Carcinogenesis is a sophisticated biological process consisting of progressive changes in somatic cells from premalignant to malignant phenotype. Despite the vast accumulating knowledge in tumor biology, the origin of cancer, the mechanisms of invasive cancer cell selection, and the geno-phenotypes required for metastasis remain enigmatic. Moreover, it is now widely accepted that the malignant behavior of cancer does not depend solely on tumor cell biology. According to Paget's original “seed and soil” hypothesis, tumor morphology and invasive phenotypes are largely determined by selection in the host tissue microenvironment.
Cell differentiation is a process by which proliferating cells gradually acquire tissue-specific function and phenotype. During carcinogenesis, the cancer cells lose tissue-specific markers developing a de-differentiated state with increased proliferative capacity and plasticity. Moreover, de-differentiation has also been implicated in therapeutic resistance among several types of solid tumors.
Generally, a cancer diagnosis is based on i.a clinical signs, radiologic findings, immunohistopathology, and genetic analysis. The treatment and outcomes of cancer depend on several factors, like age and gender of the patient, tumor size, metastatic burden, as well as functional and immuno-genetic profile of the tumor. With increasing insight into cancer biology, the clinical assessment of cancer has become more complex, with various diagnostic modalities, patient stratification systems, and treatment options. Due to this challenging complexity, there is a need for new mathematical models and stratification tools that might facilitate the clinical assessment of individual patients or patient groups based on their predicted treatment response or risk of disease.