Dear Marceline,

Carcinogenesis is a multi-step and complicated proccess implicating aspects such as microenvironment, heritable mutations, hypoxia and ROS,  physiological and genetic heterogeneity, angiogenesis, etc. 

Some of the following papers can be useful for you.

Finally, if you consider this answer appropriate, please upvote it using the green up arrow click.

Best regards,

http://neurosurgery.med.wayne.edu/pdf/evolution_of_cancer_review.pdf

http://www.sciencedirect.com/science/article/pii/S1044579X09000649

http://www.sciencedirect.com/science/article/pii/S1044579X08000400

http://www.sciencedirect.com/science/article/pii/S0304383514007332

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4233442/

Tissue stem cells and cancer-initiating cells (also referred to as cancer stem cells; CSCs) share much in common from the perspective of the phenotype characterized by self-renewal potential and multi-lineage differentiation ability leading to the heterogeneity in the tissue. Lineage tracing revealed  Paneth cells are required for the survival and proliferation of not only Lgr5-positive normal stem cells in the intestine but also APC-mutant adenoma-initiating cells However, tissue stem cells are not necessarily responsible for the establishment of CSCs. For example, dysregulated expression of the BMP antagonist caused the change in the cell fate determination by promoting the de-differentiation of Lgr5-negative progenitor cells.It is also notable that the constitutive activation of Wnt or the NF-κB signaling pathway leads to emergence of CSCs derived from non-stem cells in normal tissue. 

Article Intestinal Tumorigenesis Initiated by Dedifferentiation and ...

Article Aberrant epithelial GREM1 expression initiates colonic tumor...

Article Therapeutic Strategies Targeting Cancer Stem Cells

DMBA-TPA carcinogenesis experimental model is a good example. DMBA is called "initiation," while TPA is referred to as "promoter." DMBA causes the genetic alteration for malignant transformation such as the resistance to the cellular senescence. TPA promotes the proliferation of these minor malignant cells.   

Dear Marceline,

Carcinogenesis is a multi-step and complicated proccess implicating aspects such as microenvironment, heritable mutations, hypoxia and ROS,  physiological and genetic heterogeneity, angiogenesis, etc. 

Some of the following papers can be useful for you.

Finally, if you consider this answer appropriate, please upvote it using the green up arrow click.

Best regards,

http://neurosurgery.med.wayne.edu/pdf/evolution_of_cancer_review.pdf

http://www.sciencedirect.com/science/article/pii/S1044579X09000649

http://www.sciencedirect.com/science/article/pii/S1044579X08000400

http://www.sciencedirect.com/science/article/pii/S0304383514007332

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4233442/

Cancer development is a complicated process that in certain cases may need as much as 6 mutations (from adenoma to colorectal cancer as shown by Weimberg and as Jose established in his answer: multi-step process) and in other cases it is enough one chromosomal traslocation like in chronic myeloid leukemia,

So, we cannot speak of a universal mechanisms found in all cancers, but instead we should consider individual and specific mechanisms  for each kind of tumors.

Herewith find, please, some my papers on the topic

Dear Marceline,

Four ways by which tumors can arise : 1. disregulation(=evasion) of apoptosis (e.g. follicular lymphoma), 2. loss of tumor supressor genes (e.g. retinoblastoma, neurofibromatosis), 3. protooncogene activation (MYC, FOS, JUN overexpression), 4. viral carcinogenesis (e.g. HPV)

Hope it helps! Regards.

Source: Marusic M, Kovac Z, Gamulin S. Pathophysiology. 2013. Medicinska naklada, Zagreb. (textbook)