Cancer breakthroughs often get their first airing at the annual meeting of the American Society of Clinical Oncology. This year\u2019s meeting was no exception.<\/p>\n
One finding getting a lot of press<\/a> has its origins in a pair of <\/a>studies<\/a> in Nature<\/em> in 2005. The studies showed how to selectively kill cancer cells deficient in BRCA1 and BRCA2, genes that are mutated in some of the deadliest breast and ovarian cancers.<\/p>\n The agent that does the killing is called a PARP<\/span> inhibitor. And trial results released last week show some pretty promising results.<\/p>\n Olaparib, a PARP<\/span> inhibitor under development by AstraZeneca PLC<\/span>, shrank tumors in more than a third of women whose breast cancers had BRCA<\/span> mutations. The trial did not have a control arm, but the data look encouraging, considering the agent was given alone, without other drugs, and that the subjects had already had an average of 3 chemotherapy regimens. A similar trial showed that the drug could also shrink advanced ovarian tumors in subjects with BRCA1 or BRCA2 mutations.<\/p>\n A truer test of whether a drug is likely to help patients is whether it can prolong survival. A randomized, controlled trial of BS1-201, under development by Sanofi-Aventis SA, examined this question in 116 women with some pretty nasty tumors: their breast cancer had metastasized to other parts of their body and was \u2018triple negative\u2019, meaning it lacked receptors on their tumors for estrogen, progesterone and HER2, each of which are targets for current therapies. The drug prolonged survival by three and a half months, to 9.2 months, when added to a standard chemotherapy regimen.<\/p>\n Bigger studies are needed, but the findings so far validate a concept with deep origins in basic research. BRCA1 and BRCA2 facilitate DNA<\/span> repair, a function that emerged after years of painstaking research. PARP<\/span> (poly(ADP<\/span>)-ribose polymerase) mediates DNA<\/span> repair also, but in a distinct way. The Nature <\/em>studies exposed cells lacking BRCA1 or BRCA2 to PARP<\/span> inhibitors and showed that these cells get nailed: their DNA<\/span> is such a fragmented mess that they die.<\/p>\n Mice deficient in PARP<\/span> are viable, fertile and tumor-free, which bodes well for the side effect profile of these drugs. Subjects who received the drugs reported only mild side effects, including nausea and fatigue.<\/p>\n Other highlights at ASCO<\/span> include promising findings with multikinase inhibitors, which can block several types of proteins that go astray in tumor cells. Cancer vaccine approaches also got a boost with positive findings from trials in melanoma and non-Hodgkin\u2019s lymphoma.<\/p>\n","protected":false},"excerpt":{"rendered":" Cancer breakthroughs often get their first airing at the annual meeting of the American Society of Clinical Oncology. This year\u2019s meeting was no exception. Read more<\/a> Continue reading