Search

The median overall survival of patients with metastatic breast cancer is only 2–3 years, and for patients with untreated liver metastasis, it is as short as 4–8 months. Improving the survival of women with breast cancer requires more effective anti-cancer strategies, especially for metastatic disease. Nutrients can influence tumor microenvironments, and cancer metabolism can be manipulated via a dietary modification to enhance anti-cancer strategies. Yet, there are no standard evidence-based recommendations for diet therapies before or during cancer treatment, and few studies provide definitive data that certain diets can mediate tumor progression or therapeutic effectiveness in human cancer. This review focuses on metastatic breast cancer, in particular liver metastatic forms, and recent studies on the impact of diets on disease progression and treatment. [ABSTRACT FROM AUTHOR]

The study's objective was to determine whether orally ingested caffeine could help overcome excitation-contraction-coupling failure, which has been suggested to explain part of the strength loss associated with eccentric-contraction-induced muscle injury. A sample of 13 college students (4 men and 9 women) was used in a double-blind, repeated-measures experimental design. Each participant performed 2 experimental trials, 1 with each leg, with each trial lasting 4 consecutive days. On a given day, each participant was randomly assigned to ingest a capsule containing 6 mg/kg of either caffeine or flour (placebo). On the day of and the first 2 days after a bout of 50 injurious eccentric contractions done by the knee extensors, the interpolated-twitch technique was used to assess electrically evoked strength, maximal voluntary isometric contraction (MVIC) strength, and percent muscle activation during MVIC both before and after capsule ingestion. These variables were also measured before and after capsule ingestion the day before the eccentric-contraction bout—when the muscle was uninjured. In injured muscle, caffeine had no effect on any variable. In uninjured muscle, caffeine also had no effect on electrically evoked strength but increased MVIC strength by 10.4% compared with placebo (p = .00002), and this was attributed to an increase in muscle activation (6.2%; p = .01). In conclusion, the data provide no evidence that caffeine ingestion can help overcome excitation-contraction-coupling failure, if it exists, in injured human muscle. The data do indicate that caffeine ingestion can increase MVIC strength and activation in uninjured muscle but not in injured muscle. [ABSTRACT FROM AUTHOR]

DiPSI exists to celebrate existing diversity and enhance further polar science opportunities for historically excluded and underrepresented groups such as women, Black, Asian and minority ethnic people, the LGBTQ+ community, people with disabilities or those from lower-socioeconomic backgrounds. The desire for meaningful change led the UK Foreign, Commonwealth and Development Office, Polar Regions Department, to fund the Diversity in UK Polar Science Initiative (DiPSI; https://www.bas.ac.uk/project/diversity-in-uk-polar-science-initiative). [Extracted from the article]

Abstract: Background: Cancer genomes accumulate frequent and diverse chromosomal abnormalities as well as gene mutations but must maintain the ability to survive in vivo. We hypothesize that genetic selection acts to maintain tumour survival by preserving copy number of specific genes and genomic regions. Genomic regions and genes that remain unaltered in copy number and expression, respectively, may be essential for maintaining tumour survival. Methods: We analyzed copy number data of 243 previously reported breast tumours and computationally derived stable copy number regions. To identify genes in stable copy number regions with nominal changes in expression, datasets for tumour and normal samples were compared. Results were replicated by analysis of a series of independent copy number, expression and genomic sequencing studies. A subset of stable regions, including stable paralogous regions, were confirmed by quantitative PCR and fluorescence in situ hybridization (FISH) in 5 breast cancer cell lines. We deduced a comprehensive set of dually stable genes (i.e. maintaining nominal copy number and expression) which were categorized according to pathway and ontology assignments. The stability of genes encoding therapeutic drug targets was also assessed. Results and Conclusion: Tumour genome analysis revealed 766 unstable (amplified and/or deleted) and 812 stable contiguous genomic regions. Replication analysis of an independent set of 171 breast tumours confirmed copy number stability of 1.3 Gb of the genome. We found that 5804 of these genes were dually stable. The composition of this gene set remained essentially unchanged (<2% reduction) after accounting for commonly mutated breast cancer genes found by sequencing and differential expression. The stable breast cancer genome is enriched for cellular metabolism, regulation of gene expression, DNA packaging (chromatin and nucleosome assembly), and regulation of apoptosis functions. Stable genes participating in multiple essential pathways were consistently found to be targets of chemotherapies. Preservation of stable, essential genes may be related to the effectiveness of certain chemotherapeutic agents that act on multiple gene products in this set. [Copyright &y& Elsevier]