Infecting Just One Tumor with a Virus Could Boost the Systemic Effectiveness of Cancer Immunotherapy

“A Ludwig Cancer Research study suggests that the clinical efficacy of checkpoint blockade, a powerful new strategy to harness the immune response to treat cancers, might be dramatically improved if combined with oncolytic virotherapy, an investigational intervention that employs viruses to destroy tumors.

“Published today in the journal Science Translational Medicine, the study evaluated a combination therapy in which the Newcastle disease virus (NDV), a bird virus not ordinarily harmful to humans, is injected directly into one of two melanoma tumors implanted in mice, followed by an antibody that essentially releases the brakes on the immune response. The researchers report that the combination induced a potent and systemically effective anti-tumor immune response that destroyed the non-infected tumor as well. Even tumor types that have hitherto proved resistant to checkpoint blockade and other immunotherapeutic strategies were susceptible to this combined therapy.”

Editor’s Note: This story is about research that was performed in mice. For that reason, we cannot assume that similar results would happen for humans. However, viruses like the one explored here are already being used in people. To learn more about immunotherapy—cancer treatments that use the immune system to fight tumors—visit our Melanoma Basics.


Antioxidants May Actually Speed Lung Cancer Growth in Some Cases

Antioxidants are chemicals that neutralize particles called free radicals that can damage DNA. Preventing such damage may help lower cancer risk for some people. However, tumors themselves can contain high levels of free radicals; by eliminating these free radicals, antioxidants may help cancer cells grow. In a laboratory, lung cancer cells treated with the antioxidants vitamin E and acetylcysteine (ACC) multiplied faster than untreated cells. Vitamin E and ACC also increased tumor growth and decreased survival time in mice with lung cancer. The so-called ‘tumor suppressor’ protein p53 can sense certain free radicals to detect cells with DNA damage and stop their growth. Antioxidants may interfere with this cancer-suppressing mechanism by reducing free radical levels. Taking antioxidants may therefore not be recommended for lung cancer patients and smokers.


New Targeted Drugs May Offer Treatment for KRAS-Mutant Lung Cancer

Abnormalities in the KRAS gene are the most common mutations in lung cancer, especially in lung adenocarcinoma, a type of non-small cell lung cancer (NSCLC). However, no effective targeted therapy directed at KRAS has been found. Instead, researchers have begun to focus on blocking molecules “downstream” in the chain of chemical reactions through which KRAS affects the cell. Two such molecules are TBK1 and MEK. A recent study found that the drug CYT387 blocks TBK1. CYT387 reduced tumor growth in mice with KRAS-mutant lung adenocarcinoma. Also in mice, CYT387 and the MEK inhibitor AZD6244, given together, shrank aggressive lung tumors with mutations in both the KRAS and the TP53 gene. Researchers now hope to investigate the two drugs in people.


Lung Cancer Drug BGB324 May Counteract Drug Resistance

The protein Axl has been associated with cell transformation processes that contribute to the spread of cancer through the body and to cancers becoming drug resistant. A recent study investigated the effect of the Axl inhibitor BGB324 on non-small cell lung cancer (NSCLC) cells that had become resistant to EGFR inhibitors like erlotinib (Tarceva). BGB324 restored the effectiveness of EGFR inhibitors against these cancer cells, which had been grown either in a matrix or as tumors in mice. BGB324 also appeared to enhance the effectiveness of the chemotherapy drug docetaxel (Taxotere) and of bevacizumab (Avastin). BGB324 may therefore be a promising new candidate for treating drug-resistant NSCLC. The drug will be tested in a phase Ib clinical trial for NSCLC in 2014.


Attacking Lung Cancer Cells by Blocking Antioxidants

As a byproduct of their rapid metabolism and growth, cancer cells frequently produce high levels of so-called free radicals–highly reactive particles that can damage cells. To protect themselves, cancer cells also produce antioxidants, which deactivate the free radicals. Drugs that block these antioxidants should therefore selectively impair cancer cells, while having relatively little effect on healthy cells that do not experience high levels of free radicals. Researchers found that the antioxidant-inhibiting drug ATN-224 induced the death of non-small lung cancer (NSCLC) cells in cell culture. ATN-224 also decreased the number and size of lung tumors in mice injected with NSCLC cells.


Timing Cancer Treatment for Maximum Effectiveness

Our bodies follow a 24-hour ‘biorhythm’ that affects most of our biological functions. This fact forms the basis of cancer chronotherapy, which takes time of day into account to plan cancer treatment. Administering cancer drugs at the right time can double effectiveness while reducing toxicity up to fivefold. However, individual differences in biorhythms mean that the ‘right time’ varies from one person to another. In a recent study, researchers linked gene expression in mice with the time point at which the chemotherapy agent irinotecan (Camptosar) produced the least toxicity. They developed a mathematical model that predicts each animal’s ideal time point based on the expression of two genes. In the future, they hope to develop similar tools to help predict the best time for cancer treatment in human patients.


Timing Cancer Treatment for Maximum Effectiveness

Our bodies follow a 24-hour ‘biorhythm’ that affects most of our biological functions. This fact forms the basis of cancer chronotherapy, which takes time of day into account to plan cancer treatment. Administering cancer drugs at the right time can double effectiveness while reducing toxicity up to fivefold. However, individual differences in biorhythms mean that the ‘right time’ varies from one person to another. In a recent study, researchers linked gene expression in mice with the time point at which the chemotherapy agent irinotecan (Camptosar) produced the least toxicity. They developed a mathematical model that predicts each animal’s ideal time point based on the expression of two genes. In the future, they hope to develop similar tools to help predict the best time for cancer treatment in human patients.


Timing Cancer Treatment for Maximum Effectiveness

Our bodies follow a 24-hour ‘biorhythm’ that affects most of our biological functions. This fact forms the basis of cancer chronotherapy, which takes time of day into account to plan cancer treatment. Administering cancer drugs at the right time can double effectiveness while reducing toxicity up to fivefold. However, individual differences in biorhythms mean that the ‘right time’ varies from one person to another. In a recent study, researchers linked gene expression in mice with the time point at which the chemotherapy agent irinotecan (Camptosar) produced the least toxicity. They developed a mathematical model that predicts each animal’s ideal time point based on the expression of two genes. In the future, they hope to develop similar tools to help predict the best time for cancer treatment in human patients.


Immune System Cells from Tumors Might Control Cancer

Tumors contain immune system cells that attack cancer cells but are present in very small numbers, leading to the hope that a flood of these antitumor cells might eradicate cancer. This approach can work in melanomas, but has not yet worked against other kinds of cancers. Now, there’s a better way to concentrate antitumor immune system cells: they have a protein called CD137 on their surfaces; researchers recently used this distinction to extract these antitumor cells quickly and easily from both melanomas and ovarian cancer. The new study showed that peoples’ own antitumor cells recognized their tumors and that injections of these cancer fighting cells kept tumors from growing in mice. If other types of cancer also contain these antitumor immune system cells, this new approach could hold promise for treating a wide range of tumors.