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Bibliografia 1
pH and Chemotherapy - A., Raghunand N. B., Gillies RJ.
University of Arizona Health Sciences Center, Cancer Center Division,
Tucson 85724-5024, USA.
In vivo pH measurements by magnetic resonance spectroscopy reveal
the presence of large regions of acidic extracellular
pH in tumours, with the intracellular
pH being maintained in the
neutral-to-alkaline range.
This acid-outside plasmalemmal pH gradient acts to exclude weak base
drugs such as the anthracyclines and vinca alkaloids, a behaviour
that is predicted by the decrease in octanol-water partition
coefficients of mitoxantrone and doxorubicin with decreasing
solution pH.
This pH gradient can be reduced or eliminated in mouse models of
breast cancer by systemic treatment with sodium bicarbonate.....
PMID: 11727930
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Articoli che documentano l'acidosi che caratterizza i tessuti
tumorali
I Gliomi maligni esibiscono un'alterata regolazione dei pH, in
confronto agli astrociti non trasformati
Malignant Gliomas display altered pH regu1ation byè NHE1 compared
with non transformed astrocytes
Lee Anne McLean, Jane Roscoe, Nanna K. Jorgensen, Frederic A. Gorin,
and Peter M. Cala - Departments of Human pHysiology and Neurology,
School of Medicine, University of California, Davis, California
95616
Am J pHysiol Cell
pHysiol 278: C676-C688, 2000.
I gliomi maligni esibiscono un'alterata regolazione del pH, in
confronto agli astrociti non trasformati. I gliomi maligni
esibiscono pH intracellulare (pHi) alcalino e il pH extracellulare (pHe)
acido in confronto ad astrocití normali, malgrado l'aumento di
produzione di H+.
Il pHe riduce la disponibilità dello ione bicarbonato HC03-, perciò
riducendo la concentrazione dipendente, sia passiva che dinamica.
Questo implica che i gliomi sono dipendenti dalla concentrazione
dinamica dello ione HC03- di bicarbonato, e indipendente dallo H+,
come il tipo HC034H+ exchanger (NHE1).
In questo studio 4 gliomi a rapida proliferazione hanno esibito
stabile e significativa alcalinità intracelluiare, superiore
rispetto agli astrociti normali e un maggior riequilibrio
dell'acidosi, dopo somministrazione di C021-1-1C03.
L'inibizione di NHE1 in assenza di C021HCO3 fu il risultato di
un'alta acidificazione dei gliomi, laddove i normali astrociti non
ne risentirono..
Quando veniva sospeso il C021-HCO3, il pHi degli astrociti
aumentava, e ancora il pHi dei gliomi inaspettatamente diveniva
acido; questo suggeriva un meccanismo di acidificazione dipendente
dallo ione bicarbonato -HC03.
Le sequenze nucleotidiche dei DNA dei gliomi, dimostrarono che
alterazioni genetiche non erano responsabili della funzione
dell'NHE1.
Questi dati suggeriscono che l'attività dell'NHE1 è
significativamente alterata nei gliomi e può essere utilizzata come
bersaglio per lo sviluppo di terapie specifiche tumorali.
Cause e conseguenze dell'acidità nei tumori e implicazioni
terapeutiche
Causes and consequences of tumour acidity and implications for
treatment
Marion Stubbs, Paul M.I. McSheehy,Jhon R. Griffiths and C. Lindsay
Bashford - Molecular Medicine: Today, January 2000 (vol.6)
Le cellule tumorali
hanno un pH extracellulare (pHe) più basso delle cellule normali;
questa è una caratteristica intrinseca dei genotipo tumorale,
causata da alterazioni dovute sia al rilascio di acidi dalle cellule
tumorali. sia all'assorbimento dell'acidosi extracellulare.
Un basso pH favorisce le cellule tumorali perché promuove l'invasività,
laddove un alto pH extracellulare conferisce loro un vantaggio sulle
cellule normali, riguardo alla crescita.
Gli approcci genetico molecolari hanno rivelato che l'ipossia
indotta influenza la regolazione della glicolisi, un meccanismo
potenziale importante per stabilire il fenotipo metabolico tumorale.
La comprensione dell'acidità dei tumore apre nuove opportunità
terapeutiche.
Cause e conseguenze dell'ipossia e dell'acidità nei tumori
Causes
and consequences of hypoxia and acidity in turnors - Novartis
Foundatíon symposium
Robert J. Gillies - Arizone Cancer Center, University of Arizona,
Tucson, Arizona, Usa - Molecular Medicine Vol.7 N° 2 February 2001
Sia l'ipossia che l'acidità perpetuano un fenotipo tumorale più
aggressivo.
Ipossia e acidosi inducono instabilità genetica. Ipossia e acidità
inducono un fenotipo più metastatico e questo verosimilmente implica
l'alterazione di una proteasi (catepsina) e una selezione
metabolica. anche evidente tale che le cellule metastatiche
producono tumori che sono più ipossici e con iperacidosi
extracellulare. L'ipossia conferisce radio resistenza; il gradiente
acido extracellulare può conferire chemio resistenza. La dinamica
delle vescicole acide intracellulari è implicata sia nella chemio
resistenza fisiologica che biochimica.
Cause e conseguenze dell'ipossia e dell'acidosi nel microambiente
dei tumori
Causes and consequences of hypoxia and acidity in tumour
rnicroenvironments
J.R. Griffiths - Glia 1994 Nov:12(3):196-210
1a riga: La prima e più importante scoperta nella fisiologia e
biochimica dei tumore, fu l'anormale quantità di acido prodotta.
Anche in presenza di ossigeno, l cancri solidi ottengono energia
preferibilmente convertendo glucosio in acido lattico. Pagina 296,
17a riga: Il trattamento dei tumori con bicarbonato di sodio, può
eliminare il gradiente di pH intra ed extracellulare e amplificare
la risposta ai chemioterapici debolmente basici tipo
mitoxantrone. L'acidità tumorale è anche implicata nella
chemio resistenza.
Ultimo capoverso: Le origini dell'acidosi tumorale si stanno
chiarificando negli ultimi anni, e questo in una prospettiva
terapeutica anticancro.
pH acido nei tumori, presupposto per nuove linee terapeutiche
Acid pH in tumors and its potential for therapeutic exploitation.
Tannock IF, Rotin D. - Department of Medicine, Ontario Cancer
Institute, Toronto, Canada. - Cancer Res 1989 Aug 15;49(16):4373-84
Related Articles, Books, LinkOut
La misurazione del
pH nei tessuti ha evidenziato che il micro-ambiente è più acido nei
tumori che nei tessuti normali; la produzione di acido lattico e
l'idrolisi di ATIP nelle regioni ipossiche, rientrano probabilmente
in questo meccanismo di iperacidità, insieme ad altri pattern
metabolici.
Il pH acido allora, può influenzare lo sviluppo di nuove e
relativamente specifiche terapie anticancro, mirate a regolare il pH
intracellulare.
Potenziamento della terapia agendo sul pH del tumore
Enhancement of chemotherapy by manipulation of tumour pH.
Raghunand N, He X, van Sluis R, Mahoney B, Baggett B, Taylor CW,
Paine-Murrieta G, Roe D, Bhujwalla ZM, Gillies RJ. - Arizona Cancer
Center, Tucson 85724-5024, USA. - Br J Cancer 1999 Jun;80(7):1005-11
Related Articles, Books, Link Out
Il pH dei tumori
solidi è significativamente più acido dei tessuti normali.
Un basso pH in vitro riduce la citotossicità dei chemioterapici
debolmente basici., contribuendo ad una resistenza.
Il bicarbonato di sodio, si riporta nel lavoro, amplifica
significativamente l'effetto della doxorubicina.
Questo lavoro rappresenta la dimostrazione in vivo (in pazienti
neoplastici), della resistenza, già ben documentata in vitro e in
via teorica, verso i chemioterapici debolmente basici.
Dynamics of bioelectric activity of the brain and erythrocyte
ultrastructure after intravenous infusion of sodium bicarbonate to
oncologic patients. - Davydova IG, Kassil' VL, Raikhlin NT,
Filippova NA. -
Biull
Eksp Biol Med 1992 Apr;113(4):352-5 Related Articles, Books, Link
Out
Lo studio indica che
le cellule di criceto possiedono attività regolatorie intracellulari,
e che l'acidificazione cellulare gioca un ruolo nell'aumento di
frequenza delle trasformazioni osservate nelle cellule coltivate in
condizioni di acidità.
L’acidosi può essere evitata o ridotta artificialmente attraverso l’alcalinizzazione
del sangue.
Effetto dell'alcalosi artificiale nell'attività dei cervello e nelle
cellule dei sangue in pazienti oncologici
Characteristics of the effects of artificial alkalosis on electrical
activity of the brain and ultrastructure of blood cells in oncologic
patients. - Davydova IG, Kassil' VL, Filippova NA, Barinov MV. -
Vestn
Ross Akad Med Nauk 1995;(4):24-5 Related Articles, Books, Link Out
Vengono studiati 40
pazienti oncologici, di differenti istotipi, sedi e dimensioni.
Il lavoro evidenzia che i pazienti hanno un'acidosi intracellulare
generalizzata, che può essere diminuita con l'alcalinizzazione del
plasma, con il risultato di ridurre le degenerazioni cellulari.
Diminuzione dei volume in presenza dello ione -HC03 in cellule di
osteosarcoma
Regulatory volume decrease in the presence of HCO3- by single
osteosarcoma cells UMR-106-01.
Star RA, Zhang BX, Loessberg PA, Muallem S. - Department of
Medicine, University of Texas Southwestern Medical Center, Dallas
75235-9040. - J Biol Chem 1992 Sep 5;267(25):17665-9 Related
Articles, Books, Link Out
Si registra
simultaneamente la variazione di volume e di pH intracellulare, per
studiare il ruolo di HC03- nella diminuzione dei volume cellulare.
L'aumento di pH intracellulare - risulta - coincide con una
diminuzione del volume cellulare.
Appare evidente, in questo modo, il coinvolgimento dei Na+(HC03-)
nella regolazione del volume cellulare.
L'acidificazione intracellulare è associata ad un aumento di
trasformazioni morfologiche nelle cellule embrionali di
criceto siriano
Intracellular acidification is associated with enhanced
morpHological transformation in Syrian hamster embryo cells.
LeBoeuf RA, Lin PY, Kerckaert G, Gruenstein E. - Procter and Gamble
Co., Miami Valley Laboratories, Cincinnati, Ohio 45239-8707. -
Cancer Res 1992 Jan 1;52(1):144-8 Related Articles, Books
Lo studio indica che
le cellule di criceto possiedono attività regolatorie intracellulari,
e che l'acidificazione cellulare gioca un ruolo nell'aumento di
frequenza delle trasformazioni osservate nelle cellule coltivate in
condizioni di acidità.
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1. Chetoacidosi diabetica grave
Gamba G “Bicarbonate therapy in severe diabetic ketoacidosis.
A double blind, randomized, placebo controlled trial.” (Rev
Invest Clin 1991 Jul-Sep;43(3):234-8).
2. Miyares Gomez A. in “Diabetic
ketoacidosis in childhood: the first day of treatment
(An
Esp Pediatr 1989 Apr;30(4):279-83).
3. Rianimazione cardiorespiratoria
Levy MM “An evidence-based evaluation of the use of sodium
bicarbonate during cardiopulmonary resuscitation” (Crit Care Clin
1998 Jul;14(3):457-83).
Vukmir RB Sodium bicarbonate in cardiac arrest: a reappraisal
(Am J Emerg Med 1996 Mar;14(2):192-206).
4. Bar-JosepH G.
“Clinical use of sodium bicarbonate during cardiopulmonary
resuscitation--is it used sensibly?”
(Resuscitation 2002 Jul;54(1):47-55).
5. Gravidanza
Zhang L, “Perhydrit
and sodium bicarbonate improve maternal gases and acid-base status
during the second stage of labor”
Department of Obstetrics and Gynecology, Xiangya Hospital, Hunan
Medical University, Changsha 410008
6. Encefalomiopatia mitocondriale
Maeda Y. “Perioperative
administration of bicarbonated solution to a patient with
mitochondrial encepHalomyopathy”
(Masui 2001 Mar;50(3):299-303).
7. Emodialisi
Avdic E.
“Bicarbonate versus acetate hemodialysis: effects on
the acid-base status”
(Med Arh 2001;55(4):231-3).
8. Dialisi peritoneale Feriani M “Randomized long-term evaluation of
bicarbonate-buffered CAPD solution.” (Kidney Int 1998
Nov;54(5):1731-8).
9. Tossicosi farmacologica Vrijlandt PJ “Sodium bicarbonate infusion for
intoxication with tricyclic antidepressives: recommended inspite of
lack of scient(ific evidence” Ned Tijdschr Geneeskd 2001 Sep
1;145(35):1686-9)
10. Knudsen K,
“EpinepHrine and sodium bicarbonate independently and additively
increase survival in experimental amitriptyline poisoning.”
(Crit Care Med 1997 Apr;25(4):669-74).
11.
Epatopatia Silomon M “Effect
of sodium bicarbonate infusion on hepatocyte Ca2+ overload during
resuscitation from hemorrhagic shock.” (Resuscitation
1998 Apr;37(1):27-32).
Mariano F.
“Insufficient correction of blood bicarbonate levels in biguanide
lactic acidosis treated with CVVH and bicarbonate replacement
fluids”
(Minerva Urol Nefrol 1997 Sep;49(3):133-6).
12. Interventi di chirurgia vascolare Dement'eva II “Calculation of the dose of
sodium bicarbonate in the treatment of metabolic acidosis in surgery
with and deep hypothermic circulatory arrest” (Anesteziol Reanimatol 1997
Sep-Oct;(5):42-4).
Altra Bibliografia -
References
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Electrolyte and Acid-Base Disorders, Churchill Livingstone, New
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Consumer's Guide to Chelation Therapy and Other Heart Savers,
Sixteenth Edition, Healthsavers Press, Herndon, Virginia, 1996.
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Therapy, Medex Publishers, Second edition, Trout Dale VA, March
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4 - Cohen, R.D., The Liver and Acid-Base Regulation, in Arieff,
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Acid-Base Disorders, Churchill Livingstone, New York, NY, 1995.
5 - Ensminger, Audrey H., Ensminger, M. E., Konlande, James E.,
Robson, John R.K., The Concise Encyclopedia of Foods & Nutrition,
CRC Press, Boca Raton, FL, 1995.
6 - Feldman, Elaine B., Nutrition and Diet in the Management of
Hyperlipidemia and Atherosclerosis, in Modern Nutrition in Health
and Disease, Volume 2, Lea & Febiger, Philadelphia, PA, 1994.
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(Editors) Fluid, Electrolyte and Acid-Base Disorders, Churchill
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The Johns Hopkins U. Press, Baltimore, MD., 1982.
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Physiology, Volume 1 & 2, Springer Publishing, New York and
Heidleberg, 1996.
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Physiology, Ninth Edition, W.B Sanders Company, Philadelphia, PA.,
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Surinder, and Kamel, Kamel S., Diabetic Emergencies, in Arieff,
Allen I., and DeFronzo, Ralph, A., (Editors) Fluid, Electrolyte and
Acid-Base Disorders, Churchill Livingstone, New York, NY, 1995.
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Heart Association, Washington, DC, 1996.
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The genomic analysis of response to
lactic acidosis in human
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ALTRA BIBLIOGRAFIA (English)
[1] Vestn Ross Akad Med Nauk 1995;(4):24-5
[Characteristics of the effects of artificial alkalosis on
electrical activity of the brain and ultrastructure of blood cells
in oncologic patients].
[Article in Russian] Davydova IG, Kassil' VL, Filippova NA, Barinov
MV.
The authors examined 40 patients with malignant tumors of various
histogenesis, sites and extent, as well as 5 patients with benign
tumors and other non-tumorous diseases. They also studied their
electroencepHalograpHy and peripHeral blood lympHocytic and
erythrocytic ultrastructure in metabolic alkalosis temporarily
induced by intravenous sodium hydrogen carbonate. In cancer patients
without late metastases, alkalosis caused a transient normalization
of previously altered electroencepHalograpHy, erythrocyte
disaggregation and substantially reduced the count of killer cells
in small and middle lympHocytes.
These findings suggest that patients with malignant neoplasms have a
generalized intracellular acidosis which can be temporarily
abolished by plasma alkalinization.
PMID: 7780336
[2] Br J Cancer 1999 Jun;80(7):1005-11
Enhancement of chemotherapy by manipulation of tumour pH.
Raghunand N, He X, van Sluis R, Mahoney B, Baggett B, Taylor CW,
Paine-Murrieta G, Roe D, Bhujwalla ZM, Gillies RJ.
Arizona Cancer
Center, Tucson 85724-5024, USA.
The extracellular (interstitial) pH (pHe) of solid tumours is
significantly more acidic compared to normal tissues. In-vitro, low
pH reduces the uptake of weakly basic chemotherapeutic drugs and,
hence, reduces their cytotoxicity. This pHenomenon has been
postulated to contribute to a
'pHysiological' resistance to weakly basic drugs in vivo.
Doxorubicin is a weak
base chemotherapeutic agent that is commonly used in combination
chemotherapy to clinically treat breast cancers. This report
demonstrates that MCF-7 human breast cancer cells in vitro are
more susceptible to doxorubicin toxicity at pH 7.4, compared to pH
6.8. Furthermore 31P-magnetic resonance spectroscopy (MRS) has shown
that the pHe of MCF-7 human breast cancer xenografts can be
effectively and significantly raised with sodium bicarbonate in
drinking water.
The bicarbonate-induced extracellular alkalinization leads to
significant improvements in the therapeutic effectiveness of
doxorubicin against MCF-7 xenografts in vivo.
Although pHysiological resistance to weakly basic chemotherapeutics
is well-documented in vitro and in theory, these data represent the
first in vivo demonstration of this important pHenomenon.
PMID: 10362108
[3] Med Hypotheses 1999 May;52(5):367-72
Carcinogenesis and the plasma membrane. Stern RG, Milestone BN,
Gatenby RA.
Department of Veterans Affairs Medical Center, and University of
Arizona College of Medicine, Tucson, 85723, USA.
sternr@u.arizona.edu
Presented is a two-stage hypothesis of carcinogenesis based on: (1)
plasma membrane defects that produce abnormal electron and proton
efflux; and (2) electrical uncoupling of cells through loss of
intercellular communication. These changes can be induced by a wide
variety of stimuli including chemical carcinogens, oncoviruses,
inherited and/or acquired genetic defects, and epigenetic
abnormalities. The resulting loss of electron/proton homeostasis
leads to decreased transmembrane potential, electrical
microenvironment alterations, decreased extracellular pH, and
increased intracellular pH. This produces a positive feedback loop
to enhance and sustain the proton/electron efflux and loss of
intercellular communication.
Low transmembrane potential is functionally related to rapid cell
cycling, changes in membrane structure, and malignancy.
Intracellular alkalinization affects a variety of pH-sensitive
systems including glycolysis, DNA synthesis, DNA transcription and
DNA repair, and promotes genetic instability, accounting for the
accumulation of genetic defects seen in malignancy. The abnormal
microenvironment results in the selective survival and proliferation
of malignant cells at the expense of contiguous normal cell
populations.
PMID: 10416941
[4] FASEB J 2000 Nov;14(14):2185-97
Na+/H+ exchanger-dependent intracellular alkalinization is an early
event in malignant transformation and plays an essential role in the
development of subsequent transformation-associated pHenotypes.
Reshkin SJ, Bellizzi A, Caldeira S, Albarani V, Malanchi I, Poignee
M, Alunni-Fabbroni M, Casavola V, Tommasino M. Department of General
and Environmental pHysiology, University of Bari, Bari, Italy.
In this study we investigate the mechanism
of intracellular pH change and its role in malignant transformation
using the E7 oncogene of human papillomavirus type 16 (HPV16).
Infecting NIH3T3 cells with recombinant retroviruses expressing the
HPV16 E7 or a transformation deficient mutant we show that
alkalinization is transformation specific. In NIH3T3 cells in which
transformation can be turned on and followed by induction of the
HPV16 E7 oncogene expression, we demonstrate that cytoplasmic
alkalinization is an early event and was driven by stimulation of
Na+/H+ exchanger activity via an increase in the affinity of the
intracellular NHE-1 proton regulatory site.
Annulment of the E7-induced cytoplasmic alkalinization by specific
inhibition of the NHE-1, acidification of culture medium, or
clamping the pHi to nontransformed levels prevented the development
of later transformed pHenotypes such as increased growth rate,
serum-independent growth, anchorage-independent growth, and
glycolytic metabolism. These findings were verified in human
keratinocytes (HPKIA), the natural host of HPV.
Results from both NIH3T3 and HPKIA cells show that alkalinization
acts on pathways that are independent of the E2F-mediated
transcriptional activation of cell cycle regulator genes. Moreover,
we show that the transformation-dependent increase in proliferation
is independent of the concomitant stimulation of glycolysis.
Finally, treatment of nude mice with the specific inhibitor of
NHE-1, DMA, delayed the development of HPV16-keratinocyte
tumors. Our data confirm that activation of the NHE-1 and resulting
cellular alkalinization is a key mechanism in oncogenic
transformation and is necessary for the development and maintenance
of the transformed pHenotype.
PMID: 11053239
Studi relativi al
potere antiacido del bicarbonato di sodio nei tumori:
Anne McLean, “Malignant gliomas display altered pH regu1ation byè
NHE1 compared with non transformed astrocytes (Am J Physiol Cell
Physiol 278: C676-C688, 2000).
Marion Stubbs, “Causes and consequences of tumour acidity and
implications for treatment”, Molecular Medicine: Today, January 2000
(vol.6).
Robert J. Gillies, “Causes and consequences of hypoxia and acidity
in turners - Novartis Foundatíon symposium”, Molecular Medicine
Vol.7 N° 2 February 2001; “Causes and consequences of hypoxia and
acìdity in tumour microenvironments”.
J.R. Griffiths, “Causes and
consequences of hypoxia and acìdity in tumour microenvironments”,
Glia 1994 Nov:12(3):196-210.
Tannock, I.F., “Acid pH in tumors
and its potential for therapeutic exploitation”, Cancer Res 1989 Aug
15;49(16):4373-84.
Raghunand, N., “Enhancement of chemotherapy by manipulation of
tumour pH”, Br J Cancer 1999 Jun;80(7):1005-11.
Davydova, I.G., “Dynamics of
bioelectric activity of the brain and erythrocyte ultrastructure
after intravenous infusion of sodium bicarbonate to oncologic
patients.” Biull Eksp Biol Med 1992 Apr;113(4):352-5.
Davydova, I.G., “Characteristics
of the effects of artificial alkalosis on electrical activity of the
brain and ultrastructure of blood cells in oncologic patients”,
Vestn Ross Akad Med Nauk 1995;(4):24-5.
Star, R.A., “Regulatory volume decrease in the presence of HCO3- by
single osteosarcoma cells UMR-106-01”, J Biol Chem 1992 Sep
5;267(25):17665-9.
LeBoeuf, R.A., “Intracellular acidification is associated with
enhanced morphological transformation in Syrian hamster embryo
cells”, Cancer Res 1992 Jan 1;52(1):144-8.
Raghunand, N., “Acute metabolic alkalosis enhances response of C3H
mouse mammary tumors to the weak base mitoxantrone.” Neoplasia. 2001
May-Jun;3(3):227-35.
Raghunand, N., “pH and chemotherapy pH and chemotherapy” Novartis
Found Symp. 200 1;240:199-21 l; discussion 265 -8.
Raghunand, N., “Enhancement of chemotherapy by manipulation of
tumour pH.” Br J Cancer. 1999 Jun;80(7):1005-1 I.
Raghunand, N., “Tumor acidity, ion trapping and chemotherapeutics.
IL pll-dependent partition coefficients predict importance of ion
trapping on pharmaeokinetics of weakly basic chemotherapeutie
agents.” Bíochem Pharmacol. 2003 Oct 1;66(7):1219-29.”
Mahoney, B.P., “Tumor acidity, ion trapping and chemotherapeutics.
I. Acid plì affects the distribution of ehemotherapeutic agents in
vitro.” Biochem Phannacol. 2003 Oct 1;66(7):1207-18.
Schornack, P.A., “Contributions of cell metabolism and H+ diffusion
to the acidic pH of tumors.” Neoplasia.
2003 Mar-Apr;5(2):135-45.
Giffles,
R.J., “MRI of the tumor microenvironment.” J Magn Reson Imaging 2002
Dec; 16(6):75 l.
Torigoe, T., “Vacuolar H(+)-ATPase:
funetional mechanisms and potential as a target for cancer
chemotherapy.” Anticancer Drugs. 2002 Mar; 13 (3):23 7-43.
Griffiths, J.R., “Why are cancers acidic? A carrier-mediated
diffusion model for H+ transport in the interstitial fluid.”
Novartis Found Symp. 200 1;240:46-62; discussion 62-7, 152-3.
Webb, S.D., “Modelling tumour acidity and invasion.” Novartis Found
Symp. 2001;240:169-8 l; discussion 181-5.
Gillies, R.J., “The tumour microenvironment: causes and consequences
of hypoxia and acidity. Introduction.” Novartis Found Symp. 200
1;240:1-6.
Gillies, R.J., “Causes and
consequences of hypoxia and acidity in tumors” Novartis Foundation
symposium. Trends Mol Med. 2001 Feb;7(2):47-9.
Griffiths, JR. “Causes and consequences of hypoxia and acidity in
tumour microenvironments. Bioessays. 2001 Mar;23(3):295-6.
Gillies, R.J., “Causes and effects of heterogeneous perfusion in
tumors.” Neoplasia. 1999 Aug; 1 (3):197-207.
Stubbs, M., “Causes and consequences of tumour acidity and
implications for treatment.” Mol Med Today. 2000
Jan;6(1):15-9Stubbs, M., “Causes and consequences of acidic ph in
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Tratto da:
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su: Biblio 3 +
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