CANCERS of non-smokers are different from those of smokers. Genetically different: the mutations underlying the development of the disease in the former, in fact, are not the same as those that can be identified in the latter. To discover the differences and the two “molecular signatures” was an international group of researchers led by the Italian Maria Teresa Landi of the US National Cancer Institute. The results, published on Nature Genetics, not only provide important information on the development of neoplasms, but can direct clinical research towards the development of new targeted drugs specific for these types of cancer.
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Not just smoke
Smoking is known to be the main risk factor for lung cancer. However, it is not the only one. It is estimated that a variable percentage between 10 and 25% of cases occur in non-smokers: these are mainly women and with an average age lower than that of smoking patients. There are other defendants, such as passive smoking, exposure to radon gas and pollution, to name a few: all contribute to the onset of mutations in the DNA. To these are added the normal “errors” that are committed during cell replication and that are not always corrected. In all cases, what occurs is an accumulation of mutations which, when they involve certain particular genes, lead a cell to go mad and give rise to cancer. Research has so far focused on studying the genomes of smoking-related cancers, while the mechanisms and genes involved in the disease of those who have never touched a cigarette had not yet been investigated.
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The analysis of 232 genomes
So what did the researchers do? They sequenced the tumor genomes of 232 non-smoking patients – with an average age of almost 65 years at diagnosis, over 75% women and almost all Caucasians – with the aim of identifying the “patterns” of specific mutations. All tumors were of the “non-small cell” type (NSCLC), and mostly adenocarcinomas.
Based on the data that emerged from the sequencing, the tumors of non-smokers were classified into three categories, to which the researchers gave the names “flat”, “medium-strong” and “strong”. As the scientists explain, this classification refers to the world of music, where the amount of accumulated mutations represent the “noise” of the tumor. Note: the mutations that usually characterize smokers’ tumors were not found in these genomes, not even in the 62 patients who had been exposed to secondhand smoke.
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The new classification
The “plane” subtype appears to be associated with the activity of some stem-derived cells which are called progenitors. These tumors grow slowly and have several “driver” mutations that guide their development, which can make them more difficult to treat. Not for all these mutations, moreover, there are already targeted therapies. The “half-strong” subtype is characterized by alterations in the epidermal growth factor receptor (Egfr) gene, already associated with several tumors, and by some particular changes in chromosomes. Development is faster than that of the “flat” subtype. Finally, the “strong” subtype has many alterations like that of smokers (or former smokers), and grows rapidly. Both of these latter two subtypes have few “driver” mutations and this makes them potentially more easily attacked with targeted drugs.
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The study adds an important piece to a complex puzzle. A first step, because other analyzes on a larger number of patients will be needed to confirm these results or identify other mutations that could be used both for diagnosis and as a target for future therapies.
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