[ron123456 (OP)]

Isn't NAD+ required to sustain any glycolysis (aerobic or hypoxic) in any human normal or cancerous cell? If tumors use glycolysis for fast ATP production, then no NAD+ could mean none of this fast ATP production. Is it possible to eliminate NAD+ to just cancer cells and not normal differentiated cells and normal proliferating cells?

[Bored chemist]

Is it possible to eliminate NAD+ to just cancer cells

It is very difficult to do anything "just to cancer cells" because cancer cells are very similar to normal ones.

[ron123456 (OP)]

Are monoclonal antibodies not attracted by chemicals given off by a foreign invaders or nasty cells? Monoclonal antibodies by definition are "designed to bind to antigens that are generally more numerous on the surface of cancer cells than healthy cells". If this is true, then why can we not use the same or a similar concept to possibly eliminate NAD+ to just cancer cells and not normal differentiated cells and normal proliferating cells?

[Bored chemist]

Are monoclonal antibodies not attracted by chemicals given off by a foreign invaders

Sort of...
But cancer cells are almost identical to normal cells.
If you could get antibodies to bind to them then the immune system would destroy them without any further "medical" intervention

[ron123456 (OP)]

Could a dual purpose polymer molecule be designed that would attach to a carbine anchor for tumor injected gold nanoparticles? This molecule's dual purpose would be to temporary bind to a tumor as well as to permanently bind to Nad+ in the proximity......in time, macrophages would then perform mopup.... perhaps decreasing the Nad+ that is sustaining the tumor cell?
 

[Bored chemist]

There is still a problem.
How do you get the molecule to recognise a cancer cell?

[ron123456 (OP)]

The molecule could perhaps recognize a decreased cancer cell membrane voltage by sensing a decreased extracellular electric field force. But even if this was possible, the Nad+ produced by cancer cell glycolysis would probably be restricted to being intracellular. "NAD+ is carried into the mitochondrion by a specific membrane transport protein, since the coenzyme cannot diffuse across membranes". Perhaps if the other dual purpose of the attached anchored molecule was to temporary provide this same required transport protein to the cancer cell's membrane, then this may cause havoc to the tumor cancer cell? .. 

[ron123456 (OP)]

If the transport protein carried by the gold nanoparticle entered the cytosol by endocytosis and then engineered into ion protein channels for the cellular plasma membrane, then the entrapped Nad+ could exit the cytosol. With pulsed lasers within the therapeutic optical window (650nm-1350nm), stimulated active transport, in reverse, through these channels could eventually assist the exit of Nad+, placing the majority of it into the extracellular environment.....no Nad+, no sustaining cytosol glycolysis by fast ATP production "Malignant, rapidly growing tumor cells typically have glycolytic rates up to 200 times higher than those of their normal tissues of origin." Once into the interstitial fluid then with chemical combination a mopup could occur by macrophages.

[ron123456 (OP)]

Every problem requires a necessary starting point to be resolved? Before ending this conversation, is this conversation so far one good legitimate starting point path to follow?: i.e. If Nad+ is minimized in the cytosol of specifically cancer cells, then there can be no tumor cells' crazy growth....
Thx...

[ron123456 (OP)]

Well,.....here's a picture indicating that the Nad+ is not totally entrapped in the cytosol but can leave through a connexin CX43 hemichannel (connexon) and into the extracellular material....The problem is that these hemichannels are short lived with a half life of hours and cannot eliminate the build up of Nad+ in the cytosol and don't have a desire to do so in tumor cells (but please do note that inhibition of casein kinase 1 increases the number of surface hemichannels)......
So I guess we have to help the inflicted cell......Perhaps the attached molecule on the gold nanoparticle could be CX43 to help induce the production of additional hemichannels via the Golgi apparatus or to increase the open time of the connexon pores (Hemichannels tend to be opened by positive membrane potentials and low extracellular Ca2+)....

[syhprum]

My neighbours father survives after massive Metastasis with the aid of antibody treatment albeit at vast cost after three years it can be done but only if you live in the USA with generous insurence

[ron123456 (OP)]

Thanks for the concern....everything is cool.....