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Epigenetic alterations have been implicated in the pathogenesis of solid tumors, however, proto-oncogenes activated by promoter demethylation have been sporadically reported.
Adequate blood supply is a prerequisite in the pathogenesis of solid malignancies.
Evasion of apoptosis contributes to the pathogenesis of solid tumours including non-small cell lung cancer (NSCLC).
Evidence from experimental and clinical studies increasingly points to an important role for hypoxia in the pathogenesis of solid cancers, including pancreatic cancer.
These enzymes regulate cellular processes such as metabolism, cell survival, differentiation, DNA repair and they are implicated in the pathogenesis of solid tumors and leukemias.
Fusion transcripts are common in haematological malignancies and they are also recognized as contributing to the pathogenesis of solid tumors [ 20].
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Interleukins and cytokines play an important role in the pathogenesis of many solid cancers.
These results suggest that frequently deleted regions may harbor one or more TSGs that play important roles in the pathogenesis of various solid malignancies, including NPC.
Recently, there is increasing evidence that inflammation, both local and systemic, has a causal link in the pathogenesis of many solid tumours (Balkwill and Mantovani, 2001; Coussens and Werb, 2002).
The key assumption of the model reflecting recent biological insights into the pathogenesis of the solid tumour growth states that the tumour cell population is heterogeneous with respect to the parameters characterizing the outcome of the interaction with cytotoxic T lymphocytes.
Overexpression of c-erbB-1 or c-erbB-2 mRNA and/or protein has been implicated in the pathogenesis of various solid tumours including breast, ovarian, lung and oesophageal cancers; however, association with prognosis varied substantially between studies and tumour entities (Meden et al, 1994; Singleton et al, 1994; Schneider et al, 2000; Brabender et al, 2001; Esteva et al, 2002; Lau et al, 2002).
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