BMD Cancer Research Results

BMD, bone mineral density: Click to Expand ⟱

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The Bone Mineral Density (BMD) Test is a diagnostic tool used to measure the density and strength of bones. A bone mineral density (BMD) test measures calcium and other minerals in bone. Cancer treatments, including chemotherapy, hormone therapy, and radiation, can negatively impact bone health and lead to decreased BMD, increasing the risk of osteoporosis and fractures.
Some studies suggest that low BMD may be associated with poorer survival outcomes in certain cancer types, although the relationship can be complex and influenced by various factors.

Scientific Papers found: Click to Expand⟱

4542-

AgNPs,

Silver Nanoparticles (AgNPs): Comprehensive Insights into Bio/Synthesis, Key Influencing Factors, Multifaceted Applications, and Toxicity─A 2024 Update

Review,

NA,

AntiCan↑, cytotoxicity against human colon carcinoma (HT-29) cells. The MTT assay confirmed their anticancer potential, with an IC50 value of 150.8 μg/mL.
DNAdam↑, Ag-NPs, accumulating in the nucleus, may cause genotoxicity, DNA damage, and chromosomal aberrations
ATP↓, Ag-NP exposure disrupts calcium homeostasis, leading to mitochondrial dysfunction, ATP depletion, and apoptosis.
Apoptosis↑,
ROS↓, induce cytotoxicity through numerous mechanisms viz., oxidative stress, mitochondrial dysfunction, DNA damage, cell cycle arrest, and subsequent apoptosis.
TumCCA↑,
*Bacteria↓, effectiveness as an antibacterial agent.
*BMD↑, Bone Repair Applications

3516-

Bor,

Boron in wound healing: a comprehensive investigation of its diverse mechanisms

Review,

Wounds,

*Inflam↓, anti-inflammatory, antimicrobial, antioxidant, and pro-proliferative effects.
*antiOx↑,
*ROS↓, The antioxidant properties of boron help protect cells from oxidative stress, a common feature of chronic wounds that can impair healing
*angioG↑, Boron compounds exhibit diverse therapeutic actions in wound healing, including antimicrobial effects, inflammation modulation, oxidative stress reduction, angiogenesis induction, and anti-fibrotic properties.
*COL1↑, Boron has been shown to increase the expression of proteins involved in wound contraction and matrix remodeling, such as collagen, alpha-smooth muscle actin, and transforming growth factor-beta1.
*α-SMA↑,
*TGF-β↑,
*BMD↑, Animals treated with boron showed favorable changes in bone density, wound healing, embryonic development, and liver metabolism
*hepatoP↑,
*TNF-α↑, BA elevates TNF-α and heat-shock proteins 70 that are related to wound healing.
*HSP70/HSPA5↑,
*SOD↑, antioxidant properties of BA showed that boron protects renal tissue from I/R injury via increasing SOD, CAT, and GSH and decreasing MDA and total oxidant status (TOS)
*Catalase↑,
*GSH↑,
*MDA↓,
*TOS↓,
*IL6↓, Boron supports gastric tissue by alleviating ROS, MDA, IL-6, TNF-α, and JAK2/STAT3 action, as well as improving AMPK activity
*JAK2↓,
*STAT3↓,
*AMPK↑,
*lipid-P↓, boron may improve wound healing by hindering lipid peroxidation and increasing the level of VEGF
*VEGF↑,
*Half-Life↝, Boron is a trace element, usually found at a concentration of 0–0.2 mg/dL in plasma with a half-life of 5–10 h, and 1–2 mg of it is needed in the daily diet

3512-

Bor,

Activation of the EIF2α/ATF4 and ATF6 Pathways in DU-145 Cells by Boric Acid at the Concentration Reported in Men at the US Mean Boron Intake

in-vitro,

Pca,

DU145

TumCP↓, Treatment of DU-145 prostate cancer cells with physiological concentrations of BA inhibits cell proliferation without causing apoptosis and activates eukaryotic initiation factor 2 (eIF2α).
eIF2α↑, Phosphorylation of eIF2α occurs following BA treatment of DU-145 and LNCaP prostate cells
ATF4↑, post-treatment increases in eIF2α protein at 30 min and ATF4 and ATF6 proteins at 1 h and 30 min, respectively
ATF6↑,
GADD34↑, The increase in ATF4 was accompanied by an increase in the expression of its downstream genes growth arrest and DNA damage-induced protein 34 (GADD34) and homocysteine-induced ER protein (Herp),
CHOP↓, but a decrease in GADD153/CCAAT/enhancer-binding protein homologous protein (CHOP), a pro-apoptotic gene.
GRP78/BiP↑, The increase in ATF6 was accompanied by an increase in expression of its downstream genes GRP78/BiP, calreticulin, Grp94, and EDEM.
GRP94↑,
Risk↓, Low boron status has been associated with increased cancer risk, low bone mineralization, and retinal degeneration
*BMD↑,
Ca+2↓, LNCaP and DU-145: BA binds to cADPR and inhibits cADPR-activated Ca2+ release from the endoplasmic reticulum (ER) in a dose-dependent manner [15, 16] and lowers ER luminal Ca2+ concentrations
*Half-Life↝, lood levels of BA are dynamic, rising rapidly after a meal with an elimination half-life from 4 to 27.8 h depending on dose
IRE1∅, BA does not activate IRE1
chemoP↑, Dietary boron has been connected to three seemingly unconnected observations, increased bone mass and strength [10, 74, 75], chemoprevention

3520-

Bor,

Effect of boron element on photoaging in rats

in-vivo,

NA,

rats

*hepatoP↑, to positively affect the liver metabolism, and to promote bone density, embryogenic development and wound healing, and is known to provide significant benefits in cancer treatment through neutron capture systems
*BMD↑,
*COX2↓, Increased skin inflammatory parameters (COX-2, IL-8, NF-KB, IL-6, and TNF-α) levels in UVB-exposed groups were inhibited in all treatment groups
*IL8↓,
*NF-kB↓,
*IL6↓,
*TNF-α↓,

696-

Bor,

Nothing Boring About Boron

Review,

Var,

>3mg

upper intake level (UL) of 20 mg/d

*hs-CRP↓, reduces levels of inflammatory biomarkers, such as high-sensitivity C-reactive protein (hs-CRP) and tumor necrosis factor μ (TNF-μ);
*TNF-α↓,
*SOD↑, raises levels of antioxidant enzymes, such as superoxide dismutase (SOD), catalase, and glutathione peroxidase
*Catalase↑,
*GPx↑,
*cognitive↑, improves the brains electrical activity, cognitive performance, and short-term memory for elders; restricted boron intake adversely affected brain function and cognitive performance.
*memory↑, In humans, boron deprivation (<0.3 mg/d) resulted in poorer performance on tasks of motor speed and dexterity, attention, and short-term memory.
*Risk↓, Boron-rich diets and regions where the soil and water are rich in boron correlate with lower risks of several types of cancer, including prostate, breast, cervical, and lung cancers.
*SAM-e↑,
*NAD↝, Boron strongly binds oxidized NAD+,76 and, thus, might influence reactions in which NAD+ is involved
*ATP↝,
*Ca+2↝, Because of its positive charge, magnesium stabilizes cell membranes, balances the actions of calcium, and functions as a signal transducer
HDAC↓, some boronated compounds are histone deacetylase inhibitors
TumVol↓,
IGF-1↓, expression of IGF-1 in the tumors was significantly reduced by boron treatment
PSA↓, Boronic acid has been shown to inhibit PSA activity.
Cyc↓, boric acid inhibits the growth of prostate-cancer cells both by decreasing expression of A-E cyclin
TumCMig↓,
*serineP↓, Boron exists in the human body mostly in the form of boric acid, a serine protease inhibitor.
HIF-1↓, shown to greatly inhibit hypoxia-inducible factor (HIF) 1
*ChemoSideEff↓, An in vitro study found that boric acid can help protect against genotoxicity and cytotoxicity that are induced in lymphocytes by paclitaxel
*VitD↑, greater production of 25-hydroxylase, and, thus, greater potential for vitamin-D activation
*Mag↑, Boron significantly improves magnesium absorption and deposition in bone
*eff↑, boron increases the biological half-life and bioavailability of E2 and vitamin D.
Risk↓, risk of prostate cancer was 52% lower in men whose diets supplied more than 1.8 mg/d of boron compared with those whose dietary boron intake was less than or equal to 0.9 mg/d.
*Inflam↓, As research into the chemistry of boron-containing compounds has increased, they have been shown to be potent antiosteoporotic, anti-inflammatory, and antineoplastic agents
*neuroP↑, In addition, boron has anti-inflammatory effects that can help alleviate arthritis and improve brain function and has demonstrated such significant anticancer
*Calcium↑, increase serum levels of estradiol and calcium absorption in peri- and postmenopausal women.
*BMD↑, boron stimulates bone growth in vitamin-D deficient animals and alleviates dysfunctions in mineral metabolism characteristic of vitamin-D deficiency
*chemoP↑, may help ameliorate the adverse effects of traditional chemotherapeutic agents. boric acid can help protect against genotoxicity and cytotoxicity that are induced in lymphocytes by paclitaxel, an anticancer drug commonly used to treat breast, ovarian
AntiCan↑, demonstrated preventive and therapeutic effects in a number of cancers, such as prostate, cervical, and lung cancers, and multiple and non-Hodgkin’s lymphoma
*Dose↑, only an upper intake level (UL) of 20 mg/d for individuals aged ≥ 18 y.
*Dose↝, substantial number of articles showing benefits support the consideration of boron supplementation of 3 mg/d for any individual who is consuming a diet lacking in fruits and vegetables
*BMPs↑, Boron was also found to increase mRNA expression of alkaline phosphatase and bone morphogenetic proteins (BMPs)
*testos↑, 1 week of boron supplementation of 6 mg/d, a further study by Naghii et al20 of healthy males (n = 8) found (1) a significant increase in free testosterone,
angioG↓, Inhibition of tumor-induced angiogenesis prevents growth of many types of solid tumors and provides a novel approach for cancer treatment; thus, HIF-1 is a target of antineoplastic therapy.
Apoptosis↑, Cancer cells, however, commonly overexpress sugar transporters and/or underexpress borate export, rendering sugar-borate esters as promising chemopreventive agents
*selectivity↑, In normal cells, the 2 latter, cell-destructive effects do not occur because the amount of borate present in a healthy diet, 1 to 10 mg/d, is easily exported from normal cells.
*chemoPv↑, promising chemopreventive agents

5065-

dietSTF,

dietFMD,

Nutrition, GH/IGF-I Signaling, and Cancer

Review,

Var,

GH↓, These effects of fasting/FMD on normal and cancer cells are mediated at least in part by the reduction in GH and IGF-I signaling.
IGF-1↓,
glucose↓, In mice, cycles of a 4-day FMD have been shown to lower blood glucose levels by 40 % and IGF-I by 45 % while increasing ketone bodies 9-fold and IGFBP-1, which inhibits IGF-I, by the end of the FMD
IGFBP1↑,
OS↑, FMD cycles adopted twice a month starting in middle age extend health span and longevity, reduce visceral fat and skin lesions, promote hippocampal neurogenesis, rejuvenate the immune system, and delay bone mineral density loss in mice
Imm↑,
neuroP↑,
BMD↑,
Dose↝, FMD is a plant-based caloric-restricted dietary regimen (typically between 300 and 1100 kcal per day) characterized by low proteins, sugars, and relatively high unsaturated fats.
Risk↓, Remarkably, these bi-monthly FMD cycles started in middle age reduce tumor incidence and delay cancer onset.
other↑, The robust epidemiological evidence that high animal protein consumption increases serum IGF-I levels in humans
TumCP↓, For these reasons, the GH/IGF-I axis emerged as a promising target for cancer treatments and prevention aimed at inhibiting cell proliferation by down-regulating IGF-I

2153-

Ex,

The Impact of Exercise on Cancer Mortality, Recurrence, and Treatment-Related Adverse Effects

Review,

Var,

eff↑, The findings of this review support the view that exercise is an important adjunct therapy in the management of cancer
BMD↑, Finally, thrice weekly resistance training during 6 months of radiotherapy for metastases to the spine resulted in significantly improved spine bone density compared with passive physical therapy
cognitive↑, Two of the 5 observed significant improve- ments in cognitive function
OS↑, 28-44% reduced risk of cancer-specific mortality
Remission↑, 21%-35% lower risk of cancer recurrence
eff↑, exercise may elicit positive changes in inflammation, immunity, and oxidative stress, as well as in metabolic and sex hormones, all of which are factors believed to contribute to cancer progression

5055-

Ex,

Why exercise has a crucial role in cancer prevention, risk reduction and improved outcomes

Review,

Var,

OS↑, In 2008, a cohort study of breast cancer survivors identified that patients who consistently exercised for greater than 2.5 hours per week following diagnosis had a greater than 60% reduction in the risk of all deaths compared with patients who were
IGF-1↓, Table 1, IGF1 Decreased levels, IGFBP3 Increased levels
IGFBP3↑,
BRCA1↑, BRCA1 Increased expression
BRCA2↑, BRCA2 Increased expression
RAS↓, RAS family oncogenes Suppressed activity
P53↑, P53 Enhanced activity
HSPs↑, Heat shock proteins Enhanced activity
Leptin↓, Leptin Reduced activity
Irisin↓, Irisin Enhanced activity
Resistin↓, Resistin Reduced activity
NK cell↑, NK cells Enhanced activity
CRP↓, C-reactive protein, interleukin-6, TNFα Reduced activity
IL6↓,
TNF-α↓,
PGE1↓, Prostaglandins Reduced activity
COX2↓, Cox-2 Reduced activity
*GSH↑, Glutathione, Catalase and Superoxide dismutase Increased activity
*Catalase↑,
*SOD↑,
*monoA↑, Monoamines Higher levels
*EndoR↑, Endorphins Increased release
*testos↑, testosterone increases immediately after vigorous exercise in some but not all studies. lasting for 20–60 minutes post-exercise
ROS↑, Physical activity, especially if strenuous, produces reactive oxidative species (ROS)
QoL↑, Adverse cancer-related symptoms, which have been shown to be alleviated by exercise, include fatigue, muscle weakness, thromboembolism, weight gain, loss of bone density, quality of life (QOL), psychological distress, incontinence and sexual dysfunct
BMD↑, the rate of decline in BMD was significantly less in the resistance exercise group, with a greater benefit seen in the aerobic exercise group
BowelM↑, Exercise reduces bowel transit time and ameliorates constipation and its associated abdominal cramps

4005-

K+,

Potassium

Review,

Nor,

Review,

Stroke,

*Risk↓, Higher potassium intakes have been associated with a decreased risk of stroke and possibly other cardiovascular diseases
*Dose↝, Adequate intake: 51+ years Male:3,400 mg Female:2,600 mg
*Risk↓, those who consumed an average of more than 4,099 mg of potassium per day had a 35% lower risk of kidney stones. The potassium citrate salts significantly reduced the risk of new stones and reduced stone size.
*BMD↑, Observational studies suggest that increased consumption of potassium from fruits and vegetables is associated with increased bone mineral density
*glucose↓, Numerous observational studies of adults have found associations between lower potassium intakes or lower serum or urinary potassium levels and increased rates of fasting glucose, insulin resistance, and type 2 diabetes

4705-

MEL,

Melatonin: beyond circadian regulation - exploring its diverse physiological roles and therapeutic potential

Review,

Nor,

*CLOCK↝, In mammals, melatonin primarily serves to regulate the circadian rhythm system, which is essential for maintaining the sleep-wake cycle.
*BMD↑, Graphical Abstract
*cardioP↑,
*neuroP↑,
*Sleep↑,

2242-

MF,

Electromagnetic stimulation increases mitochondrial function in osteogenic cells and promotes bone fracture repair

in-vitro,

Nor,

2.5G, 5G, 10G, 15G, and 20G

*MMP↑, we show that application of a low intensity constant EM field source on osteogenic cells in vitro resulted in increased mitochondrial membrane potential and respiratory complex I activity and induced osteogenic differentiation.
*Diff↑,
*OXPHOS↑, effect was mediated via increased OxPhos activity
*BMD↑, EM field source enhanced fracture repair via improved biomechanical properties and increased callus bone mineralization
ATP∅, higher mitochondrial OxPhos activity leads to higher ATP production, increased cellular activity leads to increased ATP consumption.

2238-

MF,

Electromagnetic fields act via activation of voltage-gated calcium channels to produce beneficial or adverse effects

Review,

Var,

*BMD↑, Therapeutic bone-growth stimulation via Ca2+/nitric oxide/cGMP/protein kinase G. Multiple studies have implicated increased Ca2+ and nitric oxide in the EMF stimulation of bone growth
*VGCC↑, increased VGCC activity following EMF exposure and suggests, therefore, that VGCC stimulation in the plasma membrane is directly produced by EMF exposure.
*Ca+2↑, Other studies, each involving VGCCs, summarized in Table 1, also showed rapid Ca2+ increases following EMF exposure [8, 16, 17, 19, 21].
*NO↑, Multiple studies have implicated increased Ca2+ and nitric oxide in the EMF stimulation of bone growth
*eff↓, Voltage-gated calcium channel stimulation leads to increased intracellular Ca2+, which can act in turn to stimulate the two calcium/calmodulin-dependent nitric oxide synthases and increase nitric oxide.

2240-

MF,

Pulsed electromagnetic field induces Ca2+-dependent osteoblastogenesis in C3H10T1/2 mesenchymal cells through the Wnt-Ca2+/Wnt-β-catenin signaling pathway

in-vitro,

Nor,

C3H10T1/2

30 Hz, 1 mT, 2 h/day

PEMF output waveform consisted of a 400 kV/m pulsed burst (pulse width 0.2 m s; pulse wait 0.02 m s; burst width 5 m s; burst wait 60 m s; pulse rise 0.3 m s; pulse fall 2.0 m s) repeated at 30 Hz.

*Ca+2↑, intracellular [Ca2+]i in C3H10T1/2 cells can be upregulated upon exposure to PEMF
*Diff↑, PEMF-induced C3H10T1/2 cell differentiation was Ca2+-dependent.
*BMD↑, pro-osteogenic effect of PEMF on Ca2+-dependent osteoblast differentiation
*Wnt↑, PEMF promoted the gene expression and protein synthesis of the Wnt/β-catenin pathway.
*β-catenin/ZEB1↑, PEMF activates the Wnt/b-catenin signaling pathway in C3H10T1/2 cells
*eff↝, These data indicated that increased intranuclear [Ca2+]i resulted in altered electrical activity in the nucleus.

4149-

MF,

Pulsed Electro-Magnetic Field (PEMF) Effect on Bone Healing in Animal Models: A Review of Its Efficacy Related to Different Type of Damage

Review,

NA,

*other↑, The expression of placental growth factor (PlGF) was significantly higher in the PEMF-treated group compared to the expression level before PEMF treatment.
*BDNF↑, Other factors trended higher following active PEMF treatment including BDNF and BMP-7 and -5.
*BMPs↑,
*BMD↑, PEMF accelerated bone regeneration, resulting in increased BV and BMD in groups that received 0, 2.5, and 5 μg rhBMP-2.

3741-

MF,

Promising application of Pulsed Electromagnetic Fields (PEMFs) in musculoskeletal disorders

Review,

NA,

usually less than 100 Hz and the magnetic flux density is between 0.1 m T and 30 m T.

*eff↑, effectively treat numerous musculoskeletal disorders, such as delayed union or nonunion fractures, osteoarthritis (OA), osteoporosis (OP), osteonecrosis (ON), tendon disorders, etc.
*BMD↑, n 1964, Bassett et al. [8] demonstrated the effects of electric currents on new bone growth in vivo
*Inflam↓, arani et al. also demonstrated the PEMFs exerted a strong anti-inflammatory effect on the joint environment via acting as agonist of A2A and A3 adenosine receptors [
*PGE2↓, The receptor activation can reduce the release of prostaglandin E2 (PGE2) and pro-inflammatory cytokines IL-6 and IL-8, as well as inhibit the activation of the transcription factor NF-KB
*IL6↓,
*IL8↓,
*NF-kB↓,
*mTOR↝, mTOR) pathway has also been demonstrated to be the underlying signaling pathway of PEMFs involved in bone formation

3471-

MF,

The prevention effect of pulsed electromagnetic fields treatment on senile osteoporosis in vivo via improving the inflammatory bone microenvironment

in-vivo,

Nor,

PEMF with 40 min/day, five days per week

24 Sprague Dawley (SD) rats

*BMD↑, PEMF increased the bone mineral density of the proximal femur and L5 vertebral body and improved parameters of the proximal tibia and L4 vertebral body.
*NLRP3↓, PEMF also dramatically inhibited NLRP3-mediated low-grade inflammation in the bone marrow,
*proCasp1↓, PEMF inhibited the levels of NLRP3, proCaspase1, cleaved Caspase1, IL-1β, and GSDMD-N.
*cl‑Casp1↓,
*IL1β↓,
*GSDMD↓,

530-

MF,

Low frequency sinusoidal electromagnetic fields promote the osteogenic differentiation of rat bone marrow mesenchymal stem cells by modulating miR-34b-5p/STAC2

in-vivo,

Nor,

15 Hz, 0.4 -1 mT

rat bone marrow mesenchymal stem cells

*miR-34b-5p↓, expression of miR-34b-5p decreased under SEMF stimulation,
*ALP↑, significant upregulation in the relative expression levels of osteogenic markers (ALP, RUNX2, BMP2, OCN, and OPN)
*RUNX2↑,
*BMP2↑,
*OCN↑,
*OPN↑,
*β-catenin/ZEB1↑, protein expression levels of osteogenic makers, including Active-β-catenin, RUNX2, and ALP, were elevated upon SEMFs exposure at 0.4 mT, 0.7 mT, and 1 mT
*STAC2↑, subsequently increasing STAC2 level.
*Diff↑, electromagnetic fields promote the osteogenic differentiation
*BMD↑, low-frequency SEMFs promote osteogenesis

4349-

MF,

Long-term effect of full-body pulsed electromagnetic field and exercise protocol in the treatment of men with osteopenia or osteoporosis: A randomized placebo-controlled trial

Trial,

ostP,

0.01–15,000 Hz, with sinusoidal, rectangular, multi-resonance, impulse, or sawtooth waveforms, the full-body maximum intensity is 30 gauss (3,000 microTesla)

Ninety-five males with osteopenia or osteoporosis

*BMD↑, The BMD of total hip and lumbar spine was significantly increased post-treatment in all groups
*Pain↓, PEMFs also help patients with osteoporosis feel better by reducing pain, improving functional results and improving quality of life (QoL)
*QoL↑,
*toxicity↓, PEMF therapy has gained extensive use due to its quick effects, ease of use, and lack of side effects
*Dose↝, 30 min/day, with intensity 100%, and frequency 5-15 Hz, three times/week.
*Inflam↓, PEMFs have a considerable anti-inflammatory and analgesic effect on the joint environment (Varani et al., 2017).

4348-

MF,

Pulsed electromagnetic field attenuates bone fragility in estrogen-deficient osteoporosis in rats

in-vivo,

ostP,

 (40 Hz and 25 Hzk), intensities (10 mT and 36.4 μT)

*BMD↑, The application of PEMF40Hz, significantly reduced the osteoporotic bone loss in female rats

3535-

MFrot,

MF,

Pulsed Electromagnetic Field Stimulation in Osteogenesis and Chondrogenesis: Signaling Pathways and Therapeutic Implications

Review,

Nor,

*eff↑, Pulsed electromagnetic fields (PEMFs) are currently used as a safe and non-invasive treatment to enhance bone healing and to provide joint protection.
*COL2A1↑, exposure to PEMFs induced increased collagen type II (Col2) expression and glycosaminoglycan (GAG) content
*SOX9↑, PEMFs significantly increased the expression of chondrogenic genes (SOX9, collagen type II, and aggrecan) and the deposition of cartilaginous matrix (sulphated GAG)
*Ca+2↑, Intracellular Ca2+ increase
*FAK↑, FAK activation
*F-actin↑, increased F-actin network formation
*Inflam↓, anti-inflammatory effect of PEMFs exposure has been extensively described above
*other↑, PEMFs exert a strong anti-inflammatory effect protecting cartilage tissue from the catabolic activity of pro-inflammatory cytokines.
*Diff↑, commonly recognized that PEMFs exposure induces osteogenic differentiation of MSCs
*BMD↑, Emerging evidence shows that PEMFs stimulation represents a safe non-invasive approach to favor bone repair and optimize bone tissue engineering

2262-

MFrot,

MF,

Effects of 0.4 T Rotating Magnetic Field Exposure on Density, Strength, Calcium and Metabolism of Rat Thigh Bones

in-vivo,

ostP,

0.4T, 8Hz, 30min/day, 30days

Rat

*BMD↑, strong magnetic field (MF) exposure could effectively increase bone density and might be used to treat osteoporosis
*eff↓, calcium supplement tended to increase the indexes of thigh bone density, energy absorption, maximum load, maximum flexibility, and elastic deformation
*ALP↑, alkaline phosphatase (ALP), serum phosphate, and serum calcium were higher in rats exposed to RMF with calcium
*other↑, RMF is in fact capable of increasing density, strength, calcium, and metabolism in bones

193-

MFrot,

MF,

Rotating Magnetic Field Mitigates Ankylosing Spondylitis Targeting Osteocytes and Chondrocytes via Ameliorating Immune Dysfunctions

in-vivo,

Arthritis,

 Ankylosing Spondylitis arthritis:  Mouse model

BMD↑, loss reduced
Cartilage↑, more intact cartilage surfaces and denser proteoglycan
IL17↓,
IL22↓,
IL23↓,
IL28↓,
CD4+↓, tremendously attenuated
CD8+↓, In this investigation, data showed that RMF treatment decreased CD3-expressing proliferative cells via immunostaining and reduced CD4+/CD8+ T-cells via flow cytometry in AS mice
LAMB3↑,
COL4↓,
THBS2↓,
ITGA11↓,
PPARγ↑, mice have decreased expression of peroxisome proliferator-activated receptor γ (PPAR-γ), a ligand-activated transcription factor belonging to the nuclear hormone receptor superfamily, which RMF reverses.
ACAA1↓,
PLIN1↓,
FABP4↓,
PCK1↓,
UCP1↓,
TNF-α↓,

198-

MFrot,

MF,

Biological effects of rotating magnetic field: A review from 1969 to 2021

Review,

Var,

AntiCan↑, RMF can inhibit the growth of various types of cancer cells in vitro and in vivo and improve clinical symptoms of patients with advanced cancer.
breath↑, 0.4T, 7Hz RMF was applied to treat 13 advanced non-small cell lung cancer patients (2 h/day, 5 days per week, for 6–10 weeks)
Pain↓, Decreased pleural effusion (2 patients, 15.4%), remission of shortness of breath (5 patients, 38.5%), relief of cancer pain (5 patients, 38.5%), increased appetite (6 patients, 46.2%), improved physical strength (9 patients, 69.2%), regular bowel mov
Appetite↑,
Strength↑,
BowelM↑,
TumMeta↓, The same RMF (2 h/day, for 43 days) can also suppress the growth and metastasis of B16-F10 cells in vivo
TumCCA↑, The up-regulated transcription of miR-34a induced cell proliferation inhibition, cell cycle arrest, and cell senescence by targeting E2F1/E2F3, two members of E2F family which are major regulators of the cell cycle,
ETC↓, 2h exposure) effectively inhibited the growth of two types of cultured brain cancer cells, glioblastoma cells and diffuse intrinsic pontine glioma cells. They found that the mitochondrial electron transport chain was significantly disturbed by RMF,
MMP↓, which caused loss of mitochondrial integrity, decreased mitochondrial carbon flux in cancer cells, and eventual cancer cell death (Sharpe et al., 2021).
TumCD↑,
selectivity↑, same group further reported that the same RMF can also selectively kill cultured human glioblastoma and non-small cell lung cancer cells, and leave normal cells unharmed
ROS↑, Mechanistic studies revealed that RMF can increase the mitochondrial ROS level, which further activated the caspase-3 and disturbed the electron fflow in the respiratory chain pathway in cancer cells. (Helekar et al., 2021).
Casp3↑,
TumCG↓, 0.4T, 7.5Hz RMF (2 h/day, for 5 days) inhibited the growth of mouse melanoma cell line B16–F10 in vitro,
TumCCA↑, and its mechanism involved cell cycle arrest and decomposition of chromatins.
ChrMod↑,
TumMeta↓, (2 h/day, for 43 days) can also suppress the growth and metastasis of B16–F10 cells in vivo,
Imm↑, benefiting from improved immune function, including decreased regulatory T cells, increased T cells, and dendritic cells
DCells↑,
Akt↓, inhibiting the activation of the AKT pathway (Tang et al., 2016). T
OS⇅, 51 women with advanced breast cancer underwent RMF treatment. The results showed that 27 patients among them achieved signicant therapeutic effects, and there were no side-effects
toxicity↓,
QoL↑, 13 advanced non-small cell lung cancer patients the quality of life was improved in different degrees. Median survival and 1-year survival rate was 50% and 100% longer
hepatoP↑, In addition, it seems that the RMF can also attenuate liver damage in mice bearing MCF7 and GIST-T1 cells (Zha et al., 2018)
Pain↓, The results showed that the RMF treatment reduced abdominal pain by 42.9% (9/21), nausea/vomiting by 19.0% (4/21), weight loss by 52.4% (11/21), ongoing blood loss by 9.5% (2/21), improved physical strength by 23.8% (5/21) and sleep quality by 19.0%
Weight↑,
Strength↑,
Sleep↑,
IL6↓, Furthermore, decreased levels of interleukin-6 (IL-6), granulocyte colony-stimulating factor (G-CSF) and keratinocyte-derived chemokine (KC) were observed
CD4+↑, it was discovered that macrophages and dendritic cells were activated, CD4+ T and CD8+ T lymphocytes increased, and the ratio of Th17/Treg was balanced.
CD8+↑,
Ca+2↑, effects of RMF were strongly associated with increased calcium tunnel activity and intracellular Ca2+ level in CNS
radioP↑, These results suggest that RMF may be helpful to alleviate the damage of hematopoietic function caused by radiotherapy and chemotherapy
chemoP↑,
*BMD↑, 0.4T, 8Hz RMF treatment (30min/day, for 30 days) along with calcium supplement, synergistically improved bone density
*AntiAge↑, In 2019, Xu et al. reported that a 4h exposure to a 0.2T, 4Hz RMF delayed the aging of human umbilical vein endothelial cells (HUVEC)
*AMPK↑, Mechanistic research revealed that RMF treatment increased the expression of AMPK while reducing the expression of p21, p53 and mTOR.
*P21↓,
*P53↓,
*mTOR↓,
*OS↑, They also discovered that the RMF (2 h/day, for 6, 10 or 14days) can prolong the health status lifespan of Caenorhabditis elegans.
*β-Endo↑, 0.1–0.8T, 0.33Hz RMF treatment signicantly increased the β-endorphin level in the blood of rabbits and humans (23 times higher than before). Moreover, it decreased serotonin (5-HT) in brains, small intestine tissue and serum of mice.
*5HT↓,

4128-

Silicon,

Silicon as Versatile Player in Plant and Human Biology: Overlooked and Poorly Understood

Review,

NA,

*other↑, human exposure to Si imparts health benefits and essentially occurs through plant-derived food products.
*BMD↑, Si bioavailability in human diet, e.g., strengthens bones and improves immune response, as well as neuronal and connective tissue health.
*Dose↝, It is estimated that human daily intake of Si as silicic acid ranges from 9 to 14 mg, while intakes near 25 mg/d might promote bone health
*cognitive↑, low Si levels in drinking water increase the risk of cognitive impairment due to high aluminum (Al) intake
*Dose?, In order to prevent risks of developing Al-induced Alzheimer’s disease, use of silica rich water with concentrations ≥11 mg/L is recommended

2211-

SK,

Shikonin mitigates ovariectomy-induced bone loss and RANKL-induced osteoclastogenesis via TRAF6-mediated signaling pathways

in-vivo,

ostP,

mice, RANKL-induced

*BMD↑, Shikonin prevented bone loss by inhibiting osteoclastogenesis in vitro and improving bone loss in ovariectomized mice in vivo.
*p‑NF-kB↓, shikonin inhibited the phosphorylation of inhibitor of NF-κB (IκB), P50, P65, extracellular regulated protein kinases (ERK), c-Jun N-terminal kinase (JNK), and P38.
*p‑p50↓, by inhibiting phosphorylation of P65, P50, and IkB protein.
*p‑p65↓,
*p‑ERK↓, shikonin blocked the MAPK pathway via preventing phosphorylation of ERK, JNK, and P38
*p‑cJun↓,
*p‑p38↓,

2281-

VitK2,

The biological responses of vitamin K2: A comprehensive review

Review,

Var,

*ROS↓, VitK1 and MK-4 prevent oxidative cell death by blocking the activation of 12-LOX and ROS generation
*12LOX↓,
*NF-kB↓, VitK2 modulates osteoblast and osteoclast formation and activity via downregulation of basal and cytokine-induced NF-κB activation
*BMD↑, strengthens bone construction
*hepatoP↑, VitK2 significantly increased serum albumin levels with concurrent reduction of the levels of alanine and aspartate aminotransferases, suggesting that VitK2 enhances liver regeneration.
cycD1/CCND1↓, figure 5
PKCδ↓,
STAT3↓,
ERK↑,
MAPK↓,
ROS↑,
PI3K↝,
Akt↝,
Hif1a↝,
*neuroP↑, An increasing body of evidence suggests the possible role of VitK supplementation as a novel neuroprotective strategy in the maintenance of nerve integrity and normal brain function, including cognition and behavior

1818-

VitK2,

New insights on vitamin K biology with relevance to cancer

Review,

Var,

TumCG↓, A few small randomized trials support the concept that vitamin K supplementation can retard cancer development and/or progression
ChemoSen↑, phase 2 randomized placebo-controlled trial in HCC patients demonstrated that MK4 supplementation (45 mg/day orally) enhanced the efficacy of the multi-kinase inhibitor sorafenib
toxicity∅, long term vitamin K supplementation is safe and may offer survival benefit in HCC patients.
OS↑,
BMD↑, Primary Outcomes: Bone density
eff↑, In studies where both forms of the vitamin have been compared, MKs generally exerted more potent anticancer effects than PK.
MMP↓, direct effects on mitochondrial membrane depolarization and reactive oxygen species (ROS)
ROS↑,
eff↓, ROS neutralization by antioxidants (N-acetyl cysteine (NAC) and alpha-tocopherol) or BAK knockdown prevented MK4 mediated mitochondrial disruption and apoptosis
ERK↑, activates ERK, JNK/p38 MAPK
JNK↑,
p38↑,
Cyt‑c↑, cytochrome c release
Casp↑, caspase activation
ATP↓, reducing ATP production and increasing lactate production
lactateProd↑,
AMPK↑, which activates AMPK
Rho↓, via inhibition of RhoA
TumCG↓, mouse xenograft studies, treatment with MK4 administered in water at a calculated dose of 20 mg/kg/d significantly reduced growth of established HCCs
BioAv↑, Phylloquinone (K1) is the major dietary form, but it is converted into menaquinone (K2) in tissues.
cardioP↑, optimal vitamin K status is common in adults and may contribute to chronic diseases such as osteoporosis, type 2 diabetes and cardiovascular disease.
Risk↓, Observational studies suggest that low vitamin K intake increases cancer risk(more lowers risk)

1815-

VitK3,

VitK2,

Vitamin K

Review,

Nor,

*Dose↝, 19+ years - 120 mcg (male) 90 mcg(female)
BMD↑, Some, but not all, studies also link higher vitamin K intakes with higher bone mineral density and/or lower hip fracture incidence

1761-

WBV,

Low Intensity Vibration Mitigates Tumor Progression and Protect Bone Quantity and Quality in a Murine Model of Myeloma

in-vivo,

Melanoma,

mice

Dose∅, (15min/d; 0.3g @ 90Hz)
BMD↑, 27% improved retention of bone in L5 of LIV-treated mice
TumCI↓, Low intensity vibration, serving as a surrogate for exercise, slowed the degradation of the bone and marrow phenotype and suppressed the invasion of the tumor.

1754-

WBV,

Vibration Therapy for Cancer-Related Bone Diseases

Review,

Var,

*BMD↑, Studies have shown that WBV improves bone mineral density (BMD) and bone volume in patients and mice with cancer.
*toxicity∅, WBV effects on cancer patients, no adverse effects were reported for children, adolescents [51,56], adults, or the elderly
other↓, these studies indicate that vibration can suppress osteoclastogenesis through both cancer cell and osteocyte signaling.
Dose↝, Notably, low-magnitude (LM, ≤1 g) high-frequency (HF, ≥30 Hz) vibration was found to be optimal for patients with compromised bone quality [84] but not for those with healthy bones [111].
Dose↑, the intensity and duration of WBV may need to be much higher and longer to overcome the significant bone loss induced by aromatase inhibitors.
eff↑, demonstrated that a 7-day insertion, in which vibration (0.25 g, 35 Hz, 15 min/day) for 7 days was followed by a 7-day rest, significantly increased the rate of bone formation and improved micromechanical properties in rats
eff↑, However, in a recent rat study, three bouts of daily vibration (0.25 g, 35 Hz, 5 min/bout) separated by 4 h between each bout more effectively promoted fracture healing than the aforementioned 7-day rest insertion
eff↑, The benefits of inserting rest periods also can be observed at the cellular level. Twice-daily vibration (0.3 g, 90 Hz, 20 min/bout) separated by 3 h of rest decreased breast cancer invasion more than once-daily vibration treatment

1751-

WBV,

Yoda1 Enhanced Low-Magnitude High-Frequency Vibration on Osteocytes in Regulation of MDA-MB-231 Breast Cancer Cell Migration

in-vitro,

BC,

MDA-MB-231

in-vitro,

AML,

RAW264.7

BMD↑, Low-magnitude (≤1 g) high-frequency (≥30 Hz) (LMHF) vibration has been shown to enhance bone mineral density
YAP/TEAD↑, Combined treatment on osteocytes showed beneficial effects, including increasing the nuclear translocation of Yes-associated protein (YAP) in osteocytes
TumCG↓, The ability of carefully controlled high-magnitude mechanical loads to suppress breast cancer growth and maintain bone integrity has been shown using various models in vivo
Strength↑, Studies have shown the anabolic benefits of LMHF vibration (LMHFV) on the musculoskeletal system, including increased bone density [7], reduced marrow fat [8], and improved muscle and glucose metabolism
TumCI↓, Application of LMHF vibration on MDA-MB-231 cells does not affect their migration [25], cell viability, and apoptosis but suppresses their invasion and upregulates FAS, a membrane death receptor
Fas↑,
Ca+2↑, concentration of intracellular calcium in MLO-Y4 was shown to significantly increase after 90 Hz of vibration for 1 h

Showing Research Papers: 1 to 31 of 31

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 31

Pathway results for Effect on Cancer / Diseased Cells:

Infection & Microbiome ⓘ

CD8+↓, 1, CD8+↑, 1,
Total Targets: 127

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 1, Catalase↑, 3, GPx↑, 1, GSH↑, 2, lipid-P↓, 1, MDA↓, 1, OXPHOS↑, 1, ROS↓, 2, SAM-e↑, 1, SOD↑, 3, TOS↓, 1,

Mitochondria & Bioenergetics ⓘ

ATP↝, 1, MMP↑, 1,

Core Metabolism/Glycolysis ⓘ

12LOX↓, 1, AMPK↑, 2, glucose↓, 1, NAD↝, 1,

Cell Death ⓘ

BMP2↑, 1, cl‑Casp1↓, 1, proCasp1↓, 1, GSDMD↓, 1, p‑p38↓, 1,

Kinase & Signal Transduction ⓘ

OCN↑, 1, SOX9↑, 1,

Transcription & Epigenetics ⓘ

p‑cJun↓, 1, other↑, 4,

Protein Folding & ER Stress ⓘ

HSP70/HSPA5↑, 1,

DNA Damage & Repair ⓘ

P53↓, 1,

Cell Cycle & Senescence ⓘ

P21↓, 1,

Proliferation, Differentiation & Cell State ⓘ

CLOCK↝, 1, Diff↑, 4, p‑ERK↓, 1, mTOR↓, 1, mTOR↝, 1, RUNX2↑, 1, STAT3↓, 1, VGCC↑, 1, Wnt↑, 1,

Migration ⓘ

Ca+2↑, 3, Ca+2↝, 1, COL1↑, 1, COL2A1↑, 1, F-actin↑, 1, FAK↑, 1, OPN↑, 1, serineP↓, 1, STAC2↑, 1, TGF-β↑, 1, α-SMA↑, 1, β-catenin/ZEB1↑, 2, β-Endo↑, 1,

Angiogenesis & Vasculature ⓘ

angioG↑, 1, miR-34b-5p↓, 1, NO↑, 1, VEGF↑, 1,

Immune & Inflammatory Signaling ⓘ

COX2↓, 1, IL1β↓, 1, IL6↓, 3, IL8↓, 2, Inflam↓, 5, JAK2↓, 1, NF-kB↓, 3, p‑NF-kB↓, 1, p‑p50↓, 1, p‑p65↓, 1, PGE2↓, 1, TNF-α↓, 2, TNF-α↑, 1, VitD↑, 1,

Synaptic & Neurotransmission ⓘ

5HT↓, 1, BDNF↑, 1, EndoR↑, 1, monoA↑, 1,

Protein Aggregation ⓘ

NLRP3↓, 1,

Hormonal & Nuclear Receptors ⓘ

testos↑, 2,

Drug Metabolism & Resistance ⓘ

Dose?, 1, Dose↑, 1, Dose↝, 5, eff↓, 2, eff↑, 3, eff↝, 1, Half-Life↝, 2, selectivity↑, 1,

Clinical Biomarkers ⓘ

ALP↑, 2, BMD↑, 23, BMPs↑, 2, Calcium↑, 1, hs-CRP↓, 1, IL6↓, 3, Mag↑, 1, VitD↑, 1,

Functional Outcomes ⓘ

AntiAge↑, 1, cardioP↑, 1, chemoP↑, 1, chemoPv↑, 1, ChemoSideEff↓, 1, cognitive↑, 2, hepatoP↑, 3, memory↑, 1, neuroP↑, 3, OS↑, 1, Pain↓, 1, QoL↑, 1, Risk↓, 3, Sleep↑, 1, toxicity↓, 1, toxicity∅, 1,

Infection & Microbiome ⓘ

Bacteria↓, 1,
Total Targets: 108

Scientific Paper Hit Count for: BMD, bone mineral density

13 Magnetic Fields
4 Boron
4 Magnetic Field Rotating
3 Vitamin K2
3 Whole Body Vibration
2 Exercise
1 Silver-NanoParticles
1 diet Short Term Fasting
1 diet FMD Fasting Mimicking Diet
1 Potassium
1 Melatonin
1 Silicic Acid
1 Shikonin
1 VitK3,menadione

Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:538  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

BMD Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Immune & Inflammatory Signaling ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Kinase & Signal Transduction ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Protein Aggregation ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

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