cervical cancer first, then breast

Colon cancer, then breast. Told that even tho it is not a met, it is related. Is your BC hormone positive? Sounds like a STUDY to me!!!!
Hugs, Kathi

it can be so hard sometimes finding the real answer to ur very real question. Maybe try e-mailing or calling the american cancer society at a primary location and they can say something, i bet, or refer u to where u can get the info.

Just a thought, and how r u today karenack? besides all this stuff, i mean. i've decided to wake each day and throughout the day be grateful for and really allow myself to enjoy them too, if possible, with 5 things.1st one today was, how much i enjoyed how my dog slept next to me all night because she knew i was worried and upset again,i had her hot 'lil body protecting me, hehe, silly but so heartwarming. so, my very strong and courageous ladies, many (((((((((((hugs)))))))))))) and prayers, kathydaly

I was diagnosed with breast cancer, stage 1, in 2002, and then with lung cancer in August of this year, also stage 1. I've read that those folks who get one cancer should be told that their chances of getting a second cancer(not including mets) are higher than the general population. I would love to see a study determining if those folks who get multiple kinds of cancers have any genetic similarities--it might lead to some genetic similarities that lead to cancer and when blocked stop cancer from happening. Haven't seen it so far though. As a matter a fact, I found out that I can't participate in clinical studies on breast OR lung cancer now since having 2 kinds of cancer would confound the study. Is that an insult or what!!! But the pulmonologist who told me that I was knocked out of the lung study was kind enough to tell me what they're currently testing as a lung cancer preventitive and how much to take. I guess you could say I ended up getting the experimental drug guarenteed, which might be better than being in the study, if it works anyhow. Good luck on your search!

karenack said:

Hi Cabbott! I had talked to my oncologist about finding this information and he told me exactly what you are saying about being excluded because of having cancer before. That really sucks because I am wondering....is there something about me that makes me prone to cancer? Kathi M., you had asked me if my bc was estrogen positive and yes it is both estrogen and progesterone positive. I also have a hx of ovarian cysts and my oncologist is wanting me to consider having them removed. They left them after my cervical cancer surgery. I have a cyst now about 2 cm (showed up on CT), I have had it for a few weeks and the pain just keeps getting worse. I have ended up in the ER before from the pain. I hope tonight is not one of those nights. Anyway, I just want them out. I am afraid that will be where the cancer goes next.

I avoided getting a hysterectomy and my ovaries out for the longest time. I had been diagnosed with the breast cancer and got lots of cysts while on tamoxifen. None of them were so painful I ended up in the hospital, but the doctors kept worrying about ovarian cancer which can be related to breast cancer in some people. After two years I got tired of all the ultrasounds (we are talking about the internal kind, not just a take off your top kind for the breast sort). No pain, but it was worrisome and I didn't like having tests all the time. Anyhow, I finally took the time one summer to get everything out. I needed about a month to recover, but everything went well. Yes, I have hot flashes, but that's been the only side effect that stayed around. It made it so that I could take aromosin (exemestane) which is not available to premenapausal women. And now I have very little chance of getting either ovarian or uterine cancer, not to mention no more ultrasounds sans panties. I do need to take calcium supplements and exercise lots to keep from losing too much bone. But the worst of my fears about hysterectomies never materialized. I really worried before the operation if everything else would work like it should if I had the operation. It does. And now I don't have to worry about cancer there. If you are considering a hysterectomy or just ovaries out, read up on your choices (there's several ways they can do it) and go for it.

karenack said:

Hi Cabbott! I had talked to my oncologist about finding this information and he told me exactly what you are saying about being excluded because of having cancer before. That really sucks because I am wondering....is there something about me that makes me prone to cancer? Kathi M., you had asked me if my bc was estrogen positive and yes it is both estrogen and progesterone positive. I also have a hx of ovarian cysts and my oncologist is wanting me to consider having them removed. They left them after my cervical cancer surgery. I have a cyst now about 2 cm (showed up on CT), I have had it for a few weeks and the pain just keeps getting worse. I have ended up in the ER before from the pain. I hope tonight is not one of those nights. Anyway, I just want them out. I am afraid that will be where the cancer goes next.

You could be a candidate for this drug and you can obtain it via the US FMF's Compassionate Use Program:

Their website link is:
http://feminist.org/rrights/compassionateuse.asp

2000: Phase II study of mifepristone (RU486) in refractory ovarian cancer.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10831354&dopt=Abstract
• “Mifepristone has activity against ovarian cancer resistant to cisplatin and paclitaxel. The drug is well tolerated. Further studies need to be performed when this drug becomes more widely available in the United States.”


2000: RU486 increases radiosensitivity and restores apoptosis through modulation of HPV E6/E7 in dexamethasone-treated cervical carcinoma cells
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10739708&dopt=Abstract
“RU486 reverses glucocorticoid-dependent upregulation of HPV E6/E7, which corresponds to restoration of p53 expression, and restores radiosensitivity and apoptosis following gamma-irradiation. Therefore, it appears that along with radiation, RU486 may be a beneficial agent in the treatment of hormone-reactive cervical tumors.”


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.”


2003: Study of effect of mifepristone on apoptosis of human ovarian cancer cell line 3AO
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&list_uids=14728868&dopt=Abstract
• “Mifepristone inhibited significantly the proliferation and induced the cell apoptosis of cell line 3AO in dose-time dependent manner in vitro. The anti-tumor effect was related to down-regulation the expression of PR protein and bcl-2 protein, and to up-regulation the expression of p53 protein of 3AO cells.”

2003: Enhancement of antitumor effect of cisplatin against human ovarian carcinoma cells by mifepristone in vivo.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12651241&dopt=Abstract
• “At a non-toxic dose, RU486 may enhance the sensitivity of tumor cells to cisplatin in vivo, possibly through the mechanism of inhibiting GcS expression at the mRNA level.”

2003 - Study on the treatment of high dose mifepristone and progesterone in endometrial carcinoma
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14680611&dopt=Abstract
• “The study indicates that high dose progesterone could inhibit the growth, promote apoptosis and inhibit metastasis of endometrial carcinoma, MIF could inhibit the growth and promote apoptosis, MIF + MPA could more strongly inhibit the growth, promote apoptosis and inhibit metastasis of endometrial carcinoma than MIF or MPA, and synergistic effect was observed on the expression of PCNA, ER, PR, bax and bcl-2.”

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.”

2006: Prevention of Brca1-Mediated Mammary Tumorigenesis in Mice by a Progesterone Antagonist
http://www.sciencemag.org/cgi/content/abstract/314/5804/1467
• 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 cancerpreventioninindividuals with BRCA1 mutations.
2003: Glucocorticoid Cotreatment Induces Apoptosis Resistance toward Cancer Therapy in Carcinomas1
http://cancerres.aacrjournals.org/cgi/content/full/63/12/3112

• “....In conclusion, GCs are widely used in high doses in the therapy of leukemias and lymphomas and are also used as antiemetics or preservatives for normal cells during chemotherapy of solid tumors. In addition, GCs are among the most widely used anti-inflammatory drugs. 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.