A recent study has shown that chronic exposure to cigarette smoke may reprogram lung stem cells and alter their functions, making them more likely to turn into cancerous cells when specific gene mutations occur.
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The study was conducted by researchers at the Johns Hopkins University Sidney Kimmel Comprehensive Cancer Center, and it showed that the type of lung cancer that develops may not be determined by the genetic mutation alone, but is also affected by the type of cell in which the mutation occurs and its condition after continuous exposure to cigarette smoke.
The researchers used three-dimensional laboratory models known as "lung organoids," which are miniature models that mimic some of the properties of lung tissue, and exposed them to a cigarette smoke condensate, a mixture of chemicals and particles found in smoke, for six months, then monitored the changes that occurred in the cells.
The researchers found that chronic smoke exposure caused changes in gene activity and control mechanisms, leading to cellular conditions similar to those preceding cancer. Some of the cells' natural defense mechanisms were also altered, including pathways related to inflammation, immune response, and cell death.
The researchers then tested the effects of two mutations associated with lung cancer: the KRAS mutation and the loss of the tumor suppressor gene TP53. The experiments showed that tumors only formed when prior exposure to cigarette smoke was combined with one of these genetic alterations. Neither smoke exposure alone nor the introduction of the mutations into cells not exposed to smoke resulted in tumor development.
“What this tells us is that the genetic event alone is not enough,” says Dr. Michelle Vaz, the study’s lead author. The researchers emphasize that chronic smoke exposure first alters the state of cells, making them more susceptible to cancerous transformation when certain mutations occur.
One of the study's key findings was that different mutations led to different types of lung cancer. The KRAS mutation in smoke-exposed organisms resulted in tumors with characteristics resembling lung adenocarcinoma, while the loss of TP53 led to tumors with characteristics resembling squamous cell carcinoma. Researchers were able to trace the origin of these tumors to different stem cell populations. Tumors associated with the KRAS mutation appeared to originate from bronchial-alveolar stem cells, while squamous tumors resulting from TP53 loss were linked to basal stem cells, which help maintain and repair the lining of the airways.
"It was very interesting that when introducing a KRAS mutation or causing TP53 loss, both seemed to select a particular state of stem cells," Vaz says.
The findings suggest that chronic exposure to cigarette smoke may not only increase cancer risk by inducing genetic mutations, but may also reshape cells and alter how they respond to subsequent mutations. Researchers believe that understanding these early changes could help identify molecular markers that pinpoint individuals most susceptible to lung cancer, and may also reveal new targets for prevention and treatment.
The study also suggests the possibility of combining targeting epigenetic changes with immunotherapy in the future, especially for tumors that do not respond to current treatments.
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