The cell cycle is mediated by many pathways.
Let's look at the tumor suppressor protein retinoblastoma (RB) and how it affects the p53 pathway:

a) The loss of RB function contributes to the deregulation of the EF2 transcription factors, which sees an increase in E2F-1 concentrations.

b) E2F-1 directly activates expression of the human p14ARF tumour-suppressor protein

c)p14ARF,causes inhibition of the MDM2-p53 complex, therefore stabilizing p53. p53 is able to bring about cell cycle arrest at the G1/S phase.

Another cool/scary pathway for p14 activation is:
Expression of Oncogenes such as Ras or Myc, which results in the stimulation of the transcription of the p14 gene resulting in the stabilization of the p14 protein.

Patients who develop lung cancer seem to have a positive correlation with the loss of p16 and p53 functionality. Interestingly, the p14 ARF /p53 and p16 INK4A /Rb pathways are functionally linked and play distinct roles as components of the cell cycle checkpoints and growth inhibitory pathways.

In the figure presented here, you can see the complex pathways that relate these pathways.

"Molecules with frequent activating alterations in lung cancer are marked in red whilst proteins encoded by genes that are frequently or infrequently inactivated in lung cancer are denoted by dark blue and light blue respectively."

Here, we can clearly see how oncogenes such as MYC and RAS start a chain of reactions that ultimately lead to the activation of p16 and p14 which go ahead and affect the RB and MDM2 pathways respectively. Any loss of functionality to these proteins could lead to the p53 pathway being inhibited, ultimately resulting in (lung) cancers.