Despite the multiple identified common genetic, molecular, and cellular processes connecting pulmonary fibrosis (PF) and lung cancer (LC), there is still no clear answer about the contribution of each of them to the development of pathology. It is known that most cell populations involved in the development of PF are involved in LC. At the same time, there are differences that can be explained by the specificity of PF development or changes specific to LC. We evaluated the changes in the lung and blood at the modeling of PF, LC, PF+LC. To induce PF in male C57BL6 mice, we used bleomycin; on the 15th day after bleomycin administration, we modeled non-small cell LC by introducing Lewis lung carcinoma (LLC) cells. The material for this study was collected on the 28th day of the experiment and was analyzed by histology and cytometry. In the lung tissue of mice, against the background of PF and LC modeling, an increase in pathological changes in the lungs was observed compared to each pathological situation separately. Disorders of the lungs in the group of animals with PF and LC were based on increased migration from the blood to the lungs of populations of CD309+ endothelial cells, an increase in atypical/hybrid cells (CD45+CD326+), and cancer stem cell markers CD90, CD117, CD274, CD276, and EGFR in various combinations in the lung tissue. Biomarkers confirming tumor development against the background of pulmonary fibrosis are populations of cancer stem cells, atypical/hybrid cells, endothelial cells, hematopoietic stem cells, myeloid fibrocytes, and changes in the composition of CD4+ T-cells. Further clinical and experimental studies are needed to determine the role of these changes and to find biomarkers that predict the progression of pulmonary fibrosis and the risk of developing lung cancer.