cancer cells may be responsible for this effect, proposing a new molecular target that could help treat the disease.
- Dr. Frank and colleagues exposed breast cancer cell lines to HDL and noticed that signaling pathways involved in cancer progression were activated, and that the cells began to migrate in an experimental model mimicking metastasis.
- The researchers then limited the expression of the HDL receptor called SR-BI in the cells using silencing RNA to reduce the receptor’s levels. In response, the activities of the signaling pathways that promote tumor progression were reduced.
For more information:
Breast Cancer Research 2013, 15:R87 doi:10.1186/bcr3483
Published: 24 September 2013
Also check out:
Cholesterol as driver of breast cancer:
3. Researchers link protein with breast cancer’s spread to the brain and triple-negative breast cancer
- Researches have discovered that breast cancer cells harness a protein called alphaB-crystallin to help them stick to endothelial cells that line the small blood vessels in the brain.
- In addition, this protein enhances the penetration of breast cancer cells through the blood-brain barrier, which normally prevents cells and many molecules from entering the brain.
- Once in the brain, the breast cancer cells are able to form metastases.
- In addition, by examining tissue from breast-cancer patients who developed brain metastasis, the investigators discovered that women with breast tumors that expressed alphaB-crystallin had a shorter survival than women with breast tumors that did not express this protein.
- The team also found breast tumors that expressed alphaB-crystallin were more likely to be triple-negative breast cancers – an aggressive type of cancer, which lacks three receptors (estrogen receptor, progesterone receptor and HER-2) expressed in other types of breast cancer.
- Triple-negative breast cancers are known to have a high incidence of brain metastasis.
- “Our findings suggest that alphaB-crystallin may contribute to the tendency of triple-negative breast cancers to metastasize to the brain and to their poor prognosis,” said Cryns. Yet, he cautioned these findings need to be validated in additional studies.
- The study, published in Clinical Cancer Research, and featured on the journal cover, was led by Dr. Vincent Cryns, professor of medicine at the University of Wisconsin School of Medicine and Public Health and a member of the University of Wisconsin Carbone Cancer Center.
4. Mice [here we go again!] models of drug-resistant breast cancer suggest better treatments
- Human breast tumors transplanted into mice are excellent models of metastatic cancer and are providing insights into how to attack breast cancers that no longer respond to the drugs used to treat them, according to research presented at the 2013 San Antonio Breast Cancer Symposium, December 10-14, 2013.
- The transplanted tumors maintain the genetic errors that caused the original cancer, even though they are growing in mice.
- As such, mice carrying human tumors can help identify drivers of tumor growth and serve as excellent test subjects for investigating new drugs.
- The mice are particularly good models of estrogen receptor (ER)-positive tumors that have become resistant to the drugs used to treat them.
- Researchers found three different types of mutations in the estrogen receptor in patients whose cancer was resistant to antihormone therapy.
- One type of mutation is called gene amplification, in which multiple copies of the ESR1 gene are present.
- A second type is a point mutation in the part of the receptor that binds estrogen, causing the receptor to become active even without estrogen.
- The third type is a translocation, in which half of the estrogen receptor gene is swapped for a completely unrelated gene from a different part of the genome.
“We can now categorize estrogen receptor-positive breast cancer that has evolved resistance into four categories: point mutated, translocated, amplified, and none of the above. We’re planning clinical trials to study different treatment strategies for each of these types.”
5. Imaging breast cancer with light
- A team of researchers at the University of Twente in the Netherlands have developed a prototype of a new imaging tool that may one day help to detect breast cancer early, when it is most treatable.
- The new device, called a photoacoustic mammoscope, would represent an entirely new way of imaging the breast and detecting cancer.
- Instead of X-rays, which are used in traditional mammography, the photoacoustic breast mammoscope uses a combination of infrared light and ultrasound to create a 3-D map of the breast.
- The researchers describe their device in a paper published in The Optical Society’s (OSA) open-access journal Biomedical Optics Express.
For more information:http://www.opticsinfobase.org/boe/abstract.cfm?uri=boe-4-11-2555
6. A do-Ron-Ron … new cell mechanism discovery key to stopping breast cancer metastasis
- Researchers from Huntsman Cancer Institute (HCI) at the University of Utah discovered a cellular mechanism that drives the spread of breast cancer to other parts of the body (metastasis), as well as a therapy which blocks that mechanism.
- The new discovery focuses on a protein called RON kinase (RON), which signals some areas of tumor cell DNA to become active.
- Normally, RON operates mostly during embryonic development and is not highly expressed in healthy adults.
- But in about 50 percent of breast cancer cases, RON becomes re-expressed and reprograms genes responsible for metastasis, making them active
- It was found that inhibiting RON turns off the entire metastasis program in these tumor cells
- The research results were published online in the journal Cell Reports on January 2.
For more information:
7. Neoadjuvant chemotherapy in breast cancer significantly reduces number of yielded lymph nodes by axillary dissection
- Neoadjuvant chemotherapy (NC) is an established therapy in breast cancer, able to downstage positive axillary lymph nodes, but might hamper their detectibility.
- Even if clinical observations suggest lower lymph node yield (LNY) after NC, data are inconclusive and it is unclear whether NC dependent parameters influence detection rates by axillary lymph node dissection (ALND).
- The likelihood of incomplete axillary staging was four times higher in the NC group.
8. PIK3CA gene mutations make some breast cancers resistant to treatment
- Women with breast cancer characterized by high levels of the protein human epidermal growth factor-2 (HER2) and hormone receptors gained much less benefit from presurgery treatment with chemotherapy and HER2-targeted therapies if their cancer had one or more mutations in the PIK3CA gene.
- These results were presented at the 2013 San Antonio Breast Cancer Symposium, December 10-14, 2013.
For more information: