Best of Breast: news for week ending 3 January 2014

The first lot of news in 2014, and it’s the usual melange of cancer breakthroughs which turn out not to be real breakthroughs because they only work on mice and rats.  Or what seems to be a breakthrough really is a simplification and sensationalism on the part of the newspaper that published it.

Apologies for sounding so world-weary only days into the New Year, but the fact is, scientists keep coming up with “cures” which have only been tested on mice and rats and will only be commercially-available years down the road after they’ve been put the through pharmaceutical company hoops.  After several months of putting together Best of Breast, I’ve become quite suspicious and now make sure I kick the tyres on any purported cancer “cure”.

MouseSantaClaus

Sorry for the lack of new developments! Uz ratz have been partying!

After the previous three weeks’ of Best of Breast which were chockful of news from the San Antonio Breast Symposium 2013, the news has petered out.  Maybe everyone (and the mice and ratz) has been too busy enjoying Christmas and New Year to publish their research findings!

I’m fed-up of seeing my friends suffer, and facing my fears at night – I want a cure, and I want it now for this terrible disease!  It’s either that or let’s all become rats and mice!

[Fact:  Mice and humans share 98% DNA. It takes changing only 2% of mice DNA to make a human being (if it were that easy). That’s why most experiments are conducted on mice.]

On a more positive note, I’m taking this opportunity to fill this week’s black hole, to re-post a piece of news first reported in Best of Breast (w/e 27 Dec 2013) on cancer immunotherapy being voted breakthrough of the year by Science magazine.

This is backed-up by an excellent summary in Business Australia of an increase in gene-based and immune-boosting therapies because the cost of gene sequencing is coming down.  Great news!  I believe this is the future of cancer treatments – magic bullets with targetted treatments, preferably getting the immune system to do the fighting with antibody treatments and vaccines.

There’s also an article on Bcl-2 protein expression, and my personal experience of using it as a marker.

1A.  Cancer immunotherapy voted breakthrough of the year by Science magazine

Immunotherapy

image credit:  sciencemagazine.org

http://news.sciencemag.org/breakthrough-of-the-year-2013

http://www.sciencemag.org/content/342/6165/1432.full

  • Immunotherapy – a way of fighting cancer that turns the body’s immune cells into targeted tumor killers – was named the breakthrough of the year by the US journal Science today.
  • Immunotherapy has only worked for a small number of patients, and only in certain cancers, including melanoma and leukemia, but experts believe its promise is huge.
  • “Oncologists, a grounded-in-reality bunch, say a corner has been turned and we won’t be going back,” said the magazine.

Well, that’s not entirely true that immunotherapy only works for a small number of patients.  There are antibody treatments that work – Herceptin, a monoclonal antibody that is used for Her2 positive breast cancers is one.  And there are antibody treatments that are available, but not on a commercial basis, or as off-label use only (cf Removab at Hallwang Private Oncology Clinic).  And as for cancer vaccines, they are available in both trials, and for private patients.

1B.  Cancer Drugs: Getting Close And Personal

http://www.businessinsider.com.au/cancer-drugs-getting-close-and-personal-2014-1

  • A new wave of cancer treatments is coming to market.
  • Three trends are helping to fill this cancer-drug cornucopia:
    1. One is the increase in demand as people live longer, and thus become more likely to develop cancer.
    2. The second trend is the rising price of cancer drugs, particularly in America, the biggest market. More expensive drugs increases profitability.
    3. The third is a rapid expansion of scientific knowledge about cancer, the result of both the plummeting cost of genetic sequencing (see chart) and a better understanding of how to recruit the immune system to attack the disease.
Economist Cancer Drugs
  • Understanding the genetic changes that cause particular cancers may suggest ways to attack them with specially tailored drugs.
  • DNA sequencing means it is becoming possible to track mutations, one tumour at a time. This helps in understanding how cancers in different tissues work and it also holds out the hope of treatments tailored even more closely to an individual’s needs.
  • The first example of such a targeted treatment came in 2001, when Novartis launched Gleevec, a treatment for chronic myeloid leukaemia.
  • Before Gleevec, less than a third of those diagnosed with chronic myeloid leukaemia were still alive five years later. After it became available, that figure jumped to 90%.
  • Pfizer came up with crizotinib (sold under the brand name Xalcori), for lung-cancer patients with a mutated version of a gene called ALK, which encodes a protein that instructs lung cells to divide uncontrollably.
  • And Roche developed vemurafenib (sold as Zelboraf), which goes after another rogue protein, generated by a mutated version of a gene called BRAF. It tells skin cells to reproduce, causing melanoma.
  • The other novel approach to treating cancer is to rally the immune system to join the fight.
  • Ipilimumab, a drug to treat melanoma, was launched in 2011 by Bristol-Myers Squibb, branded as Yervoy. It is a so-called “checkpoint inhibitor”, which by removing a blocking mechanism allows immune-system cells called T-lymphocytes to attack cancer cells.

2A.  New Noninvasive Procedure Targeting Single Gene May Halt Breast Cancer Development

  • A new, non-invasive therapy could soon be used to thwart breast cancer in its early stages, according to a new study.
  • Scientists from the Wyss Institute of Biologically Inspired Engineering at Harvard University have shown that the silencing of a single gene inhibits the formation of tumors in lab mice afflicted with a breast cancer model.
  • According to the authors, the research represents a significant step forward for oncological treatment and diagnosis as well as systems biology.

Apparently the treatment consists of an injection into the breast, and is currently only used for ductal carcinoma in situ breast cancer.  It is gene therapy.  And they’re talking about using it for people with familial tendencies (i.e. inherited breast cancer) to prevent breast cancer from developing.  What I don’t understand is, if it’s effective for DCIS, why not just use it for all breast cancers?  What’s so different about the genes for DCIS and invasive breast cancers?  Why not use it as adjuvant therapy, post-surgery, say?  Why am I not a mouse?

http://www.medicaldaily.com/new-noninvasive-procedure-targeting-single-gene-may-halt-breast-cancer-development-266143

For more information:

Science Translational Medicine, “Silencing HoxA1 by Intraductal Injection of siRNA Lipidoid Nanoparticles Prevents Mammary Tumor Progression in Mice”

or, same breakthrough, reported by The Daily Mail – got me excited and then I realised it was only for DCIS:

2B.  Breast cancer jab ‘prevents the disease in 75% of cases’: Treatment could spare thousands of women the trauma of surgery

  • New intravenous drug fights development of ductal carcinoma in situ (DCIS)
  • In Britain 5,000 women a year are diagnosed with the condition
  • The drug stopped three-quarters of mice [argh!] treated from developing cancer
  • Much more research is needed but, eventually, women with DCIS or genes that put them at high risk of breast cancer could be given a six-monthly jab to keep the disease at bay.

http://www.dailymail.co.uk/health/article-2532301/Breast-cancer-jab-prevents-disease-75-cases-Treatment-spare-thousands-women-trauma-surgery.html

3.  Bcl-2 expression predicts sensitivity to chemotherapy in breast cancer: a systematic review and meta-analysis

  • Numerous studies have yielded inconclusive results regarding the relationship between anti-apoptotic protein Bcl-2 expression and the sensitivity to chemotherapy in the patients with breast cancer.
  • The purpose of the current study was therefore to elaborate their relationship.
  • Conclusion: The results of the present meta-analysis suggest that Bcl-2 expression is a predictive factor for chemotherapy sensitivity in breast cancer patients.

For more information:  Author: Dong YangMin-Bin ChenLi-Qiang WangLan YangChao-Ying LiuPei-Hua Lu
Credits/Source: Journal of Experimental & Clinical Cancer Research 2013, 32:105

This is not new research, it’s a meta-analysis of other pieces of research on Bcl-2 for exaple:  “Bcl-2 Is a Prognostic Marker in Breast Cancer Independently of the Nottingham Prognostic Index

I got interested in the Bcl-2 expression when I was trying to find out if the complementary therapies I was using (IV C and other infusions) were working.  My tumour markers had always been within reference range, so I felt I could not rely on them.  I got a special series of gene-based tests done, including the P53 gene expression and Bcl-2, by the Galkina Lab (also known as Neuro Lab), in the UK:

What is Bcl-2 expression?  

Here’s what’s on Galkina’s website:

Cells produce BCL-2 protein to protect themselves against Apoptosis (programmed cell death). Cancerous and virally infected cells can use this BCL-2 protective capacity to avoid their elimination by the body’s immunological defence system, leading to further malignant growth.

The assay for BCL-2 clarifies the resistance levels of these Abnormal Cells to such programmed elimination. High BCL-2 quantities indicate that cancerous and infected cells are effectively resisting Apoptosis, while minimal quantities suggest the possibility of successfully targeting them for destruction. Particularly low BCL-2 quantities may also signify the inappropriate eradication of normal cells, including cells of the Immune System.

http://www.thegalkinalab.co.uk/#/bcl2-gene-expression/4572911336

So, high levels of Bcl-2 indicate that the cancer cells are more capable of resisting apoptosis (or cell death).  When my Bcl-2 level leaped up in 6 months from within reference range to way-way beyond that, I knew that something was up (my tumour markers, CA125, CA15-3, CEA were all normal at this time), and that’s when I made the decision to switch course of action.  However, I was also told that high levels of Bcl-2 indicated good response to chemotherapy – small consolation!

Where to get the Bcl-2 test done

In the UK, all you need is a blood draw and for the blood sample to be sent to the Galkina Lab.  However, Galkina Lab will only process the sample if it is authorised by a doctor.  The doctor I used was Ziggy Trefzer of Hightree medical who also did the blood draw and posted it off to Galkina Lab for me.  You can also get the tests done through Christopher Etheridge (a cancer advocate) but he does not do blood draws.  In London, you can get blood draws done through Biolab.

Please note, the Bcl-2 test is not the only test you should be using to keep tabs on how well you are doing.  It is another piece of the diagnostic/prognostic toolkit.  They are not a substitute for scans and tumour markers.  You also need someone who is experienced with interpreting the tests to tell you what’s happening.

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