Yesterday was Day 1 at the American Society of Clinical Oncology’s annual conference in Chicago and among the many things I’m excited to learn more about is what current ASCO president Dr. Michael Link described in the kickoff press conference as the molecular era of cancer. I’m still new to covering the cancer space, and this is my first time at ASCO, so my goal is to find out what these sorts of intriguing phrases mean to cancer patients.
In the next decade, explained Dr. Link, doctors and researchers won’t be so concerned about cancer in terms of where it first developed in the body, be it the lung, brain or breast, but they’ll be more focused on each tumor’s unique molecular makeup. Certain genetic mutations within tumors spur cancer on and they will be creating, more and more, therapies that target those specific abnormalities.
“In effect, every patient has his or her own rare form of cancer,” explained Dr. Link, a leader in the field of pediatric oncology. The tricky part is finding which patient has what genetic mutation and then getting them the right treatment.
One study Dr. Link mentioned that tested this customized form of medicine is a Phase I trial in which the oral targeted agent Xalkori (crizotinib) was used to treat three rare and aggressive pediatric cancers: neuroblastoma, anaplastic large cell lymphoma (ALCL) and inflammatory myofibroblastic tumors (IMTs). Most of the 70 children in this study, conducted by the Children’s Oncology Group, had already received every available therapy before they were given crizotinib.
Crizotinib works by targeting genetic abnormalities in the anaplastic lymphoma kinase (ALK) gene. ALK mutations, which can drive tumor growth, occur in 80 to 95 percent of all ALCL cases, half of all IMTs, and 10 to 15 percent of all aggressive neuroblastomas. Response rates to crizotinib seemed to correspond to these percentages. Seven out of eight children, or 88 percent, with ALCL on the study had a complete response to the therapy. The majority of the patients with IMTs, which previously had no other effective alternatives, had tumor shrinkage or a regression. For those with aggressive neuroblastoma, two out of 27 had a complete response and eight experienced stable disease, meaning the cancer had not grown.
Patients on the study were, when possible, tested for having this ALK mutation, although it was not a requirement. But it is still thought that perhaps whether or not these patients have this genetic mutation could indicate whether or not crizotinib will be effective. This is, of course, a Phase 1 study, which examines such things as toxicity (crizotinib was well-tolerated by the patients), and more studies need to be performed. But, as Dr. Link explained, this is the sort of studies we’ll be seeing in the coming decade.
“Are we ready for the molecular era?” asked Dr. Link. “Not yet. Clinical trials haven’t kept pace with the molecular era.” But the belief is that trials like this Phase 1 study will become the new norm.