Mets Day 915: Consultation with my clinical oncologist

Today I met with my clinical oncologist, Dr. Aragon-Ching of GW's Medical Faculty Associates. She and I had traded emails and spoken by phone last week. The purpose of today's meeting was to further discuss whether I should stay on Lovenox long-term, or eventually switch over to an oral anticoagulant. I also wanted to get her thoughts on my clinical trial options.

Prior to my meeting with her, I did some research on whether Lovenox can help suppress growth of my cancer. Along the way, I got an education on the use of low molecular weight heparins (LMWHs) to combat venous thromboembolism (VTE). VTE includes deep vein thrombosis (DVT) and pulmonary embolism (PE). Patients with cancer -- especially metastatic cancer, and who have had chemotherapy -- are at increased risk for VTE. A good overview of VTE, and the emerging use of oral anticoagulants, is available here.

The question I was looking into is whether LMWHs such as Lovenox can help inhibit the growth of my metastatic bladder cancer. Lovenox is an injected form of LMWH, with the generic name of enoxaparin sodium. I'm currently injecting myself with 120 mg of Lovenox twice a day. If there is evidence that enoxaparin can help slow the spread of my cancer, then I'm willing to continue with the shots. If not, I'd prefer switching to rivaroxaban (Xaralto).

In the 2009 book, Coagulation and Cancer, by G.F. Pineo and R.D. Hall, the authors write, "Some LMWH compounds were effective in the suppression of tumor cell growth, metastases (nandroparin, tinzaparin, enoxoparin), and antiogenesis (tinzaparin, dalteparin, and enoxoparin), whereas fondaparinux (as selective factor Xa inhibitor) was not." Id. at 266, endnotes omitted. Elsewhere in the chapter, the authors cite other studies that support the idea that LMWHs may inhibit tumor growth. Id. at 261. The authors conclude:

Over the years it has become increasingly evident that the thrombotic process plays a vital role in cancer cell development, proliferation, migration and metastasis leading to the hope that suppression of the coagulation cascade could have a beneficial effect on the cancer. Data from clinical trials initially aimed at the treatment of venous thromboembolism in cancer patients and later directly in cancer patients who did not have thrombosis provided evidence that LMWH could improve survival in the patients who had a wide variety of primary tumor sites . . . .

Id. at 270. Unfortunately, the excepts of the book that I was able to pull up on Google books omitted the pages with the critical endnotes, so I could not readily locate the studies cited for those propositions.

Duly prepared, I met with Dr. Aragon-Ching. She said that the evidence that Lovenox can inhibit metastatic activity is very limited. She said that she would not give much weight to that possibility in making the decision of whether to continue using Lovenox, or switching to Xaralto. She acknowledged that Xaralto was a relatively new drug for DVT and PE, but was satisfied that Xaralto was as effective as Lovenox. She said that NIH would recommend that I stay on Lovenox, because they do clinical trials for a living, and Lovenox is well-known for its lack of interactions with most drugs. Because Xaralto is a newer drug, there is not as much evidence about its lack of interactions, although she said that it should be as safe and effective as Lovenox. She recommended that I have the Lovenox injections for 4 weeks, then switch over to Xaralto, unless I was to enter a clinical trial.  She added that, if I went on Xaralto and then later entered a clinical trial, I could switch back to Lovenox with no problems.

Dr. Aragon-Ching also said that I should not go on coumadin. It doesn't work as well, has too many side effects, and is too diet-dependent. It's simply an older drug that has been superseded by newer drugs.

On the subject of clinical trials, Dr. Aragon-Ching said that the key issue was whether my nodes were large enough to meet the clinical trial threshold. I learned that the standards for lymph node sizes in clinical trials are set forth in a document called "Response Evaluation Criteria in Solid Tumors" (RECIST). The 2009 version of the RECIST standards -- version 1.1 -- requires that lymph nodes be at least 15 mm on their short axis before they can be considered a "target lesion" for purposes of a clinical trial. As stated in an article summarizing the new guidelines:

Lymph nodes with a short axis of ≥15 mm are considered measurable and assessable as target lesions, and the short-axis measurement should be included in the sum of target lesion measurements in the calculation of tumor response as opposed to the longest axis used for measurements of other target lesions. Lymph nodes with a short axis of < 10 mm are defined as “nonpathologic” (Fig. 8A). All other pathologic nodes—that is, those with a short axis of ≥10 mm but <15 mm—should be considered nontarget lesions.

Since all US clinical trials follow the RECIST 1.1 guidelines, until my nodes are of sufficient size, I'm not eligible.  Which is fine: I'd much rather have my nodes stay small and not enter a trial, than have them growing and then enter a trial. 

Nevertheless, as Dr. Aragon-Ching and I discussed, it's highly likely that my cancer is going to progress. If and when that happens, then she recommended that I enter an immunotherapy clinical trial relating to PD-L1. She didn't think it mattered which PD-L1 trial it was -- either the Hoffman-LaRoche MPDL-3280A trial, or the soon-to-open NIH study which I'll learn more about tomorrow when I meet with Dr. Apolo.