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Lauredhel is an Australian woman and mother with a disability. She blogs about disability and accessibility, social and reproductive justice, gender, freedom from violence, the uses and misuses of language, medical science, otters, gardening, and cooking.

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7 responses to “Women’s health: Are we taking a risk by dumping the Democrats?”

  1. Barry

    While the demise of the Democrats is a sad loss, you’re completely ignoring the presence of the Greens as the third political force in Australian politics. I predict they will be the voice of reason that is sorely needed in Parliament. Not to denegrate the ALP, but sometimes their judgement can be a little off.

  2. TheDailyMagnet

    I have no idea how long it will take for the new federal government to undo the horrible ‘moral high-ground’ erosion of our rights to adequate healthcare.

    Mary Lander has been unrelenting in her determination to obtain this treatment and for someone who’s health has suffered from the meningioms that is all the more amazing.

    I think she would in fact make an excellent federal health minister and wish – once she’s recovered – that she would join one of the parties and run for election – we’d certainly all be better off with her common-sense approach and can-do-ism.

    The cost should be rebated retrospectively at the very least – the government has a moral obligation to do that not only for Mary Lander, but for all those who have this type of meningioma.

    TheDailyMagnet’s last blog post..Like blamonge through the hour glass

  3. Mary Lander

    Thanks to everyone for their interest. In fact the loss of Senator Allison is a great loss for women’s rights and health matters and she was the only one prepared to run with this issue. Kerry Nettle from the Greens came on board first but unfortunately she has lost her seat as well (she was the one to introduce social issues into the Greens Agenda so I expect they will no longer have that focus). Julia Gillard, the then Opposition Health Minister refused my request to her to tackle this issue and I still have her letter stating just that in response so the initiative came about no thanks to the ALP. However, after Senator Allison ran with it, Julia Gillard then eventually came on board and so did the majority of ALP MP’s voting 74 for and 11 against the amendment to overturn the legal status of the drug. The Liberal National Party Coalition voted predominantly AGAINST changing the legislation.

    How Did your MP’s Vote on Conscience:
    http://www.australiavotes.org/conscience/index.php#allelectorates

    While not outlined in my article in the MJA (due to word count limits), the issue also has implications for senior public sector managers in the Department of Health who think nothing of misrepresenting medical opinions. In this case and in the first instance, by the Chief Medical Officer noting the (then) Minister was also considering the appointment of his wife as the new CEO of a new government organsisation. Nepotism over women’s rights and health issues – see:
    Abortion drug anger
    http://www.news.com.au/dailytelegraph/story/0,20281,17262842-5001022,00.html

    It’s not over yet but I can’t do this alone so thankyou everyone for your support.

    Mary Lander

  4. Anne McGinnis Breen

    Dear Good People,
    I have been in long distance email contact with Mary Lander for a few years. I have faced a similar year long battle with institutional red tape and personal expense starting in March 2004 to take the drug in the USA again for my own similar condition.
    Please read my webpage resources about my personal medical experiences with meningioma and mifeprex the past twenty years using Ru-486 (mifepristone) brand name Mifeprex to control and stop or stall the progesterone related regrowth of recurrent meningioma instead of brain radiation which has been recommended by many neurosurgeons for me since 1992. I am on it again now since Feb 2005, my recent Nov 07 head MRI shows no significant change and no side effects in the almost three years I have been on a small daily dose 200 mg of the “early option pill” this time. THANK GOD

    Unfortunately, the same political/religious ideology opposition to the drug in the United States has prevented thousands of other meningioma patients from being told by their doctors of this possible alternative to brain surgery or brain radiation for their condition. I believe if I had been offered this drug after its discovery and successful use in France and Germany in the mid 1980’s for meningiomas after my first craniotomy in 1986, I might never have had a recurrence of this brain tumor in 1992 or the other benign uterine fibroids removed by total hysterectomy in 1992 or needed the second craniotomy in 2000.

    http://journals.aol.com/anne91547/anne-mcginnis-breens/articles/

  5. Mary Lander

    Thanks Laurel,
    I thought it interesting to note that the Department of Health “could see no reason to change the status of this drug” (as per their own advice to the Minister), yet if you look at breast cancer as another example noting that women with progesterone receptor positive (PR+) breast cancers have an increased risk of mortality of 1.5 – 2.1 fold as per recent findings below. Alas, mifepristone (also called RU486), the most effective progesterone antagonist and one that would be suitable to use for PR+ breast cancers is not readily available. The patient would need to pay the full cost of the drug mifepristone themselves and obtain it via the Special Access Scheme if they wanted to access it and not only that, but they would have to wait until they have exhausted other treatments first and could die within a matter of months to be eligible via the Special Access Scheme at which time the cancer has spread so extensively it’s a moot point as to whether anything can save them at that stage.

    Question: Why would Australian women need to wait that long to access the drug mifepristone?
    Answer: Because the Australian governmement has not done clinical trials using the drug here?
    Question: How many women die of breast cancer every year?

    By way of a comparison, through which I can demonstrate the disparity that exists, depending on the hormone status of a cancer, those women with ER+ breast cancers can get tamoxifen (an oestrogen antagonist) via a prescription for ER+ breast cancers and that drug is subsidised and available to them at any time (it’s not necessary for those women to wait until they are on their death bed to get it). Quite a different story for those women with PR+ breast cancers (they have a 1.5 – 2.1 fold increased risk of mortality). The drugs work in similar ways just on different hormones. Is it fair that women with PR+ breast cancers should be disadvantaged simply because the drug that could help them is caught up in controversy due to another of the drug’s uses?

    Also might be worth noting that recent studies have shown promise using mifepristone for familial types of breast cancer such as that which result from the BRCA-1 gene as well as those breast cancers that are ER+/PR+ and for use on a subset of this combination of hormone receptors that are antiestrogen resistant.

    Hormone Receptor Status, Tumor Characteristics, and Prognosis: A Prospective
    Cohort of Breast Cancer Patients

    10 April 07
    http://www.medscape.com/viewarticle/553850
    Results: Compared to ER+/PR+ cases, elevations in risk of mortality were observed across all subcategories of age at diagnosis, ranging from 1.2- to 1.5-fold differences for ER+/PR- cases, 1.5- to 2.1-fold differences for ER-/PR+ cases, and 2.1- to 2.6-fold differences for ER-/PR- cases. Greater differences were observed in analyses stratified by grade; among women with low-grade lesions, ER-/PR- patients had a 2.6-fold (95% confidence interval [CI] 1.7 to 3.9) to 3.1-fold (95% CI 2.8 to 3.4) increased risk of mortality compared to ER+/PR+ patients, but among women with high-grade lesions, they had a 2.1-fold (95% CI 1.9 to 2.2) to 2.3-fold
    (95% CI 1.8 to 2.8) increased risk.

    1998 – Additive effect of mifepristone and tamoxifen on apoptotic pathways
    in MCF-7 human breast cancer cells:
    http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9879777&dopt=Abstract
    “Our data further suggest that a combination of an antiprogestin with tamoxifen may be more effective than tamoxifen monotherapy in the management of human breast cancer.”

    2006: Prevention of Brca1-mediated mammary tumorigenesis in mice by a
    progesterone antagonist.
    http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=17138902

    Women with mutations in the breast cancer susceptibility gene BRCA1 are predisposed to breast and ovarian cancers. Why the BRCA1 protein suppresses tumor development specifically in ovarian hormone-sensitive tissues remains unclear. We demonstrate that mammary glands of nulliparous Brca1/p53-deficient mice accumulate lateral branches and undergo extensive alveologenesis, a phenotype that occurs only during pregnancy in wild-type mice. Progesterone receptors, but not estrogen receptors, are overexpressed in the mutant mammary epithelial cells because of a defect in their degradation by the proteasome pathway. Treatment of Brca1/p53-deficient mice with the progesterone antagonist mifepristone (RU 486) prevented mammary tumorigenesis. These findings reveal a tissue-specific function for the BRCA1 protein and raise the possibility that antiprogesterone treatment may be useful for breast cancer prevention in individuals with BRCA1 mutations.

    2004: Mifepristone Induces Growth Arrest, Caspase Activation, and Apoptosis
    of Estrogen Receptor-Expressing, Antiestrogen-Resistant Breast Cancer Cells
    http://clincancerres.aacrjournals.org/cgi/content/abstract/10/15/5215
    “We demonstrate that: (a) estrogen receptor+progesterone receptor+, 4-OHT-resistant clonal variants can be isolated from an MCF-7 cell line in the absence of antiestrogen selection; and (b) MIF and MIF plus 4-OHT combination therapy induces growth arrest and active cell death of the antiestrogen-resistant breast cancer cells. These preclinical findings show potential for a combined hormonal regimen of an antiestrogen and an antiprogestin to combat the emergence of antiestrogen-resistant breast cancer cells and, ultimately, improve the therapeutic index of antiestrogen therapy.”

    Also note: The research shows that the mild antiglucocorticoid effect of
    mifepristone could also help to stop metastatis in some breast cancers
    (effects are dose dependant). Previous studies have demonstrated that 58% of
    all and 85% of invasive breast carcinomas expressed CSF-1R and this study
    shows that RU486 (mifepristone) therefore has the potential to prevent
    invasiveness (metastatis) by acting on CSF-1R:

    1985: [Glucocorticoid receptors and the histological structure of breast cancer]
    http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=2581364&dopt=Abstract
    Glucocorticoid receptors (GR) were studied in tumor cytosols from 140 breast cancer patients. The level of GR depended upon tumor histology. The highest GR level was found in medullary cancer, while the lowest–in a mucinous one. The GR level in ductal-invasive cancer was significantly higher than in the lobular infiltrative type. The frequency of GR in tumors of the 1st grade of malignancy was significantly lower than in those of the 2nd and 3rd grade of malignancy. The 1st grade of malignancy tumors which contained GR had estrogen and progesterone receptors, too. The increasing malignancy was matched by the rising percentage of such tumors which was as high as 47% among 3rd grade of malignancy tumors.

    2003: Glucocorticoid Cotreatment Induces Apoptosis Resistance toward Cancer Therapy in Carcinomas1
    http://cancerres.aacrjournals.org/cgi/content/full/63/12/3112

    a.. ….In this study, we have shown that application of GCs renders
    certain tumors resistant or less susceptible to apoptosis after cancer
    therapy. This finding urges to carefully reconsider the widespread use of
    GCs in almost all treatment protocols for patients with solid cancers. In
    the clinical setting of cancer therapy, e.g., in antiemetic regimens,
    corticosteroids are usually given transiently to suppress acute side effects
    of cancer therapy. Although our experiments did not mimic precisely the
    clinical situation because we administered DEX daily to achieve steady-state
    levels, short-term exposure to DEX may nevertheless be sufficient to
    abrogate or diminish the efficacy of concomitant chemotherapy in cancer
    patients in vivo. This is suggested by our experiments where DEX was found
    to down-regulate basal and cisplatin-induced expression of apoptosis
    effectors within 24 h in vitro. Also, endogenous levels of GCs and those
    existing as a consequence of administered hormones may render solid tumors
    less susceptible to apoptosis after cancer therapy. The administration of
    steroid/receptor agonists such as RU486 might be beneficial before
    chemotherapy and radiotherapy to enhance cell death of solid tumor cells.

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