Positron emission tomography with 2-[18F]-fluoro-2-deoxy-D-glucose in oncology

B, van der Hiel; Ek, Pauwels; Mp, Stokkel

doi:10.1007/s004320000191

Cited by 27 publications

(3 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…They reported that the total dietary fibre is inversely associated with C. hathewayi, which has been implicated in clinical conditions such as infection and sepsis [46], while soluble fibre is inversely associated with Clostridium. Insoluble fibre was positively asso-ciated with B. uniformis, currently used as an indicator of malignancy since it represents an evident characteristic of many cancers due to an expanded glycolytic capability of its strains, related to a higher glucose uptake [47,48]. Our results showed a significantly increased abundance of C. hathewayi in group 1, which may reflect a low dietary fibre intake.…”

Section: Discussionmentioning

confidence: 56%

Breast Cancer Survivors and Healthy Women: Could Gut Microbiota Make a Difference?—“BiotaCancerSurvivors”: A Case-Control Study

Caleça

Ribeiro²,

Vitorino

et al. 2023

Cancers

View full text Add to dashboard Cite

In this first analysis, samples from 23 BC survivors (group 1) and 291 healthy female controls (group 2) were characterised through the V3 and V4 regions that encode the “16S rRNA” gene of each bacteria. The samples were sequenced by next-generation sequencing (NGS), and the taxonomy was identified by resorting to Kraken2 and improved with Bracken, using a curated database called ‘GutHealth_DB’. The α and β-diversity analyses were used to determine the richness and evenness of the gut microbiota. A non-parametric Mann-Whitney U test was applied to assess differential abundance between both groups. The Firmicutes/Bacteroidetes (F/B) ratio was calculated using a Kruskal-Wallis chi-squared test. The α-diversity was significantly higher in group 1 (p = 0.28 × 10−12 for the Chao index and p = 1.64 × 10−12 for the ACE index). The Shannon index, a marker of richness and evenness, was not statistically different between the two groups (p = 0.72). The microbiota composition was different between the two groups: a null hypothesis was rejected for PERMANOVA (p = 9.99 × 10−5) and Anosim (p = 0.04) and was not rejected for β-dispersion (p = 0.158), using Unifrac weighted distance. The relative abundance of 14 phyla, 29 classes, 25 orders, 64 families, 116 genera, and 74 species differed significantly between both groups. The F/B ratio was significantly lower in group 1 than in group 2, p < 0.001. Our study allowed us to observe significant taxonomic disparities in the two groups by testing the differences between BC survivors and healthy controls. Additional studies are needed to clarify the involved mechanisms and explore the relationship between microbiota and BC survivorship.

show abstract

Section: Discussionmentioning

confidence: 56%

Breast Cancer Survivors and Healthy Women: Could Gut Microbiota Make a Difference?—“BiotaCancerSurvivors”: A Case-Control Study

Caleça

Ribeiro²,

Vitorino

et al. 2023

Cancers

View full text Add to dashboard Cite

show abstract

“…However, the early investigations into metabolic energy alterations in tumours by Otto Warburg and Carl and Gerty Cori in the 1920s revealed the paradoxical observation that cancer cells preferentially respire using glycolytic lactate production despite the presence of oxygen; later known as 'The Warburg effect' (41). This phenomenon, also referred to as the process of 'aerobic glycolysis' i.e.…”

Section: Altered Metabolism In Gscsmentioning

confidence: 99%

Glioma Stem-Like Cells and Metabolism: Potential for Novel Therapeutic Strategies

et al. 2021

View full text Add to dashboard Cite

Glioma stem-like cells (GSCs) were first described as a population which may in part be resistant to traditional chemotherapeutic therapies and responsible for tumour regrowth. Knowledge of the underlying metabolic complexity governing GSC growth and function may point to potential differences between GSCs and the tumour bulk which could be harnessed clinically. There is an increasing interest in the direct/indirect targeting or reprogramming of GSC metabolism as a potential novel therapeutic approach in the adjuvant or recurrent setting to help overcome resistance which may be mediated by GSCs. In this review we will discuss stem-like models, interaction between metabolism and GSCs, and potential current and future strategies for overcoming GSC resistance.

show abstract

“…Breast cancer cells with high glucose metabolism are associated with more aggressive behavior and greater invasiveness [10, 11]. Accordingly, the magnitude of breast tumor FDG uptake offers useful information for decision making and prognostication [8, 9], as well as for predicting response to therapy [12, 13]. Our group recently discovered that breast tumor FDG uptake is more strongly influenced by EGFR status than by other major biomarkers [14].…”

Section: Introductionmentioning

confidence: 99%

EGF receptor stimulation shifts breast cancer cell glucose metabolism toward glycolytic flux through PI3 kinase signaling

et al. 2019

View full text Add to dashboard Cite

Breast cancers that express epidermal growth factor (EGF) receptors (EGFRs) are associated with poor prognosis. Our group recently showed in breast cancer patients that EGFR expression is strongly correlated with high tumor uptake of the glucose analogue, 18F-fluorodeoxyglucose (FDG). Here, we explored the cellular mechanism and signaling pathways that can explain the relation between EGFR and breast cancer cell glucose metabolism. FDG uptake, lactate production and hexokinase (HK) activity were measured, and proliferation assays and western blots were performed. EGF stimulated an increase of FDG uptake in EGFR-positive T47D and MDA-MB-468 cells, but not in MCF-7 cells. In T47D cells, the effect was dose-dependent and was accompanied by increased lactate production, indicating a shift toward glycolytic flux. This metabolic response occurred through enhanced HK activity and upregulated glucose transporter 1 (GLUT1) expression. EGFR stimulation also increased T47D cell proliferation. Blocking EGFR activation with BIBX1382 or gefitinib completely abolished both FDG uptake and proliferation effects. EGFR stimulation induced MAP kinase (MAPK) and PI3 kinase (PI3K) activation. Increased cell proliferation by EGFR stimulation was completely abolished by MAPK inhibition with PD98059 or by PI3K inhibition with LY294002. Increased FDG uptake was also completely abrogated by PI3K inhibition but was uninfluenced by MAPK inhibition. These findings suggest that the association between breast tumor EGFR expression and high FDG uptake might be contributed by stimulation of the PI3K pathway downstream of EGFR activation. This was in contrast to EGFR-mediated cell proliferation that required MAPK as well as PI3K signaling.

show abstract

Positron emission tomography with 2-[18F]-fluoro-2-deoxy-D-glucose in oncology

Cited by 27 publications

References 28 publications

Breast Cancer Survivors and Healthy Women: Could Gut Microbiota Make a Difference?—“BiotaCancerSurvivors”: A Case-Control Study

Breast Cancer Survivors and Healthy Women: Could Gut Microbiota Make a Difference?—“BiotaCancerSurvivors”: A Case-Control Study

Glioma Stem-Like Cells and Metabolism: Potential for Novel Therapeutic Strategies

EGF receptor stimulation shifts breast cancer cell glucose metabolism toward glycolytic flux through PI3 kinase signaling

Contact Info

Product

Resources

About