Researchers give insight into novel therapeutics development for metastatic tumor advances
New York, US: Researcher Paul Dent of Virginia Commonwealth University's Department of Biochemistry and Molecular Biology found that tumours that have metastasized to distant locations, such as the brain, are most often impossible to treat and cure, despite recent successes in some tumour types such as NSCLC and cutaneous melanoma.
There is, however, substantial evidence that immune therapy may cause hyper-progression in some NSCLC patients, perhaps including Dr. Blagosklonny, whose tumour contains METex14 and MDM2 amplification, as well as melanoma and NHSCC patients.
A new editorial paper was published in Oncoscience (Volume 11) on February 9, 2024, entitled, "A very long and winding road: developing novel therapeutics for metastatic tumors."
"There are several issues that presently preclude more effective control of solid tumors both in situ and as metastatic disease."
The first is that the mutations which drive a cancer phenotype are generally the combination of subtle alterations in cell biology, any one of which, if targeted, if it can be targeted, will only have modest effects on tumor growth and survival. Conceptually, this calls for an immediate use of two- and three-drug combinations blocking key signaling pathways to achieve effective tumor control regardless of whether resistance mechanisms evolve. Second, a corollary of altered cell biology, and highlighted in the article, is that fewer tumors have a single recognizable driving oncogene to which the tumor cell is specifically addicted for growth and survival, e.g., mutant RAS proteins, mutant EGF receptors and other mutant receptors of MET, RET, and HER2.
"And even under these circumstances based on a large body of evidence from the past 20 years is that such tumors also require treatment with two- and three-drug combinations that simultaneously interdict the primary driving oncogene, block signaling from the primary evolving resistance mechanism and even block signaling from a secondary survival pathway."
