Link between Wellbutrin and increased BC risk?

Wellbutrin is not a SSRI (which you may know as you mentioned that it works on dopamine and norepinephrine receptors).  Yes, it is contraindicated while taking tamoxifen.  My oncologist recommended Wellbutrin when I was diagnosed to help me with anxiety/worry (not really depression).  It really helped.  I would talk to your oncologist about it, but from the little I have read it was the SSRI's specifically and I'm not sure why or how large of a study it was. I think that I have read a side effect of SSRI's is weight gain and I wonder if the weight gained then increases estrogen, which would possibly increase bc?  Hmmm.

I saw a post in this forum somewhere about this. I am taking effexor xr for anxiety and wellbutrin for depression. My psychiatrist said it didn't do much for anxiety but I guess everyone is different. I took a very high dose to start and it caused chest pain and my blood pressure went up so we cut it to 1/2 and now I just get tired. I am looking for something to give me energy. I have tried numerous antidepressants. She mentioned she may switch me to MAO Inhibitors. Just the name scares me.

2009 abstract (by a psych dept) There is consistent evidence that paroxetine and fluoxetine have a large effect on the metabolism of tamoxifen and should not be used. Indirect evidence indicates that bupropion may also have a large effect on the metabolism of tamoxifen. Venlafaxine has little or no effect on the metabolism of tamoxifen and may be considered the safest choice of antidepressants. Desvenlafaxine is not metabolized by the P450 system and may consequently be another option. Mirtazapine has not been extensively studied, but existing research suggests minimal effect on CYP2D6. The remaining commonly prescribed antidepressants have mild to moderate degrees of CYP2D6 inhibition. http://www.ncbi.nlm.nih.gov/pubmed/20141708

Paroxetine, fluoxetine and bupropion are strong CYP2D6 inhibitors which should be avoided in tamoxifen users.  http://www.ncbi.nlm.nih.gov/pubmed/20880642

This 2008 abstract opines: Second-generation antidepressants differ in their potential for pharmacokinetic drug interactions. Fluoxetine and paroxetine are potent inhibitors of CYP2D6, fluvoxamine markedly inhibits CYP1A2 and CYP2C19, and nefazodone is a substantial inhibitor of CYP3A4. Therefore, clinically relevant interactions may be expected when these antidepressants are coadministered with substrates of the pertinent isozymes, particularly those with a narrow therapeutic index. Duloxetine and bupropion are moderate inhibitors of CYP2D6, and sertraline may cause significant inhibition of this isoform, but only at high doses. Citalopram, escitalopram, venlafaxine, mirtazapine, and reboxetine are weak or negligible inhibitors of CYP isozymes in vitro and are less likely than other second-generation antidepressants to interact with co-administered medications. http://www.ncbi.nlm.nih.gov/pubmed/18691982

Use of concomitant strong or intermediate inhibitors of CYP2D6 should be avoided when alternate medications are available.  http://www.ncbi.nlm.nih.gov/pubmed/19200418

The interaction may also be a judgement call for your onc:  for example, in my (somewhat unusual) case, I am taking tamoxifen to help prevent bc as I only have classic LCIS and nothing worse.  Classic LCIS may confer an approximate 25-40% lifetime risk of breast cancer.   (I take sertraline which is a mild-moderate inhibitor.)

For other women, tamoxifen may play a much more crucial role in their therapy than in mine.

In this paper of over 1500 women with primary invasive breast cancer who took SSRIs (it does NOT state whether or not these women took tamoxifen).

Overall, SSRI use was not associated with an increased risk of breast cancer regardless of our definition of cumulative use (total number of prescriptions dispensed and total dosage). In addition, our results indicate that prolonged SSRI use does not have a latent effect on breast cancer risk. Also, our findings are not suggestive of an increased risk of breast cancer with the use of individual SSRIs. http://www.ncbi.nlm.nih.gov/pubmed/21176215

(all emphasis is mine)

Wellbutrin is what's known as a TNF Inhibitor (tumor necrosis factor) - Wellbutrin blunts the body's ability to fight abnormal cell production.  I wouldn't take it.  I don't know why they don't make this crystal clear to those with cancer.  Also causes low white blood cell count - all sorts of problems for those with cancer or who have had it.  

When I search quickly the Pubmed site for Wellbutrin + TNF, it looks like the studies I see are all in rodents.  One study reports a case report in an anorexic woman, which of course interesting, but hardly evidence.  To me, it looks like they have discovered more than 1 TNF inhibitor receptor. I don't know enough to say if one receptor has different actions than another.

To me, your oncologypractice article is referring to biologic TNF inhibitors.  Wellbutrin is not a biologic TNF inhibitor.

This abstract states that Wellbutrin's major action is dopamine and norepinephrine reuptake inhibitor.  http://www.ncbi.nlm.nih.gov/pubmed/17136226

so that makes it difficult to know if, and if so, why Wellbutrin may be contraindicated.

I don't know if Wellbutrin is a weak or strong TNF inhibitor, or even whether they know if TNF inhibition occurs in humans.

Since Wellbutrin has multiple mechanisms of action, and I can find no Pubmed studies (as opposed to case reports) on Wellbutrin anti-TNF activity in humans,  I don't think there is a whole lot of evidence that has looked at Wellbutrin in human breast cancer.  So I don't think we can know for sure whether Wellbutrin has any effect on cancer or not.

There is a lot we don't know about cancer and drug interactions.

Maybe you can locate Pubmed references I have missed, especially since I just did a quick look.  Sometimes information gets lost in translation.