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Estrogen and Lung cancer 2005 study


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dadstimeon actually already posted this. But it is interesting that this connection was made on this board by members before.

http://my.webmd.com/content/Article/100 ... nting=true

Combined targeting of the estrogen receptor and the epidermal growth factor receptor in non-small cell lung cancer shows enhanced antiproliferative effects.

Stabile LP, Lyker JS, Gubish CT, Zhang W, Grandis JR, Siegfried JM.

Department of Pharmacology and Otolaryngology, University of Pittsburgh and Lung and Thoracic Malignancy Program, University of Pittsburgh Cancer Institute, Pittsburgh, Pennsylvania, USA.

Identifying new effective therapeutic treatments for lung cancer is critical to improving overall patient survival. We have targeted both the estrogen receptor (ER) and the epidermal growth factor receptor (EGFR) pathways using an ER antagonist, fulvestrant ("Faslodex"), and the selective EGFR tyrosine kinase inhibitor, gefitinib ("Iressa"), in non-small cell lung cancer (NSCLC) cells. Rapid activation of phospho-EGFR and phospho-p44/p42 mitogen-activated protein kinase by estrogen was observed, indicating nonnuclear ER transactivation of EGFR. Additionally, EGFR protein expression was down-regulated in response to estrogen and up-regulated in response to fulvestrant in vitro,

suggesting that the EGFR pathway is activated when estrogen is depleted in NSCLC cells. Cell growth and apoptosis were examined in several NSCLC lines that express varying amounts of ERbeta, EGFR, and Neu but no full-length ERalpha. One cell line contained an EGFR mutation. Cells were exposed to 10 nmol/L estrogen and 10 ng/mL EGF and either 1 mumol/L fulvestrant or 1 mumol/L gefitinib alone or in combination. In all cell lines, the drug combination decreased cell proliferation up to 90% and increased apoptosis 2-fold. The relative responses to gefitinib and fulvestrant were similar regardless of ER and EGFR expression and mutation status. In an in vivo lung tumor xenograft model, the drug combination decreased tumor volume in severe combined immunodeficient mice by approximately 60% compared with 49% and 32% for gefitinib and fulvestrant treatment alone, respectively. Antitumor effects of the combination therapy were accompanied by biochemical and histologic evidence of increased apoptosis, decreased phospho-p44/p42 mitogen-activated protein kinase expression, and increased Ki-67 expression compared with individual treatment. These studies provide evidence of a functional interaction between the ER and the EGFR pathways in NSCLC.


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I've read this before and still don't understand what it means :oops:

Is it saying that estrogen is a no-no? I know there was some question a while back in studies that women w/ breast cancer shouldn't eat soy foods because of the estrogen levels or something. Is this suggesting that soy foods would be harmful in LC as well?

Anyone have a clue?? :roll:

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I think the main point is that estrogen DOES seem to fuel lung cancer growth in some cases.

So soy maybe isn't a good thing, not sure sbout this.

I looked on some studies and it stated that Asian women have a higher incidence of lung cancer (my mom was Asian). *Maybe* it is related to soy and of course genetics.

The study basically used a anti-estrogen drug with Tarceva and the results were better than Tarceva or fulvestrant (anti-estrogen drug) as a single drug.

I think it is the same as estrogen dependent breast cancer in a way. So maybe armoatase or Tamoxifen will be used in lung cancer in women someday (again just a guess).

Look at the link below. It is easier to understand than the study in my previous post.

http://my.webmd.com/content/Article/100 ... nting=true

My mom was on HRT and some women on this board were on HRT who did not smoke, so the estrogen replacement may have been a factor in the lung cancer.

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When I read this I really am thankful that my tumor did not return. I say this because, with chemo I went into instant menopause and was having tremendous hot flashes, sweats etc so the doctor put me on hormone replacement therapy, while on treatment.

About a year later my sister told me she had breast cancer, bothe my grandmothers died of breast cancer. I knew this and the fact I had never been pregnant, never had missed a menstual cycle, never had breast fed a baby all added up to me being at high risk for breast cancer I quit taking the HRT. After lung cancer I certainly didn't want to increase my risk of getting another cancer.

Little did I know at that time it could also increase my risk of the lung cancer. Donna G

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I am pretty sure it probably depends on the person. I would guess that all lung tumors are not fueled by estrogen, just as all breast cancers are not estrogen dependent.

Just a guess, but I think one reason any cancer is so hard to treat is because they are all slightly different.

Also I just read a 2005 study where it said there was no connection between HRT and lung cancer, though of course the study could be flawed. It definitely is complicated.

Department of Epidemiology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas, USA.

PURPOSE: To date, there are few published data regarding the use of hormone replacement therapy (HRT) and lung cancer risk. Therefore, we analyzed data regarding HRT use from a large case-control study designed to study genetic susceptibility to lung cancer to determine whether HRT affected risk of lung cancer. Experimental Design: In a secondary analysis, we compared self-reported HRT use among 499 women with lung cancer and 519 healthy age-matched controls. RESULTS: HRT use was associated with an overall reduced risk of 34% [odds ratio (OR), 0.66; 95% confidence interval (CI), 0.51-0.89] of lung cancer, after adjusting for age, ethnicity, smoking status, education, body mass index, and menopausal status. The use of estrogen replacement therapy alone was associated with a 35% reduction in lung cancer risk (OR, 0.65; 95% CI, 0.47-0.89) and the use of combination therapy (estrogen and progestin) was associated with a 39% reduction in lung cancer risk (OR, 0.61; 95% CI, 0.40-0.92). HRT use was also associated with a statistically significantly reduced risk of lung cancer in current smokers (OR, 0.59; 95% CI, 0.38-0.92), but the risk estimates were not statistically significant in never (OR, 0.72; 95% CI, 0.37-1.40) or former smokers (OR, 0.73; 95% CI, 0.46-1.15). In addition, as the cigarette pack-years increased among ever smokers, the protective effect diminished, so that light smokers appeared to benefit the most from HRT use. Decreased lung cancer risks were also evident when the data were stratified by age, ethnicity, and body mass index. The joint effects of HRT use and mutagen sensitivity suggest that HRT use modifies lung cancer risk for genetically susceptible women. HRT use was also associated with a lower risk of death and improved survival compared with the women not taking HRT. To provide a possible biological mechanism to explain our findings, we compared plasma levels of insulin-like growth factor I in users and nonusers, and demonstrated that HRT use was associated with statistically significantly lower insulin-like growth factor I levels for both cases and controls compared with non-HRT users. CONCLUSIONS: These data suggest an association of HRT use with a decrease in lung cancer risk. However, there are several limitations to this secondary analysis, requiring that the data be viewed with caution, and confirmation is required in well-designed hypothesis driven studies. The biological role of HRT in lung cancer remains understudied, and only extensive research can yield new insights into the mechanisms underlying a protective effect of HRT for lung cancer.

Hormonal factors and risk of lung cancer among women?

Kreuzer M, Gerken M, Heinrich J, Kreienbrock L, Wichmann HE.

Institute of Radiation Hygiene, BfS-Federal Office for Radiation Protection, Neuherberg, Germany. mkreuzer@bfs.de

BACKGROUND: Gender differences in the histological distribution of lung carcinoma and a possibly greater susceptibility of women than men to tobacco carcinogens, suggest a possible influence of sex-specific hormones. This study examines endocrine factors and risk of lung cancer among women by smoking status and histology. METHODS: We used data of a case-control study on lung cancer conducted from 1990 to 1996 in Germany, including 811 histologically confirmed female cases and 912 female population controls. Information on various menstrual and reproductive factors, use of oral contraceptives (OC), hormone replacement therapy (HRT), and smoking was gathered through personal interviews using a structured questionnaire. Odds ratios (OR) and 95% CI adjusted for age, region, smoking, and education were calculated via logistic regression. RESULTS: A reduction in lung cancer risk was observed with the use of OC (OR = 0.69; 95% CI: 0.51-0.92), but no trend in risk with increasing duration of use, age at first use, or calendar year of first use was present. A history of HRT was associated with a reduced risk (OR = 0.83; 95% CI: 0.64-1.09), particularly after long duration (>/=7 years) (OR = 0.59; 95% CI: 0.37-0.93). No clear association was found with regard to age at menarche, length of menstrual cycle, number of live-births, and age at menopause. Overall results did not differ much by histological cell subtype. The reduction in lung cancer risk associated with the use of exogenous hormones was primarily seen among smoking women. CONCLUSIONS: Our data provide evidence for a possible role of hormonal factors in the aetiology of lung cancer in women.

John Plaschke

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I've read this study before as well and couldn't understand it at all. It's interesting to me though, because I had been taking tamoxifen (anti-estrogen) for two years when I was diagnosed with the lung tumor.

I'm supposed to go off the tamoxifen next year because 5 years is the protocol, but it makes me a little antsy knowing this.

On the other hand, tamoxifen isn't the easiest drug to be on for years on end.

Only good thing is that I'll never have to make the choice about HRT because that's not even an option post breast cancer.

The more you think you know, the more confusing it all gets!!!!!!


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I don't know if the protocol has changed, but so far I can't take arimidex because I am not post-menopausal. I have heard some rumblings about tamoxifen with no end in sight, but I'll have to check with the oncologist again in May. I know when I went on tamox, it was five years, and then you went off because studies showed no benefit to staying on any longer.

Arimidex is supposed to be a superior drug to tamoxifen and I was on it for 3 months last year, until we did some hormone function tests and found out it was not appropriate for me at this point. It does not block estrogen as strongly as tamoxifen does.

I'll find out early May when I see the onc.


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This whole issue of lung cancer and estrogen has had me perplexed -- I wasn't sure if it meant we should be avoiding soy foods (which concerns me because I do eat soy and was told that was a GOOD thing....)

So, I called the nutritionist at my cancer center to see what she could come up with. She did some research and returned my call this morning.

From what she could find, it seems that they are discovering a link between LC and estrogen, similar to that of breast cancer and estrogen. (The recent research done at The University of Pittsburgh seems to have found some evidence that LC cells seems to grow more rapidly in the presence of estrogen) The problem is that they don't know if soy (foods, powders, supplements) act like estrogen in the body, or if they actually can help BLOCK the estrogen receptors. . .for this reason, they are recomending that we treat soy foods much like breast cancer patients are told to do, which is to limit soy foods to once a day, or once every other day, and not take soy in the form of powders or supplements.

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  • 4 weeks later...

I heard about this study last night on TV and read about it online today. I know that this particular study was done with BREAST cancer, HOWEVER....since they seem to be linking lung cancer and estrogen, similar to breast cancer and estrogen, it would make sense that perhaps exercise would help lung cancer too. (The study states that exercise helps to reduce estrogen levels in the body). In any event, at the very least, walking for 30 minutes a day will expand our lungs and might possibly have the same benefits they are linking w/ breast cancer.

Breast cancer patients should walk to live

Women who exercise have better survival rates, study finds

Updated: 6:06 p.m. ET May 24, 2005 CHICAGO -

Women with breast cancer who walk at least an hour a week have a better chance of beating the disease than those who don’t exercise at all, researchers said on Tuesday.

But the study said many women hurt their chances of survival by cutting back on exercise after they are diagnosed.

“It is well established that exercise plays an important role in preventing many diseases, including breast cancer,â€

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