My car was towed. It happens. A few more unfortunate situations later, and I was crying. It wasn’t that I was feeling sorry for myself. I was just mad, and the tears wouldn’t stop.

I didn’t feel comfortable talking to a friend at the moment, so I grabbed my phone and called the Y-ME National Breast Cancer Organization’s 24-hour hotline. I had saved the number (800-221-2141) on my phone when I was diagnosed in August, but I had never used the free service before. I should have.

“Before, I would have just fixed the problem, and that was that. Tears were never an option,” I told the woman named Lauren who answered my call.

The kind stranger, who survived breast cancer 12 years ago, gently turned my focus back on a plan of action. I needed to drink a glass of water. And commit to asking for help to cope with my fears.

“You are not overreacting. It’s completely normal for you to feel this way,” Lauren said. “It’s going to be a difficult transition. You are going to need help.”

I’m extremely independent, so I don’t like asking for help. I don’t trust easily. And I have been extra fearful lately. The more afraid I am, the more I want to know. And this sometimes works against me.

My current fears have to do with Tamoxifen, the anti-tumor drug my oncologist has prescribed. I felt the need to read about other drugs and genetic variations that interfere with Tamoxifen’s power to neutralize estrogen, which can feed breast-cancer cells. It made me wish I was an expert in pharmacogenetics, the study of genetic variations that affect patients’ response to pharmaceuticals.

Human liver enzymes are supposed to metabolize Tamoxifen. Two enzymes (Cytochrome P2D6 and YP3A) are responsible for changing it into a chemical called Endoxifen. And for the drug to work, the enzymes have to do their job. Endoxifen is then supposed to bind to estrogen receptors to prevent or slow the growth of breast cancer cells.

A few years ago the American Society of Clinical Oncology and the Food and Drug Administration’s Clinical Pharmacology Subcommittee attributed Tamoxifen’s failure in some patients to a genetic variation (of the CYP2D6 gene), and deemed it an important predictor of the drug’s efficacy. Some doctors were requesting genetic testing before prescribing the drug.

In 2010, however, researchers presented data from two clinical trials at the San Antonio Breast Cancer Symposium that showed women who had the genetic variation were not more likely to have a recurrence. Soon after, an editorial in the Journal of Clinical Oncology said that there was a “hesitancy and uncertainty about (CYP2D6) genetic testing in clinical practice.” My oncologist did not prescribe the test. And that seems to be in line with current research.

Drug interactions can also affect the way Tamoxifen is metabolized, and when I learned that two medications I was taking for depression and anxiety, Buproprion and Escitalopram, were on a red list as having “high” and “moderate” impact on the efficacy of Tamoxifen, I did something foolish: I abruptly stopped taking them without discussing it with my doctors. It was a mistake on both counts — patients are almost always taken off these drugs gradually — and probably explained my crying episode.

When I talked it over with the doctor who had prescribed the antidepressants, M. Beatriz Currier, the director of the Courtelis Center for Psychosocial Oncology at the University of Miami, she told me my worries were overblown.