Implications of common mutations in a gene between specific cancers

The predominance of domain-specific mutations for a given gene in different cancers is mainly a manifestation of the functions driven by those domains, the upstream and downstream signaling processes, and ligand interactions that are intertwined with such domains. When a similar pattern of mutations for a gene gets reflected in another form of cancer like ESCC but not in yet other forms of cancers e.g., lung cancers, then there is a possibility of similar interacting ligands or signaling interactions in EGFR. This opens up the need to look into the basic binding mechanisms of EGFR  and its interactions. Questions arise as to what is common in this gene function in these two tissues. 
There have been very few studies on the presence and distribution of EGFR mutations and their relevance in the process of oncogenesis in ESCC. Their presence is rare and insignificant \cite{Guo2016} OR their significance has been less studied. Either way, their copy number is directly related to poor prognosis\cite{Barsouk2019} and changes associated with them, including copy number OR mutations, are one of the changes associated with the development of ESCC \cite{Mandard2000}.
Keeping these in the backdrop, we propose that the interacting partners unique to the mutation-specific domains of the EGFR gene in Glioblastoma might match up in functional aspects with those involved in Esophageal Squamous Cell Carcinoma. It is worth looking into the interacting partners of the EGFR-vIII domain in these two cancers. For example, the OSMR gene (Oncostatin M Receptor beta) is a  critical regulator of glioblastoma tumor growth that orchestrates a feed-forward signaling mechanism with EGFRvIII \cite{Jahani-Asl2016}. Interestingly, an RT-PCR detected overexpression of the alternatively spliced OSMR β transcript in 9 of 11 ESCCs \cite{Kausar2011}. Are these phenomena concomitant in these two cancers? How many other interacting partners of EGFR in vIII and vIV exist that are affected in these cancers? Addressing these can provide greater insights into the role of these genes in the signaling network.