Cancer, Oxidative Stress, and Metastasis

Gill, Jennifer G.; Piskounova, Elena; Morrison, Sean J.

doi:10.1101/sqb.2016.81.030791

Cited by 207 publications

(147 citation statements)

References 172 publications

Supporting

Mentioning

141

Contrasting

Unclassified

Order By: Relevance

“…Although mtDNA has been implicated in the regulation of tumor development and progression (26, 40–42), it has been challenging to dissect the precise contributions, largely because the models have been limited. Off-target effects of pharmacologic inhibitors, exposure to mutagenic agents, and challenges associated with cross-over between nuclear genomes have been raised as possible limitations for previously published studies (27, 28).…”

Section: Resultsmentioning

confidence: 99%

“…In contrast, PyMT has rapid tumor onset (~30 days) and high penetrance of metastasis (~94% of females presenting with metastasis at 3 months; ref. 26). The former develops tumors mimicking the HER2 subtype of human breast cancers, while the latter more closely mimic luminal breast cancers.…”

Section: Discussionmentioning

confidence: 99%

“…Using pharmacologic inhibitors, Felding-Habermann and colleagues established NAD/NADH ratios as critical determinants of metastatic efficiency (18). Still others have compared mitochondrial profiles and demonstrated mitochondrial mass (19, 20), metabolic profiles (21–23), and reactive oxygen species (24–26) as contributors to processes critical to invasion and metastasis.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Mitochondrial Haplotype Alters Mammary Cancer Tumorigenicity and Metastasis in an Oncogenic Driver–Dependent Manner

et al. 2017

View full text Add to dashboard Cite

Using a novel mouse model, a mitochondrial-nuclear exchange model termed MNX, we tested the hypothesis that inherited mitochondrial haplotypes alter primary tumor latency and metastatic efficiency. Male FVB/N-Tg(MMTVneu)202Mul/J (Her2) transgenic mice were bred to female MNX mice having FVB/NJ nuclear DNA with either FVB/NJ, C57BL/6J, or BALB/cJ mtDNA. Pups receiving the C57BL/6J or BALB/cJ mitochondrial genome (i.e., females crossed with Her2 males) showed significantly (P < 0.001) longer tumor latency (262 vs. 293 vs. 225 days), fewer pulmonary metastases (5 vs. 7 vs. 15), and differences in size of lung metastases (1.2 vs. 1.4 vs. 1.0 mm diameter) compared with FVB/NJ mtDNA. Although polyoma virus middle T–driven tumors showed altered primary and metastatic profiles in previous studies, depending upon nuclear and mtDNA haplotype, the magnitude and direction of changes were not the same in the HER2-driven mammary carcinomas. Collectively, these results establish mitochondrial polymorphisms as quantitative trait loci in mammary carcinogenesis, and they implicate distinct interactions between tumor drivers and mitochondria as critical modifiers of tumorigenicity and metastasis.

show abstract

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Mitochondrial Haplotype Alters Mammary Cancer Tumorigenicity and Metastasis in an Oncogenic Driver–Dependent Manner

et al. 2017

View full text Add to dashboard Cite

show abstract

“…Increased production of ROS beyond capability to cope by antioxidants leads to progressive augmentation of oxidized lesions that further promote pathogenic process such as in aging [63], atherosclerosis [64], neurodegenerative diseases [18,65,66] and cancers [67][68][69][70][71].…”

Section: Oxidative Stressmentioning

confidence: 99%

Oxidative Stress in Urolithiasis

Boonla¹

2018

Reactive Oxygen Species (ROS) in Living Cells

View full text Add to dashboard Cite

Oxygen is absolutely essential for the survival of our life. However, metabolic consumption of oxygen inevitably yields reactive oxygen species (ROS). Imbalance of ROS production and antioxidant capacity causes oxidative stress that potentially damages biomolecules leading to cell injury and death. In fact, ROS have two-faceted functions. Under physiologic condition, ROS function as signaling molecules and participate in maintaining redox balance. In pathology, ROS induce oxidative stress that critically involves in the development of several diseases including urolithiasis (UL). UL or urinary stone disease is a common urologic condition in all countries with progressively increasing prevalence. Most of UL are multifactorial with polygenic susceptibility and highly recurrent nature. Formation of urinary stones is driven by supersaturation of urinary lithogenic ions, and calcium oxalate (CaOx) is the most prevalent stone type. Oxidative stress clearly plays an active role in UL development. In vitro, lithogenic crystals induce ROS generation in renal tubular cells leading to oxidative stress, cell injury and release of inflammatory mediators. In nephrolithic rats, oxidative stress and CaOx deposit are gradually increased in the rats' kidneys. Intervention with antioxidants efficiently reduces oxidative damage and crystal deposits. Human studies show that patients with UL have increased oxidative stress and renal tubular injury relative to the non-stone-forming individuals. Increased oxidative lesions and inflammation are observed in the stone-containing kidneys of the patients. Furthermore, renal fibrosis mediated through tubular epithelial-mesenchymal transition is observed in kidneys of stone patients. Increased renal fibrosis is significantly associated with decreased kidney function. From therapeutic point of view, nutraceutical regimens that are able to reduce oxidative stress may be clinically useful alternatives for preventing stone formation and recurrence. This chapter has an intention to provide a basic knowledge of ROS generation and oxidative stress and up-to-date research findings of oxidative stress in UL based on the published articles as well as the author's studies.

show abstract

“…Enzymatic antioxidants can protect from breast cancer by neutralizing the over-generated ROS [57] and hence, antioxidant enzymes (SOD, GPX and catalase) are established markers for assessing the beneficial effect of physical training on antioxidant status [58,59]. As a consequence, oxidative stress has been recently proposed as an innovative biomarker to investigate in oncology [60]. To our knowledge, the links between the level of physical activity, biological mechanisms involved in the oxidative stress, and tumor progression have never been studied in metastatic breast cancer patients.…”

Section: Introductionmentioning

confidence: 99%

A Personalized Physical Activity Program With Activity Trackers and a Mobile Phone App for Patients With Metastatic Breast Cancer: Protocol for a Single-Arm Feasibility Trial (Preprint)

Delrieu¹,

Pérol²,

Fervers³

et al. 2018

Preprint

View full text Add to dashboard Cite

BACKGROUND About 5% of breast cancer cases are metastatic at diagnosis, and 20%-30% of localized breast cancer cases become secondarily metastatic. Patients frequently report many detrimental symptoms related to metastasis and treatments. The physical, biological, psychological, and clinical benefits of physical activity during treatment in patients with localized breast cancer have been demonstrated; however, limited literature exists regarding physical activity and physical activity behavior change in patients with metastatic breast cancer. OBJECTIVE The primary objective of this study is to assess the feasibility of a 6-month physical activity intervention with activity trackers in patients with metastatic breast cancer (the Advanced stage Breast cancer and Lifestyle Exercise, ABLE Trial). Secondary objectives are to examine the effects of physical activity on physical, psychological, anthropometrics, clinical, and biological parameters. METHODS We plan to conduct a single-center, single-arm trial with 60 patients who are newly diagnosed with metastatic breast cancer. Patients will receive an unsupervised and personalized 6-month physical activity program that includes an activity tracker Nokia Go and is based on the physical activity recommendation. Patients will be encouraged to accumulate at least 150 minutes per week of moderate-to-vigorous intensity physical activity. Baseline and 6-month assessments will include anthropometric measures, functional tests (eg, 6-minute walk test and upper and lower limb strength), blood draws, patient-reported surveys (eg, quality of life and fatigue), and clinical markers of tumor progression (eg, Response Evaluation Criteria In Solid Tumors criteria). RESULTS Data collection occurred between October 2016 and January 2018, and the results are expected in August 2018. CONCLUSIONS The ABLE Trial will be the first study to assess the feasibility and effectiveness of an unsupervised and personalized physical activity intervention performed under real-life conditions with activity trackers in patients with metastatic breast cancer. CLINICALTRIAL ClinicalTrials.gov NCT03148886; https://clinicaltrials.gov/ct2/show/NCT03148886 (Accessed by WebCite at http://www.webcitation.org/71yabi0la) REGISTERED REPORT IDENTIFIER RR1-10.2196/10487

show abstract

Cancer, Oxidative Stress, and Metastasis

Cited by 207 publications

References 172 publications

Mitochondrial Haplotype Alters Mammary Cancer Tumorigenicity and Metastasis in an Oncogenic Driver–Dependent Manner

Mitochondrial Haplotype Alters Mammary Cancer Tumorigenicity and Metastasis in an Oncogenic Driver–Dependent Manner

Oxidative Stress in Urolithiasis

A Personalized Physical Activity Program With Activity Trackers and a Mobile Phone App for Patients With Metastatic Breast Cancer: Protocol for a Single-Arm Feasibility Trial (Preprint)

Contact Info

Product

Resources

About