Many of the tumors exhibit acidosis with an acidic cytoplasm. It could be effectively used for designing pH sensitive drug releasing particles. Many such particles with Doxorubicin are still in trial.

As to alkalinity-cancer theory, which posits potentially beneficial effects on cancer processes and tumorigenesis as well as possible therapeutics, via modulation of the tumor PH environment, we must proceed cautiously and first appreciate (1) the distinction between intracellular pH versus  extracellular pH: we simply cannot assume that failure to modify the intracellular pH of tumors implies a corollary failure to modulate the  extracellular pH, and (2) the extracellular pH may have significant consequence in the tumor environment.

Furthermore, from the fact that food regardless of initial acidity and alkalinity cannot materially affect systemic levels, but rather only - and transiently - urine pH status, it does not  follow  that we cannot do so through non-food supplementation, and although again we lack human clinical confirmation, non-food supplementation to this end appears to affect extracellular pH (pHe), and it may further be possible  to affect  extracellular pH with potentially clinical relevant consequences on the tumor environment: the extracellular pH (pHe) of malignant solid tumors, including breast cancer, is acidic, in the range of 6.5 to 6.9, whereas the extracellular pH of normal tissues is significantly more alkaline, in the range of 7.2 to 7.5, and there is compelling preclinical data strongly suggesting that we can influence the extracellular pH milieu of tumors.    

The best case for this I would submit comes from the research of Ian Robey at the University of Arizona and Robert Gillies at the H. Lee Moffitt Cancer Center and Research Institute and colleagues who investigated metastatic MDA-MB-231 (triple negative) adenocarcinoma  cells in an experimental mouse model in order to test the hypothesis that neutralizing the acid pH of tumors by treatment with oral NaHCO3 (sodium bicarbonate) will inhibit invasion and consequently reduce the incidence of spontaneous metastases.  They found that although bicarbonate effectively increased the extracellular pH (pHe) of these large tumors, it did not affect the intracellular pH (pHi), reflected in a lack of an effect on growth rates.  But growth is not everything: despite lack of any effect on primary tumor growth inhibition, the bicarbonate therapy led to significant reductions in the number and size of metastases to lung, intestine, and diaphragm, and this reduction in metastases led to increased survival, via it  would appear the bicarbonate-induced reversal of tumor acidosis  at the extracellular pH level. 

Some Reservations: My Own Critical Appraisal

However, the authors acknowledged that the idea of treating cancer through oral buffering administration although theoretically attractive has some significant caveats.  At the dose of oral bicarbonate used (200 mmol/L) the buffering was not saturating, and the administered dose translates to an intake of ∼1.5 μmol/h/g of whole mouse, but the acid production rate of tumors can be ∼100 μmol/h/g of tumor weight, as demonstrated by the work of Xin Lin Xu and and Michael Guppy at the University of Western Australia.

What does all this matter? I would submit that it entails that should these findings be replicable and verifiable in human clinical trials, not just  experimental mouse models, then at best, even it true, the doses of oral bicarbonate that may be able to counteract the acid load of a 15 mg tumor translates to a 1 cubic millimeter (mm3) micrometastasis, and given that, therefore - again under ideal conditions -  the effectiveness of this therapy will necessarily be vastly reduced with larger clinical realistic tumors, so that under the  best of  circumstances, as yet unrealized, the clinical relevance of this effect is highly  questionable, suggesting that these effects warrant further investigation but require demonstration of clinical significance in human clinical trials, and the safety and sustainability, in addition to the efficacy, of such dosing needs still to be established before recommendation can be warranted.

Furthermore, the dose used in the experimental mouse model can be calculated to be the equivalent of a daily dose of 37 grams in a 70-kg human (Rober Gatenby at the Moffitt Cancer Center and colleagues), solely to affect a cubic millimeter  micrometastasis.  Yet I note  that for the treatment of moderate metabolic acidosis, doses of 325 to 2000 mg orally, 1 to 4 times a day, are used in this emergency context, to a max of 8 grams daily, and comparable does are  used for urinary alkalinization and dyspepsia, and even at these levels may induce metabolic alkalosis and hypernatremia, among other adverse sequelae, and even if we relax these application levels to say as much as 50 grams, to effect even a centimeter tumor would require does at of many manifold greater than typical upper  thresholds in humans, a wholly contraindicative and unsupportable level, still leaving the clinical feasibility of chronic bicarbonate ingestion for putative tumor reduction tumor invasion under severe doubt and without compelling  support.

Alkalinity-cancer theory is demonstrably not as yet ready for prime time and lacks human clinical evidence to support any deployment in the human context, and as I have suggested above, even the preclinical data is insufficient methodologically to dispositively deduce appreciable antitumor benefit, but it is unfair and narrow to brand it irrational or absent plausibility. The  research of dedicated investigators in cancer metabolism as a wider hypothesis inclusive of many of the tenets of cancer-alkalinity theory - like Ian Robey and Robert Gilllies, and Robert Gatenby and colleagues at Moffitt, of Pawel Swietach and colleagues at Oxford, Stefano Fais and colleagues in Rome, Nihal Alltan at Rockefeller University, Melvin Schindler and colleagues at Michigan State, Salvador Harguindey and colleagues in Spain, You Han Bae and colleagues in Korea, Eyal Gottlieb in Glasgow, José Cuezva and colleagues in Madrid, David Sabatini at MIT, Sten Orrenius and colleagues at the Karolinska Institutet (Sweden), Robert Cummings and colleagues at the University of Western Ontario, Alexei Vazquez at the Cancer Institute of New Jersey, Miguel López-Lázaro and colleagues at the  University of Seville, and Leonardo Ferreira in Portugal, among many others - is reasonable, plausible, and verifiable, with ever stronger preclinical foundations, and emerging human-context clinical confirmation, so we cannot as yet judge wanting the cancer-alkalinity theory until the broader fabric of cancer metabolism matures, as it is rapidly doing.