Sunday, August 23, 2015

Ovarian Cancer Awareness Month: September Events

September is Gynecologic Cancer Awareness month and Ovarian Cancer Awareness month.

There are many ovarian cancer awareness organizations in NJ holding events over the next few weeks toraise awareness and funds for research. Check below for an event near you.

August 30

Hoboken, NJ

September 1-30 
Teal Awareness Ribbons
Statewide


September 9
 Princeton, NJ


September 13
Newark ,NJ
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The Gail MacNeil Morristown Walk - Loantaka Park  
Morristown,NJ



September 19
Concert for a Cure
Edison,  NJ

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Dance for Life 
A Bollywood and Zumba Dance Workout
with Arya Dance Academy
Monmouth Junction , NJ


September 20
Lyndhurst Walk - Richard W. DeKorte Park
Lyndhurst, NJ

Ewing , NJ 


September 26
Avon By the Sea Walk- On the Boardwalk
Avon by the Sea, NJ 
Bristol , PA


September 27 
NOCC - New Jersey Chapter
West Orange, NJ
Registration here.





If you know of other events taking place in NJ please contact me with the information and I will update the page OR simply include the information in the comment section of this post. Thanks!

Dee 
Every Day is a Blessing   

Tuesday, August 18, 2015

MedX 2014 : A Year Later


Last year, I had the privilege of attending the Stanford MedX Conference as an e-patient and IDEO Challenge participant. I wrote two posts about that experience here on my blog (MedX - A Place for Conversations  , Design Thinking and Health Care- My MedX IDEO Challenge Experience)

While other e-patients prepare for the MedX Conference this year I started to reflect back on my experience and what impact it has made on my role as an e-patient and cancer advocate.

Connections With Other E-patients
I met Janet Freeman-Daily for the first time at MedX. Janet, a metastatic lung cancer patient, and one of the best lung cancer advocates I know.  After the conference Janet and I continued to interact via Twitter and e-mail. In June, at the ASCO Annual Meeting in Chicago I joined her and a few other lung cancer advocates for dinner. Other ovarian cancer advocates might want to limit their interacts with only other ovarian cancer advocates but I have found that interacting with other cancer advocates from MedX like Janet and  Marie Ennis-O’Connor allows me to be an empathetic well-rounded cancer advocate. It helps to understand the latest treatments for other cancers as the treatments are becoming more mutation based than organ based.

While at MedX I didn’t just develop friendships with other e-patients who were cancer survivors . I learned what is was like to live with rheumatoid arthritis from Annette McKinnon, the importance of patient safety from Meredith Hurston (my roommate), the difficulties patients with prosthesis experience from Joe Riffe and our rights as patients to use and analyze our own data from diabetes e-patient,  Doug Kanter.

Putting It Into Practice
I read two books and a number of articles on design thinking in preparation to the MedX IDEO challenge. (Thanks Dennis Boyle.) But actually putting that type of thinking into practice at the conference was invaluable. I loved working in a team to come up with a solution to my problem: How Might We help cancer survivors understand what to expect after treatment ends?

To this day I find myself putting design thinking into practice as the co-moderator of the #gyncsm community / chat. I have even used it when discussing problems and their solutions in the 55 + community I belong to. When I read health articles online I wonder if the authors asked the patients/survivors what information would be important to them. I actually asked a question along those lines at an ASCO Annual Meeting session on integrating survivorship care plan information into electronic medical records. By the way , the researchers said they had not asked the patients what information was important to them. I suggested they may want to ask them in future studies.

I hope that all the e-patients who attend this year’s Med X conference will not only share their stories with others but will be open to the stories of the other conference attendees. Those stories may move you to tears or make you laugh but I assure you they will make an impact on your life. Oh and don't forget to take Zoey for a walk!

Dee
Every Day is a Blessing! 

 

Friday, August 14, 2015

Interview with Virginia Tech Professor and Ovarian Cancer Researcher Eva Schmelz, Ph.D. - Part Two






Part two of my  interview with Dr Eva Schmelz (Virginia Tech) regarding her ovarian cancer research. You may find part one here.







4.   Other research you are doing involves synthetic sphingolipid metabolites. What are they?
Sphingolipids are a large, very diverse group of membrane-bound lipids, containing a sphingoid backbone, a fatty acid and a more or less complex headgroup.  This individual components vary among species (plants and bacteria contain different sphingolipids than mammals) and several hundreds of different sphingolipids have been identified. They are structural components of the cell membranes, affect the membrane fluidity, can mediate cell-cell or cell-matrix interactions and have many more functions depending of the types of sphingolipids present, their concentrations and where in the cell and in which cell they are located.  Most interestingly for our research is their function as second lipid messengers, mediating the response of cells to growth factors, stress, inflammatory compounds etc., and regulate cell growth and cell death, motility and many other functions that are also important for cancer cells.  Most of our daily foods contain sphingolipids, the highest amounts are found in soybeans and dairy products.  In the intestinal tract, they are digested to the same bioactive molecules that are generated in the cells to regulate cell growth and death.  By feeding sphingolipids in the diet, we can expose the cancer cells in mice to these bioactive molecules and suppress their growth and reduce tumor formation while not affecting normal cells.  Natural sphingolipid metabolites are very quickly cleared from the circulation and from cells; we have used synthetic sphingolipids developed in Dr. Merrill’s lab that avoid clearance and stay active in the cells for longer.  They have therefore a higher toxicity towards cancer cells but also a higher toxicity towards normal cells, causing more side effects than natural sphingolipids. The correct dosing is therefore very important in order not to cause severe side effects of the treatment.

5.   What role does synthetic sphingolipid metabolites play in ovarian cancer prevention?
We have used synthetic sphingolipids administered directly into the peritoneal cavity to eradicate metastatic cells but have not yet found a formulation that guarantees a slow release that kills cancer cells but only minimally affects the normal cells lining the organs and the peritoneal cavity.  Orally adnminitstered synthetic sphingolipids have been used in other rodent cancer models but they seem to cause more side effects  than the natural compounds.

6. How will this research be translated to prevent ovarian cancer or treat it?
We have used dietary sphingolipids to suppress metastatic ovarian cancer in mice (manuscript in preparation) – similar to many other natural compounds, the success of this way of administration is restricted to the less aggressive cancer or earlier stages.  We have not been able to stop fast-growing tumors of any kind (breast, ovarian) that develop lethal disease in 3 weeks. However, less aggressive disease can be reduced in mice, significantly enhancing the lifespan of these mice. Other groups have also shown that non-toxic doses of sphingolipids can enhance the effect of conventional drugs, thus reducing the side effects.  We have not yet had an opportunity to test this in women but this is an exciting possibility.

     7. We are hearing more every day about immunotherapy and targeted therapies to treat cancer. Which avenues of ovarian cancer research do you find most exciting?

I think immunotherapy for ovarian cancer is very promising since it utilizes the specific gene changes in the tumor of an individual woman to train the immune system to detect these cancer cells- even the dormant ones- rather than trying to kill cancer cells with highly toxic compounds that by themselves can cause severe DNA damage in normal cells. The same would be true for targeted therapies if we can get the information of the response of the individual cancer.  Especially ovarian cancer has such diverse and individual genetic changes and redundant pathways to bypass targeted signaling pathways that make it more difficult to suppress cancer growth by specifically inhibiting one target.  I believe that taking a step back, looking at the tumor microenvironment rather than only the tumor cells alone and identify the factors that are important for ovarian cancer cell implantation at the omentum and other metastatic sites independent of the specific genotype of the cancer cell is a novel avenue to deal with this heterogeneity.  We then can develop drugs that prevent the interaction of the supporting factors with the cancer cells and thereby suppressing the deadly metastatic outgrowth irrespective of the individual genetic changes.  This is a more preventive approach against metastasis compared to the immune or chemotherapeutic approaches.
Novel treatment approaches that also do not rely on the individual genetic changes in the cancer cells have also been subject to investigation here at Virginia Tech.  Dr. Rafael Davalos, also featured in the VT magazine article, uses the bioelectrical fingerprint of cancer cells to either selectively eradicate cancer cells or enrich for cell populations of interest- tumor cells, stem-like cells, tumor associated cells- for diagnostic purposes or treatment decision making and efficacy control.  To this end, we have published the first reports that indicate we can identify ovarian cancer cells by their unique bioelectrical fingerprint which are different in benign and aggressive cells.  I believe that in addition to individualized medicine that specifically utilizes the individual genetic makeup of a cancer cell for treatment decisions, the methods that utilize biophysical or bioelectrical properties that are altered in cancer cells independent of their specific mutations, epigenetic changes or changes in non-coding DNA are a promising  way to detect and treat many cancers including ovarian in the future.


Thank you Dr. Schmelz for your responses and your continued research to better understand what causes metastasis and how to treat and prevent ovarian cancer. 

Dee 
Every Day is a Blessing! 

Thursday, August 13, 2015

Interview with Virginia Tech Professor and Ovarian Cancer Researcher Eva Schmelz, Ph.D. - Part One

Last month I read my son's copy of the Summer 2015 edition of  VT Magazine. My son has a BA and MA from Virginia Tech. The cover had a photo of ovarian cancer cells and the inside held articles on the cancer research being done at Virginia Tech including a piece on Professor Eva Schmelz's research. 
I was fascinated by the cover and so interested in her line of research that I looked on the Tech website and found her e-mail. I wrote to her as an ovarian cancer survivor, blogger and Hokie Mom.  I asked her if she would answer questions about her research for my blog.  Professor Schmelz was gracious enough to agree to answer some of my questions. While the answers are lengthy, the details are so important that I did not want to edit them. I will be presenting the questions and answers in multiple posts. In this first post you will hear about Prof Schmelz's  background, what got her interested in ovarian cancer research and the research she is doing with Dr. Chris Roberts. 
--> 1. You are currently an Associate Professor of human nutrition, foods, and exercise at the College of Agriculture and Life Sciences at Virginia Tech. Tell us more about your academic background and what sparked your interest in ovarian cancer research?

I received a MS degree in Human Nutrition from the Justus-Liebig University in Giessen, Germany, and a Ph.D. in Human Biology/Nutrition from the same University in 1992.  This provided me a strong background in biochemistry, physiology and nutrition although at that time, my research projects were not cancer related. I had the opportunity to join Dr. AH Merrill’s lab in the department of Biochemistry at Emory University in 1992 for post-doctoral research, investigating the potential of dietary sphingolipids to suppress chemically-induced colon cancer in mice.  This was a very successful project and we found a 50-70% reduction of tumor incidence in mice fed doses of complex sphingolipids that could be achieved in the human diet—not pharmacological doses. There were also no deleterious side effects of the treatment.  This encouraged us to investigate if cancer of other organs could also be suppressed. When I moved to the Karmanos Cancer Institute in Detroit, we next focused on breast cancer and found that dietary sphingolipids could suppress the progression of early stage breast cancer but had little effect on fast-growing tumors.  Taking a step back from considering only at the cancer cells as target cells for our treatment (toxicity, molecular mechanisms etc.), we wanted to investigate the impact of our treatments on the tumor microenvironment, focusing on female cancers.  Ovarian cancer is especially challenging because it is so genetically and histologically heterogeneous, deadly when detected late and early stages cannot be investigated because of the lack of a model. However, there was no mouse cell model available that could be used in mice with an intact immune system- most researchers use human cells in immune-deficient mice so these can grow aggressive human tumors. The immune system is important since inflammatory cells are now directly linked to the generation of a “permissive niche” that allows for the survival and growth of the tumor cells.  I therefore collaborated with researchers who had developed a model for progressive ovarian cancer that could be injected into mice and would allow for investigations of multiple stages of the disease.  This model is called the Murine Ovarian Surface Epithelial or MOSE model, and consists of benign cells that do not form tumors, cells that are transitioning to the aggressive disease, cells that can form tumors albeit slowly (slow-developing disease) and those that can develop lethal disease in a very short period of time with few cells (fast-developing disease). In collaboration with Dr. Chris Roberts, we have since then characterized the molecular changes in the ovarian cancer cells that are associated with their progression, and identified important functional categories that could be targeted for the suppression of metastatic disease.
Other information: I am also the co-director of the Cancer Biology Focus of the new Translational Biology, Medicine and Health graduate program.  This is a new doctoral program that integrates genetics, molecular biology with tumor physiology and novel approaches to treat and detect cancer. This is intended to broaden the view of the new cancer researchers of how to tackle cancer.

2.     The cover of VT Magazine was a photo of ovarian cancer cells credited to you. How was the photo taken? How do those cells differ from normal cells?

Researchers usually grow cancer cells on plastic culture dishes for their experiments, taking advantage of the programming of epithelial to attach to a surface in order to grow.  However, ovarian cancer cells metastasize throughout the peritoneal cavity as single cells that can cluster together (sometimes named spheroids or tumor spheres).  When we grow our cells under conditions that prevent attachment, tumorigenic cells very rapidly form these spheroids also in cell culture. Benign cells that cannot form tumors in mice are not able to form spheroids and they will die off over a short period of time. The images were taken of live spheroids with an inverted microscope with 40-fold magnification, documenting the clustering of aggressive MOSE cells.  However, if you put about a million cancer cells into the culture dish, in a few days all of them have aggregated and we are able to see those without magnification.  The images in the article itself show the aggressive cells forming spheroids and –in green- macrophages that loosely associate with those cells. When we inject cancer cells into the mouse and after several days flush the peritoneal cavity and take the cells back out, many cells have aggregated similarly to what is shown in the picture and we are currently using this culture technique for our studies to mimic more closely what is happening in the peritoneal cavity.

3.     The VT Magazine article “Cancer Under Attack- Virginia Tech community forms a strong front against cancer” noted that you are collaborating with virologist P. Christopher Roberts (Virginia-Maryland College of Veterinary Medicine) to develop an animal ovarian cancer model. Tell us more about that research. Which animals are you using? Are the studies conducted in vitro or in vivo? How will this model help you discover the initial changes that occur when cancer develops?


As mentioned above, Dr. Roberts was instrumental in the generation of the progressive MOSE model.  This model can be used in 2D and 3D tissue culture but also can be injected into mice with a functioning immune system (syngeneic model= the cells were derived from C57BL6 mice that are also used for all our in vivo cancer studies). This is a unique model in that we can compare benign, transitional and aggressive cancer cells both in vivo and in vitro (this is limited to tumorigenic cells as the benign cells do not form tumors).  Dr. Roberts has also isolated the stem-like cells of these lines and we are beginning to investigate those since these are critical for tumor recurrence.  In collaboration, we have shown the genetic changes that are important in ovarian cancer progression, focusing on the differing cellular organization and the metabolism of these cells since most genes that are differentially expressed in the aggressive cells and can be modulated by the sphingolipids are in these functional categories. These studies are critical in order to identify targets for the sphingolipids or other drug treatments to prevent metastasis, and, most importantly,  to control the efficacy in future human trials. 
We are at this point not trying to prevent primary ovarian cancer but are focusing  on the characterization of cellular and molecular factors that are critical for progression and metastasis since most women die of recurrent disease. Dr. Roberts’ expertise in virology and vaccine development has led to the generation of ovarian cancer cells that express various anti-cancer cytokines on their surface.  In a just accepted paper in the Journal of Interferon and Cytokine Research we report that the local expression of IL-12 on the cancer cells reduced their tumorigenic potential and impacts the immune cell profile in the main site of ovarian cancer metastasis, the omentum. This is important because while IL-12 has been used before to suppress tumor growth, the systemic administration leads to severe side effects – the local expression in the omentum, however, does not.
Epidemiological studies have demonstrated that obesity - specifically in the increase in abdominal (visceral) fat- is associated with an increase risk of metastatic ovarian cancer and a lower survival rate.  We are interested in the changes in the peritoneal cavity that convey or contribute to the increased risk, using the MOSE model to characterize specific changes that could support tumor cell adhesion and outgrowth. Again, any identified molecular mechanism could be used as a drug target to prevent secondary tumor outgrowth after the removal of the primary tumor.  Dr. Roberts was also instrumental in the design and analyses of these studies, investigating changes in inflammatory markers associated with obesity and obesity-mediated disease.  We have since characterized the immune profile of the omentum in virgin and parity mice and showed differences that could contribute to a lower risk in the parity group; epidemiological studies have also shown that child-bearing lowers the risk of ovarian cancer. Currently, we are investigating if and how obesity alters the conditions in the peritoneal cavity to support metastatic growth.

Tomorrow's post will discuss Dr Schmelz's research on 
-->synthetic sphingolipid metabolites, the role they play in ovarian cancer and what avenues of research she finds most exciting. 

Dee
Every Day is a Blessing!  

Monday, August 10, 2015

Paying it Forward- 7 years

This arrived in the mail from Cancer Hope Network .


I love the sentiment on the front. Then I opened it and saw that it was a thank-you for the seven years I have been a support volunteer. Wow! I remarked to my husband that it sure hasn't seemed like seven years.

Back in 2005 I was upset. I knew the statistics about women diagnosed with late stage ovarian cancer. Jeez I knew that Gilda Radner died from that disease. I just wanted to talk to someone who had the disease and lived. Heck I didn't even meet any women in my cancer center with the disease. So when I saw a brochure for Cancer Hope Network in the waiting room I picked it up and brought it home. I hesitated at first to call. I'm not too keen on cold calling someone. But one afternoon as I sat in bed I went ahead and called. I told the person who answered that I just needed to talk to someone who had been in my situation and lived. She took all my information and said she would call back when she had a match. The very next day she called and said she could connect me right then and there with a volunteer. I spent the next half hour talking to a women diagnosed with 3b, lived in my state,  had the same chemotherapy and surgery and was a 5 year survivor. It was wonderful. I was not alone. I could survive too!

When I was out of treatment one year I called Cancer Hope Network and said I wanted to be one of their support volunteers. I did training and within a week or two I was talking to other women with ovarian cancer. I have been volunteering ever since. Although I did take a break when I recurred and was back in treatment but once treatment was done I was back on the phone.

I have spoken to women from NYC, Florida, California, Indiana and Kentucky just to name a few. I have spoken to women treated in the top cancer centers in the country and those going to community cancer centers and oncologists. I have talked to women who are a short ride from their doctor and center and those that drive eight hours or take a plane and stay at hotels when then go for treatment.But each and every time I remark "I felt that way too" the reply is the same " thank goodness I thought it was just me."

Thank you Cancer Hope Network and all their volunteers for supporting those diagnosed with cancer. If you are newly diagnosed with any cancer or a caregiver for someone diagnosed with cancer you may call( 1-800-552-4366 )  or visit the Cancer Hope Network website online  to be matched with a survivor.

Dee
 Every Day is a Blessing !

Friday, August 7, 2015

One Characteristic - Age

 A study looking at characteristics of women who are long-term survivors of ovarian cancer was recently published in the journal  Obstetrics & Gynecology . The study " Characteristics of Long-Term Survivors of Epithelial Ovarian Cancer" is currently pre-published
online and I am happy to say you can read the entire article for free. So I took the opportunity to download the article and read it and looked at the data.


This study is a retrospective study of over 11,500 women in California diagnosed between 1994 and 2001 with epithelial ovarian cancer. The California Cancer Registry was used.  Thirty one percent of the women in the study were long term survivors. Since I reached 10 years of survivorship last month I was interested to see how my characteristics matched those of women in California who were long term survivors. 

The study found the predictors of long-term survival were 
younger age ( 18-50)
early stage 
low grade 
non-serous


Out of all those predictors I have one characteristic - younger age - and I barely made that one. I was diagnosed one month after my 50th. 

I found it interesting that 1/3 of the long term survivors were women who were  late stage /high grade serous. The authors explained this result as better surgical techniques that offered these women advantages as well as possible IP or BRCA mutation status. But that information was not available in the data set studied. 

I appreciate that the authors made note of the issues associated with long term survival. The paper ends with this paragraph- 
Long-term survival may bring its own challenges beyond worry about recurrence. Studies have shown that patients with ovarian cancer are challenged with problems of anxiety, fatigue, sexual, social, and financial problems, which should be amenable to appropriate interventions. These studies highlight that physicians, especially those who provide primary care, should be prepared to address cancer survivor- ship needs in this group of patients.
"

It would be interesting to see if similar studies were conducted in other states if the characteristics would be the same. 
Dee
Every Day is a Blessing!