Where don't we dance enough: managing life span, an independent factor in managing cancer patient, and may increase the cure rate!

Because of limited resources available in research, society falls short in the management of cancer patients.  The notion that cancer patient should be managed by affecting only their driver Mutation has been popular lately and most research has focused on this emphasis.  There is a rush to discovering  the driver mutation in each disease.   The truth is that driver mutation although very effective (ie. BRAF inhibitor) for a short time, are quickly overwhelmed by what we have come to know as "mechanisms of resistance"  The point is that cells are constantly exposed to new environmental stimulants.  And their natural TASK is to die or adapt.  And naturally we try to forget or underestimate the adaptative capability of cells, including neoplastic (cancer) cells.  Cure will remain fleeting until a closer look is taken into these adjustment techniques used by the cancer cells.  and it is within that contest that I bring this statement to your mind:

" that SHC-1 not only opposes IIS but also activates JNK signaling. Loss of shc-1 function results in accelerated aging and enhanced sensitivity to heat, oxidative stress, and heavy metals, whereas expression of human p52Shc rescues the shc-1 mutant phenotype. SHC-1 acts upstream of the insulin/IGF receptor DAF-2 and the PI3 kinase AGE-1 and directly interacts with DAF-2. Moreover, SHC-1 activates JNK signaling by binding to MEK-1 kinase. Both aspects converge on controlling the nuclear translocation and activation of the FOXO transcription factor DAF-16." Elke Neuman-Haeflin et al.

If you are shocked and troubled by the placement of this statement here, you are completely within the norm! but let's go back and recapitulate.   Most cells succumbs to external pressure by cellular environmental stimulations.   Hypoxia, autocrine cytokines, chemicals and minerals end up exciting receptors including VEGFRs  (the MEK is close by).  But really when you speak of the VEGF, you imply SHC1,2 and stimulation of Annexins and from there p52, p42, and the famous p66SHC....then you can understand the above sentence...In Gastric cancer for example,  VEGFR2 is stimulated and therefore the effectiveness of Ramucirumab.  (CYRAMZA.)

Please note that the statement speak about p52 and does not even address the main RAS cofactor p66 which may affect Cyclin D and deplete MCI-1 the main depletor of SHC-1. (through PTPNs)
RAS autophosphorylation driving the cancerous process may be hidden here.

These facts point to the truth that independent of cancer driven mutation, control of these processes must occur concurrently to improve the cure!  cancer deaths are produced by progression of cancer but also involvement of cellular maturation and lifespan determinants that most Oncologist do not measure! (we dance very little away from guidelines (NCCN))...