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Identification of candidate processes and mechanisms involved in lung cancer initiation and progression

Identification of the cell that initiates lung cancer is still a controversial issue.

(a). It has been speculated that different lung tumour subtypes arise from different cells of origin, which are localised in defined microenvironments. A common theory is that cancer-initiating cells may originate from early progenitors or stem cells. Importantly, cancer-initiating cells with stem-like properties may not necessarily originate from the transformation of stem cells but also from the acquisition of an aberrant “plastic state”. Our laboratory is involved in the study of the interplay between cellular plasticity, stemness and lung cancer.

(b). Among the processes associated with lung cancer my group is also interested in cellular senescence. Senescence is a cell autonomous response to damage and oncogenic stress characterised by a permanent cell cycle arrest. Cellular senescence is a defining feature of a wide variety of human premalignant tumours. Experiments performed on lung cancer models convincingly concluded that senescent cells accumulate in adenomas (precancerous lesions) but not in adenocarcinomas (advanced malignant tumours). We are studying the role of cellular senescence during lung cancer initiation and progression. Although senescence has been reported as a barrier to prevent the expansion of premalignant cells in a cell autonomous manner, it is believed that senescent cells can also implement a complex pro-inflammatory and pro-tumorigenic secretory phenotype (SASP) that affects nearby cells accelerating tumour growth. A complete understanding of the underlying triggers, regulatory pathways, master regulators, and specific effects of the SASP in the tumour microenvironment has so far escaped elucidation. 

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