This is a personal website page. I'm in the habit of putting my professional work on the web (www.wayfinding.net), and many of my hobbies as well. This is more personal than usual, but I'll post the notes anyway in case they are helpful for others (these ARE my notes). This is not the work of researchers, doctors, or cancer experts. You cannot be sure that interpretations below are correctly stated or understood. The intention is simply to track news items over time- as they pop up on the internet. There are several sites that do this nicely, but few provide personal input or interpretations/speculations; just be aware that these are my thoughts and not facts.
I am especially worried that people may come to this site and take the alternatives section too seriously. If alternative therapies worked consistently, then the disease would disappear. Please don't decide to forgo medical help and just do diet or supplements; that seems a recipe for disaster (personal opinion). On the other hand, if the conventional therapies worked- the chemo and surgery- the disease would also have disappeared. It has not been cured, so patients do everything they can think of to address their disease. Eating healthy, drinking lots of water, this is what we are supposed to be doing anyway.
As time passed, I received occasional emails from people across the globe who came to this web site. These individuals have personal experience with ovarian cancer; they added to the knowledge on this web site. I want to thank these people for their insights. I'll continue to add to the site as I hear from people. In particular, I have received detailed information from Anne Helman (Needham, Massachusetts). Anne established the "Anne Rogal Helman Ovarian Cancer Fund" dedicated to raising money for quality of life research, for women in financial need, and for promoting awareness of the risks and symptoms of Ovarian Cancer. I urge you to visit Anne's non-profit organization.
Anne died in May 2006. Her website remains where she left off. I'll leave the link as it is in tribute to her and in the hope that someone will take over where she left off.
"After she was diagnosed with ovarian cancer in February 2003, went through surgery, treatment and remission, Helman's cancer recurred in May 2004. Her humanitarian spirit kicked in, and Anne established the fund to provide support for a three-year, quality-of-life study for ovarian cancer patients." (Massachusetts General Hospital statement). "The online guest book for Mrs. Helman's newspaper death notice has postings from states across the country and from the Netherlands -- many from people she had contacted about ovarian cancer, and who had received her information kits." (Boston.com News).
One of the best (maybe the best) way to understand ovarian cancer and to find support is through the ovarian cancer listserve. Here you can ask questions and get accurate and emotionally honest answers from other women who have the disease (you can just "lurk"- listen in on conversations if you want):
This page got quite large as time rolled on, so I decided to break it into quick access links. I also added my internal search engine. Just be aware that this software engine searches my whole web site which has genealogy, blindness, and other personal documents; if you get some weird result, try again with different terms.
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If you come to this page after just discovering that you have ovarian cancer, understand that your surgery should be done by a gynecological oncologist; a specialist in both the female reproduction system and cancer. These specialists do a very thorough exploration and eradication (called de-bulking) of all the cancer that they see. They also rinse the body cavity in solutions that kill microscopic cells that are "free" in the abdomen. This initial surgery goes a long way toward extending your life and preparing the body for the chemotherapy to follow.
Research in 2005 showed that the most effective treatment for advanced ovarian cancer was a combination of intravenous chemotherapy along with high doses of chemotherapy dripped directly into the abdomen. This procedural change was shown to have significant survival benefits.
Ovarian cancer is divided into four stages.
In stage 1, the cancerous growth is limited to the ovaries. If there is free abdominal fluid (ascites) containing cancer cells, then it becomes Stage Ic.
Stage II growth is limited to the pelvic organs. This indicates spread to nearby structures. If the uterus or fallopian tubes are involved, then it is stage IIa; if other nearby tissues are involved, it is stage IIb; and again, if there is free abdominal fluid containing cancer cells, the stage becomes IIc.
In stage III the growth is limited to the abdominal cavity. Here the tumor involves other organs in the abdomen.
Stage IV the growth involves some distant structure. This stage indicates cancerous involvement away from the abdominal cavity, such as in the chest cavity or neck lymph nodes.
As you read the depressing statistics about life expectancy with ovarian cancer, understand two things. First, these are backward-leaning statistics; they tell us how things were in the past. New drugs and therapies come out every month (it seems), and these statistics get less predictive as the days roll forward. Secondly, there is a "left over" fear from the days when a diagnosis of ovarian cancer meant death in a predictable number of months. Now, the disease is chronic. That is not such a good thing either, but it beats the alternative by a life time. Stay positive. This disease will become more and more "manageable" as the years unfold.
Ovarian cancer is a very difficult disease to completely wipe out. Seventy percent of the time, the disease returns, even after remission and successful first treatments and surgery. What looks like a "long term battle" can better be described (tolerated emotionally) as "living with cancer". Modern medications control most side affects, so it is possible, no matter how many times the cancer returns, to live a normal, happy, and quality life between the treatments- that is our observation at this time in our understanding of the disease (it may not be true for everyone, of course, but we wish you well)......
The current standard of treatment (carboplatin and paclitaxel) for patients with advanced ovarian cancer has been established in light of the results from various clinical trials. After debulking surgery, a combination of carboplatin and paclitaxel is considered to be the best treatment option in terms of survival and quality of life (November, 2005). However, since most patients on this chemotherapy will experience relapse, several studies have explored, and continue to do so, various modifications and alternatives to standard therapy in order to attain improved efficacy. Various modifications of dose, schedule, or route of standard regimens have shown no benefit, apart from intraperitoneal therapy, which has produced mixed results.
Recurrent disease is complicated by the development of drug resistance by the tumor cells. The chemical process describing this resistance is "methylation". In this process, genes that support a positive response to chemotherapy are shut down by the cancer cells at some time in the treatment phase. Clinical trials are underway to use de-methylation agents combined with chemotherapy to see if drug sensitivity can be restored. Telcyta is an example of this kind of drug.
Studies of maintenance/consolidation therapy have been mainly negative, although a small number of trials have produced enough positive data to prompt new studies powered to detect survival benefits. Various phase II trials have investigated "targeted therapies," but until now no positive results have been recorded. Translational studies are needed to identify patients who will benefit from such specific treatment strategies. The current most evaluated modification of standard therapy is the addition of a third non-cross-resistant drug to carboplatin and paclitaxel. Data for the addition of anthracyclines have either been negative (epirubicin) or not yet analyzed (pegylated liposomal doxorubicin), while evaluable data are shortly expected for the addition of topotecan. Data on the addition of gemcitabine are eagerly awaited from two phase III trials.
For those patients who have recurrence of disease at least 6 months after initial therapy, the paclitaxel-platinum combination has been shown to be a superior treatment to platinum monotherapy; in other words, you are "platinum sensitive" and can have the same therapy again and again as long as it works. However, many patients develop clinically relevant neurotoxicity (allergic reaction), frequently resulting in treatment discontinuation (with platinum based drugs).
Allergic reactions to Carboplatin occur usually after the 6th treatment. My wife (Katherine) developed an allergic reaction after her 18th treatment- so it varies widely, I guess. There is a desensitizing protocol being done br Dr. Ursu la Matulonis at Dana Farber Hospital in Boston. If you get desensitized (whatever this means?) you can do carbo treatments again. (I am getting a lot of this information from Anne Helman in Boston).
The side affects of carboplatin and paclitaxel (current first-line treatments of choice in 2005) differ with individual circumstances. One very common side affect is "chemobrain"; a usually temporary mental response that comes after treatment- found in other cancer regiments besides ovarian; breast cancer for example (sometimes lingering after treatments end). It is characterized by various degrees of memory problems, concentration difficulties, and occasional confusion. Under investigation in 2005, was a medication called d-MPH (Beth Israel Cancer Center, New York) that was effective in combating fatigue and chemobrain in a 14 month study.
If you experience clumsiness, tingling and numbness in your limbs, loss of positional sense, or hearing problems during your treatment, you are probably experiencing peripheral neuropathy. Patients who take drugs such as Taxol, Cisplatin, Paraplatin and Hycamtin (Topotecan) have a higher risk of suffering from it. The symptoms are exacerbated in those who have a longer chemotherapy treatment series or faster treatment series. You can help prevent injury from these nerve problems by stretching your hands and feet often, protecting your feet with sturdy, non-slip shoes, and being extra careful with sharp objects. Acupuncture treatments and massage therapy ease neuropathy and produce general well-being. Herbs such as ginkgo biloba and blue-green algae, and vitamins such as B-6, B-complex, B-12, B-3, and E help ease side effects. To find out what combinations could work for you, see an herbalist or nutritionist. Also, keep yourself as hydrated as possible during and after chemotherapy.
One of the major problems with diagnosis and treatment of ovarian cancer is that it is not a single disease. Each form of the disease has its own unique behavior. Researchers at the University of Texas Department of Molecular Therapeutics (April 10, 2005 Journal Nature) explained how and why different forms of ovarian cancer evolve. There are three kinds of epithelial ovarian cancer, each with a very distinctive cell shape: serous; endometroid; and mucinous. A specific kind of gene called a HOX gene is involved (MD Anderson Study) in activating these cancer types. HOX genes direct immature embryonic tissue to form various body structures during development. They normally shut off after doing their job. HOX genes get reactivated in ovarian cancer. The HOX genes are sensitive to estrogen and progesterone levels, so that abnormal surges in these hormones may "turn on" ovarian cancer. Most of the known risk factors for ovarian cancer are related to levels of estrogen and progesterone. The individual cancer cell types (unique shapes) are activated by HOX gene varieties A9, A10, A11 and A7. Turning on the HOXA9 gene causes tumors that resemble serous cancer.The HOXA10 genes cause an endometroid look-alike cancer cell. HOXA11 genes resemble mucinous ovarian cancer. Activation of HOXA7 results in low-grade, less aggressive tumors. .
The CA-125 blood test is an important marker in the identification of ovarian cancer. It is quite often highly elevated when active disease is present (usually before surgery). There are false positives and false negatives with CA 125 testing, so it is not a reliable marker for diagnosing and screening for ovarian cancer. It is, however, relatively accurate for indicating a recurrence. When the CA-125 number starts to rise, and moves above the normal 35 mark, cat scans are done to locate lesions, and chemotherapy is begun as soon as possible (if lesions show up on the scans).
It is important to understand (this information from Anne Helman) that the CA 125 number varies considerably depending on the individual. It is not always an indicator of recurrent disease, nor does it indicate the absence of cancer. Doctors used to routinely do second look surgery. What they found was that even when CA 125 levels were normal, and when cat scans were normal, 40% of the time (our doctor's comment) surgery showed that the disease was still in the body. CT/PET scans, for example, can show active disease even when all other indications are negative. Also, some women whose cancer starts out expressing CA 125 values that are reliable enough to determine diagnosis or recurrence, over time, find their cancer stops producing the antigen, or produces it at a slower rate.
(Anne Helman) The use of positron emission tomography (PET) with the radio tracer fluorodeoxyglucose (FDG) is “under utilized” in diagnosing and treating cancer of the reproductive organs—the cervix, uterus, ovaries, fallopian tubes, vagina and vulva—according to an article in the November 2005 issue of the Journal of Nuclear Medicine. Doctors are beginning to see the potential of using PET to look inside a woman’s body to find gynecologic disease and its progression—and to follow how a treatment works. PET imaging with FDG is having a “great impact” in determining the extent of spread of cancers of the reproductive system, especially when doctors get ambiguous results from other conventional imaging tests such as ultrasound, magnetic resonance imaging (MRI) or computed tomography (CT). Some studies have shown that PET imaging with FDG is “superior” to CT or MRI in detecting recurrent ovarian cancer.
There is a special technology where a cat scan is combined with a PET scan, called a ctPET. Some doctors believe it to be the best tool for seeing ovarian cancer in the body. The PET component picks up seeding and microscopic activity; particles too small for the cat scan to detect. If there are microscopic remnants of the disease they will only be detected with the PET scan. PET does not however show tumor detail as clearly as the cat scan. Combining the two technologies allows the visualization of microscopic activity overlaid on mass tumor detail.
Doctors may be reluctant to use PET scans if they feel that additional imaging would add nothing to what they already know, especially since PET scans cost over $4,000, compared to the CAT scan at $1,500, and ultrasound at $400. PET scans would probably show additional disease, just as second look surgery would. The doctors know there is no cure for ovarian cancer at the moment. When the cure comes, the microscopic disease will go away. That being said, you, as the patient, may want to know the full details of your disease. If you ask for a PET scan, the doctor will probably be supportive (as is our doctor).
I like Anne Helman's personal comments on PET scans: "A ct/pet scan (or pet) would show you things that are less than one cubic centimeter in size, i.e. microscopic seeding. This microscopic stuff is dangerous and aggressive, and not uncommon in ovarian cancer. It can cover organs faster than one can blink an eye. So, be forewarned; you think, for example, there are only 2 lesions - if you get a pet scan it may show stuff in other areas and while you want to know what's going on, at the same time it's unnerving. The first time I saw my disease on a combined ct/pet (on the doctor's computer screen), it flipped me out because there was then no denying what was going on. And, knowing where it is, seeing it, well, it brings it crashing down around you. It took me a long time to process it. I would still ONLY have ct/pet scans though because they do give a more complete picture of what's going on.
Promising new medications pop onto the radar screen almost monthly, while last months hopefuls move slowly through the clinical stages (it takes years to go through phases one, two, and three, unless a drug is "fast-tracked" by the FDA (in the United States)- because it shows so much promise). Many times, promising drugs move through the clinical trials only to be found no better than the current line of treatment. Sometimes the side affects eliminate drug candidates. The press tends to hype everything, raising the world's expectations, but most of these press announcements have to do with initial animal studies. All kinds of drugs wipe out cancer in petri dishes and in rats. But they fail in humans. Some of the newer drugs avoid the harsh effects of chemo therapy; they use injections or pills. Below are some examples of promising treatment strategies:
1. Vaccines against cancers, including ovarian, are being studied and tested. Genetically modified viruses can be designed to attack individual, patient-specific tumors. It sounds too good to be true, and right now it hasn't arrived, but it is a very exciting line of research with great promise.
2. Cancer cells are very good at directing the body to make the blood vessels that are needed to nourish rapidly growing cancer tissues. There is now considerable support for the idea of attacking cancer on two fronts, directly using chemotherapy and indirectly by cutting off the blood supply to the tumor. Cancer cells produce cytokines that stimulate growth of vessel buds around the cell- this process is called angiogenesis. Scientists are working on several promising drugs that shut down cancers ability to make abundant blood vessels- thus starving the cancerous tissue. One of the drugs under investigation (for example) is called A6 (being studied by two dozen centers in the USA as of April, 2005). A6 is in clinical trials to determine if it can prevent recurrence of ovarian cancer. Patients in clinical trials give themselves injections of the drug daily. A6 was also showing encouraging responses in Phase One trials involving patients with advanced ovarian cancer.
3. Cancer cells, ovarian included, over-produce telomerase inside the cell. The biotech firm Geron has the patents on this line of research. They are working on vaccines to identify and destroy "telomerase saturated" cells, and they are developing compounds that are anti-telomerase drugs. This is a global cancer approach. Several research companies have identified specific cancer cell characteristics and they are exploiting these eccentricities of cancer tissues to make drugs that target cancer cells (and leave normal cells unaffected).
4. Cytotoxic agents are designed to prevent the replication of cells that divide rapidly (like some cancer cells, including ovarian). Caelyx is an example of this kind of drug, as are the platinum based drugs like Carboplatin.
5. Debulking surgery and paclitaxel/carboplatin chemotherapy induce good initial responses in most patients, although most cases of advanced disease are not controlled. Monoclonal antibodies hold promise as a potential incremental advance for the treatment of the disease. Antibodies can be used to stimulate the immune response, target tumor-specific receptors to induce antibody-dependent cellular cytotoxicity or interfere with biologic pathways. They can also be used to deliver therapeutic radioisotopes to malignant cells. Oregovomab is in Phase III clinical trials as a consolidation treatment post front-line therapy to trigger tumor-specific cellular immunity. Bevacizumab, which blocks vascular endothelial growth factor, will be entering Phase III as an adjuvant to front-line chemotherapy with a direct effect on angiogenesis. Additional immunostimulating, immune counter-regulatory and receptor-targeting approaches are also under review. The family of epidermal growth factor receptors including epidermal growth factor receptor 1 (HER-1) and 2 (HER-2) are both expressed in ovarian cancer and are the subject of ongoing research.
Standard (2005) initial chemotherapy uses a combination of the following:
1. A platinum-based agent, such as carboplatin or cisplatin. Carboplatin is preferred over cisplatin in the combination because carboplatin is as effective as cisplatin but is less toxic and can be administered in a more convenient, outpatient regimen. Patients with relapsed ovarian cancer, but who respond positively to repeated regiments of the standard treatment are referred to as platinum-sensitive. Patients are considered platinum-sensitive if recurrence occurs more than six months after remission induction. If the standard treatment does not halt the progression of the disease or if recurrence happens before six months then patients are referred to as platinum-resistant, and they would be put on alternative treatment strategies.
2. A taxane, such as paclitaxel (Taxol) and docetaxel (Taxotere). Currently, paclitaxel is the drug most often used as initial therapy in combination with a platinum agent. Docetaxel, however, is less toxic to the nervous system (but has more adverse effects on blood cell production). Taxotere is commonly substituted for Taxol.
The healing properties of Taxol were known to at least one community long before Western medicine recognized the drug's potential. According to an article in the Sept. 4, 1991, Journal of the American Medical Association, around the turn of the century, a British official in the Indian subcontinent noted that parts of the European yew, Taxus baccata, were used in an Indian clarified butter preparation for treating cancer.
It wasn't until 1962, however, that the U.S. Forest Service delivered crude bark extracts of the Pacific yew, Taxus brevifola, to the National Cancer Institute. A series of NCI experiments showed the extract was effective against several kinds of cancer in mice.
In 1971, researchers at the Research Triangle Institute in Durham, N.C., isolated Taxol from the extract, but interest in the compound waned until the mid-1970s. In 1979, a researcher at Albert Einstein College of Medicine in New York described how Taxol works to defeat cancer by inhibiting cell division.
Today, Taxol--alone or in combination with other drugs--is being studied for a wide variety of adult and childhood cancers. In July 1992, FDA authorized use of the drug for ovarian cancer under a "treatment IND." Treatment INDs permit earlier and wider access to experimental drugs by patients with life-threatening conditions for which there is no satisfactory treatment.
Taxol was approved in December, 1992 for advanced disease unresponsive to other therapies. The drug was approved in a record five months.
Most clinical trials are designated as phase I, II, or III, based on the type of questions that a study is seeking to answer:
In Phase I clinical trials, researchers test a new drug or treatment in a small group of people (20-80) for the first time to evaluate its safety, determine a safe dosage range, and identify side effects.
In Phase II clinical trials, the study drug or treatment is given to a larger group of people (100-300) to see if it is effective and to further evaluate its safety. Only 30% of all drugs make it past Phase Two trials.
In Phase III studies, the drug or treatment is given to large groups of people (1,000-3,000) to confirm its effectiveness, monitor side effects, compare it to commonly used treatments, and collect information that will allow the drug or treatment to be used safely. Only 67% of all drugs make it past Phase Three.
These phases (in the United States) are defined by the Food and Drug Administration in the Code of Federal Regulations.
You should have this book in your library: "Ovarian Cancer: Your Guide to Taking Control", by Kristine Conner and Lauren Langford; May 2003 first edition
Dancing with Cancer; By Priscilla Grover
Anne Rogal Helman Ovarian Cancer Fund Anne is a wealth of intelligent information and she freely and kindly shares her knowledge.
The Ovarian Cancer National Alliance has a newsletter, and they host a yearly national conference.
My wife has a favorite poem by Jack Gilbert (it was in the New Yorker Magazine); it is very special to her (me too). Maybe it can be special for you as well; I'll share it and hope Mr. Gilbert approves of this use of his excellent poetry.
Sorrow everywhere. Slaughter everywhere. If babies
are not starving someplace, they are starving
someplace else. With flies in their nostrils.
But we enjoy our lives because that's what God wants.
Otherwise the mornings before summer dawn would not
be so fine. The Bengal tiger would not
be fashioned so miraculously well. The poor women
at the fountain are laughing together between
the suffering they have known and the awfulness
in their future, smiling and laughing while somebody
in the village is very sick. There is laughter
every day in the terrible streets of Calcutta,
and the women laugh in the cages of Bombay.
If we deny our happiness, resist our satisfaction,
we lessen the importance of their deprivation.
We must risk delight. We can do without pleasure,
but not delight. Not enjoyment. We must have
the stubbornness to accept our gladness in the ruthless
furnace of this world. To make injustice the only
measure of our attention is to praise the Devil.
If the locomotive of the Lord runs us down,
we should give thanks that the end had magnitude.
We must admit there will be music despite everything.
We stand at the prow again of a small ship
anchored late at night in the tiny port
looking over to the sleeping island: the waterfront
is three shuttered cafes and one naked light burning.
To hear the faint sound of oars in the silence as a rowboat
comes slowly out and then goes back is truly worth
all the years of sorrow that are to come.