Recently, scientists have found an approach to block one of the most tantalizing yet elusive target proteins in cancer cells, giving rise to tumor's shrinkage with little or no harm to normal cells in pre-clinical study.

In the study appearing in the journal Cell, they used a specially crafted compound to disrupt the protein's ability to spur its own production and that of other protein involved in tumor cell growth. The result, in laboratory samples of neuroblastoma, was death of the cancer cells and no harm to healthy cells.

The study are mainly performed on a protein called MYCN, one of a family of proteins that are notorious not only for stimulating the growth and proliferation of cancer cells, but also for their ability to evade targeted drug therapies. The molecule has proved very difficult for targeted agents to reach and latch onto, making it "undruggable". Scientists expect that the novel approach may prove effective against some of the other cancer also characterized by a surplus of MYC-family proteins.

Recent studies have shown that when transcription factors like MYC are mutated or overabundant, they can have a cancerous effect. They cause a global rise in gene expression, making genes throughout the cell more active.

Transcription factors like MYCN work by evoking certain "co-factor" proteins to attach themselves to specific sections of DNA. They act to spur nearby genes into activity .Using a covalent inhibitor of cyclin-dependent kinase 7 (CDK7) to disrupt the transcription of amplified MYCN in neuroblastoma cells, researchers demonstrate downregulation of the oncoprotein with consequent massive suppression of MYCN-driven global transcriptional amplification, and significant tumor regression in a mouse model.

Their study also has limitations to acknowledge. Firstly, they did not analyze CT characteristics of thymic carcinoma according to their specific pathological classifications. Certain subtypes of thymic carcinoma such as neuroendocrine carcinomas have differentiated CT manifestations and prognosis, which warrants further study. Secondly, the complete survival data of these patients are not available, which intimidates the possibility to determine the relationship bettheyen survival and variables of risk of aggressiveness and degree of CT enhancement. The fact that survival rates of TETs patients, especially for those in low risk subgroups, are relatively high and a very long follow up will be required to collect these data. Further study for elucidating this research question is warranted. Thirdly, the hemodynamic analysis of TETs based on histopathology was not conducted, and further study for resolving this research question will be needed to clarify the mechanism of CT enhancement finding in this study.

In conclusion, using the largest sample up to date, they identified that several variables which are largely unreported before, including degree of CT enhancement, risk of aggressiveness, and multiple nodule with fibrous septum could preoperatively help determine the WHO pathological classification of TETs patients, especially for the low risk and high risk subtypes. A combined prediction using these variables will provide a better guidance for appropriate therapeutic strategies for TETs patients.