Evidence map›Paper›PMID 24862761›Full record

ArticleNeoplasia (New York, N.Y.)2014

Mechanisms of buffer therapy resistance.

Kate M Bailey, Jonathan W Wojtkowiak, Heather H Cornnell, Maria C Ribeiro, Yoganand Balagurunathan, Arig Ibrahim Hashim, Robert J Gillies

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.9field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 32 citations in OpenAlex.

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  7. Cancer heterogeneity and metastasis: life at the edge.Clinical & experimental metastasis · 2022
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Kate M BaileyDepartment of Cancer Imaging and Metabolism, Tampa, FL, USA; Cancer Biology Ph.D. Program, University of South Florida, Tampa, FL, USA.
Jonathan W WojtkowiakDepartment of Cancer Imaging and Metabolism, Tampa, FL, USA.
Heather H CornnellDepartment of Cancer Imaging and Metabolism, Tampa, FL, USA.
Maria C RibeiroDepartment of Cancer Imaging and Metabolism, Tampa, FL, USA.
Yoganand BalagurunathanDepartment of Cancer Imaging and Metabolism, Tampa, FL, USA.
Arig Ibrahim HashimDepartment of Cancer Imaging and Metabolism, Tampa, FL, USA.
Robert J GilliesDepartment of Cancer Imaging and Metabolism, Tampa, FL, USA; Department of Radiology, H. Lee Moffitt Cancer Center, Tampa, FL, USA. Electronic address: robert.gillies@moffitt.org.
Moffitt Cancer Center · USUniversity of South Florida · US

Funding

TRANSLATIONAL RESEARCHP30CA076292 · NCI · UNIVERSITY OF SOUTH FLORIDA · PI KENNETH Lynn WRIGHT · 1998 to 2026
$93.5M
The Physi(ologi)cal Microenvironment and its Role in Tumor Invasion and MetastaseU54CA143970 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI GATENBY, ROBERT A · 2009 to 2014
$9.3M
Causes & Consequences of Acid pH in TumorsR01CA077575 · NCI · UNIVERSITY OF ARIZONA · PI GILLIES, ROBERT J. · 1999 to 2018
$8.5M
VisEn Fluorescence Molecular Tomography (FMT) scannerS10RR031726 · NCRR · H. LEE MOFFITT CANCER CTR & RES INST · PI MORSE, DAVID L · 2011 to 2011
$299k
NCI NIH HHS P30 CA076292NCI NIH HHS R01 CA 077575NCI NIH HHS R01 CA077575NCI NIH HHS U54 CA143970NCRR NIH HHS 1S10RR031726-01NCRR NIH HHS S10 RR031726
6 · The paper itself

Abstract

Many studies have shown that the acidity of solid tumors contributes to local invasion and metastasis. Oral pH buffers can specifically neutralize the acidic pH of tumors and reduce the incidence of local invasion and metastatic formation in multiple murine models. However, this effect is not universal as we have previously observed that metastasis is not inhibited by buffers in some tumor models, regardless of buffer used. B16-F10 (murine melanoma), LL/2 (murine lung) and HCT116 (human colon) tumors are resistant to treatment with lysine buffer therapy, whereas metastasis is potently inhibited by lysine buffers in MDA-MB-231 (human breast) and PC3M (human prostate) tumors. In the current work, we confirmed that sensitive cells utilized a pH-dependent mechanism for successful metastasis supported by a highly glycolytic phenotype that acidifies the local tumor microenvironment resulting in morphological changes. In contrast, buffer-resistant cell lines exhibited a pH-independent metastatic mechanism involving constitutive secretion of matrix degrading proteases without elevated glycolysis. These results have identified two distinct mechanisms of experimental metastasis, one of which is pH-dependent (buffer therapy sensitive cells) and one which is pH-independent (buffer therapy resistant cells). Further characterization of these models has potential for therapeutic benefit.

Indexed as

BuffersHydrogen-Ion ConcentrationAnimalsCell Line, TumorCell MovementDisease Models, AnimalHumansLysineMelanoma, ExperimentalMiceNeoplasm MetastasisNeoplasmsBuffersLysine

Identifiers

PMID24862761
PMCPMC4094835
OpenAlexW2086664463

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.