Bristol plans big lung cancer study, pairing immunotherapies Reuters (Reuters) - Bristol-Myers Squibb Co on Tuesday said it plans this year to begin a late-stage trial testing whether a combination of two of its high-profile immunotherapies can...
"Tabulated below are “targeted” or novel agents that are being or have been evaluated in non-small cell lung cancer and small cell lung cancer. Only compounds that have entered clinical trials have been listed. The compounds are listed by class, and within each class, they are listed in the order of their phase of clinical development, with those in the latest phase being listed first"
Infection with high-risk types of human papillomavirus (hrHPV) is associated with cervical, anogenital, and oropharyngeal cancers. Since a causal contribution of hrHPV infection to lung cancer (LC) is still a matter of debate, a comprehensive study was performed to delineate hrHPV involvement in LC.
hrHPV presence in a tumor with primary presentation in the lungs signifies pulmonary metastasis from a primary hrHPV-positive cancer elsewhere in the body. No support was found for an attribution of hrHPV infection to the development of primary LC.
"The discovery of RET fusions in lung cancers has uncovered a new therapeutic target for patients whose tumors harbor these changes. In an unselected population of non-small cell lung cancers (NSCLCs), RET fusions are present in 1-2% of cases. This incidence rises substantially, however, in never-smokers with lung adenocarcinomas that lack other known driver oncogenes. While pre-clinical data provide experimental support for the use of RET inhibitors in the treatment of RET fusion-positive tumors, clinical data on response are lacking. We report preliminary data for the first three patients treated with the RET inhibitor cabozantinib on a prospective phase 2 trial for patients with RET fusion-positive NSCLCs (NCT01639508)..."
"The U.S. Food and Drug Administration has designated a compound developed by Novartis AG to treat a type of non-small cell lung cancer for fast-track development and review, the Swiss drugmaker said on Friday."
"The LKB1 (also called STK11) tumor suppressor is mutationally inactivated in ∼20% of non-small cell lung cancers (NSCLC). LKB1 is the major upstream kinase activating the energy-sensing kinase AMPK, making LKB1-deficient cells unable to appropriately sense metabolic stress. We tested the therapeutic potential of metabolic drugs in NSCLC and identified phenformin, a mitochondrial inhibitor and analog of the diabetes therapeutic metformin, as selectively inducing apoptosis in LKB1-deficient NSCLC cells. Therapeutic trials in Kras-dependent mouse models of NSCLC revealed that tumors with Kras and Lkb1 mutations, but not those with Kras and p53 mutations, showed selective response to phenformin as a single agent, resulting in prolonged survival. This study suggests phenformin as a cancer metabolism-based therapeutic to selectively target LKB1-deficient tumors."
Aubrey Anderson is a 30-year-old single mum with a 14-week-old baby and like all parents she just wants to watch that baby grow, but because of a tumour in her lung behind her heart, doctors say that's unlikely.
Single mum, new born baby, lung cancer ABC Local Aubrey Anderson is a 30-year-old single mum with a 14-week-old baby and like all parents she just wants to watch that baby grow, but because of a tumour in her lung behind her heart, doctors say...
Editorial Advisory Board member Dr. Socinski discusses the key clinical insights brought to light by the POINTBREAK trial, presented at the 2012 Chicago Multidisciplinary Symposium in Thoracic Oncology.
The advent of novel therapeutics that specifically target signaling pathways activated by genetic alterations has revolutionized the way patients with lung cancer are treated. Here, we have summarized these developments into six conceptual paradigms that illustrate the transition from empirical cancer medicine to mechanistically based individualized oncology.
"In patients with non-small cell lung cancer (NSCLC), knowledge of the epidermal growth factor receptor (EGFR) mutation status is fundamental for selecting the treatment involving EGFR-tyrosine kinase inhibitors (EGFR-TKIs). Little information is available regarding the response and progression-free survival (PFS) in platinum-based chemotherapy (CT) versus EGFR-TKIs in the presence or absence of KRAS mutation, particularly in patients without EGFR mutation..."
Vall d’Hebron Institute of Oncology (VHIO) scientists eradicate lung tumours in a pre-clinical mouse model. Previous studies had already shown that Myc was a key protein in tumour development and had established how to inhibit Myc through gene therapy. The protein Myc is involved in the development of diverse tumours and so Myc-targeted therapy could make a positive contribution to the therapeutic options for different types of cancer.
The study has managed to eliminate mouse lung tumours by inhibiting Myc, a protein that plays a key role in the development of many different tumours. The results, published in the journal Genes & Development, confirm that repeated, long-term treatment does not cause side effects. Even more importantly, no resistance to treatment has been encountered, which is one of the biggest concerns with anticancer therapies. These results show that anticancer therapies based on Myc inhibition are a safe, effective therapeutic option in new drug development.
Myc is a protein that plays a big role in regulating gene transcription and it is involved in cell processes such as proliferation, differentiation and apoptosis (programmed cell death - an essential part of regenerating tissues and eliminating damaged cells). It acts as a regulator gene that controls the expression of some 15% of human genes. However, imbalances in this protein bring about uncontrolled cell growth which in turn can lead to the onset of cancer in different tissues. In fact, deregulated Myc is found in most tumours, including cervical, breast, colon, lung and stomach cancer.
The work conducted by the Mouse Models of Cancer Therapy group at the VHIO, led by Dr Laura Soucek, shows that Myc can be controlled and inhibited through a mutant called Omomyc that hijacks Myc and prevents it from acting. “Even if we clearly identify a mechanism behind tumour development, it is still extremely complex to pinpoint how to intervene in cells' internal machinery or modify genetic processes,” explained Dr Soucek. “We have found a way to inhibit Myc through Omomyc,” she continued. “We induced Omomyc expression in mice through gene therapy and managed to activate and deactivate it by administering an antibiotic to the mice in their drinking water.”
In the study, multiple lung tumours were induced in the mouse (up to 200 tumours in each individual) and Myc inhibition episodes were achieved by activating Omomyc expression for 4-weeks, followed by 4-week rest periods. This therapy - known as metronomic therapy - was maintained for more than a year, regularly checking tumour progress in each mouse. All mice became tumour free after the first inhibition period, but 63% of cases then relapsed. After the second Myc inhibition period, only 11% of the initial tumours reappeared. According to Dr Soucek, “the most important finding was that there were no signs of resistance to treatment. This is one of the biggest disadvantages of many anticancer therapies: the disease develops resistance and can return even more aggressively.”
Finally, only two remaining tumours were found after more than one year of treatment among the mice that received eight inhibition and rest cycles. Dr Soucek found that Omomyc expression had been suppressed in these tumours, and this was the only adaptive mechanism that mice developed to treatment. “These results are hugely positive for us, because one year of life in a mouse is equivalent to almost 40 human years. The fact that the results are maintained over time, that there is no tumour relapse and no resistance, suggests that Myc-targeted therapy may offer an unprecedented way forward."
These encouraging results provide sufficient scientific evidence to consider taking the next step: inhibiting Myc in patients. “Now our challenge for the future is to make Myc inhibition feasible from a pharmacological point of view, so that it can be administered, and done so safely. This will be the last step before designing clinical trials with Myc inhibitors,” explained Dr Soucek. “We're so excited about reaching this turning point and I am quite certain that it will change the course of cancer therapy, despite there being a long road ahead.”
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