Database Query Results : diet FMD Fasting Mimicking Diet, ,

dietFMD, diet FMD Fasting Mimicking Diet: Click to Expand ⟱
Features:
5-day diet to mimic fasting without fasting.
FMDs are caloric-restricted plant–based diets containing low proteins, low sugar and high fats which represent a more feasible and safer option to water-only fasting.
Scientific Papers found: Click to Expand⟱
1853- dietFMD,    Impact of Fasting on Patients With Cancer: An Integrative Review
- Review, Var, NA
*toxicity∅, Data suggest overall good compliance, no malnutrition, minimal side effects. No significant changes were identified to suggest increased harm.
QoL∅, unchanged quality of life (QOL),
eff↑, improved endocrine parameters
eff↝, mixed results for cancer outcomes
ChemoSideEff↓, decreasing chemotherapy-related side effects
TumCG↓, limiting tumor growth
Dose↑, When fasting is used as an adjunct to chemotherapy, a minimum fasting period of at least 48 hours is currently recommended for nutritional interventions in order to achieve a measurable metabolic response at the cellular level
toxicity↝, The increased risk for poor outcomes associated with malnutrition, weight loss, and cachexia poses an obvious safety concern for patients with cancer who participate in calorie-restricted fasting
eff↑, short-term fasting involving water-only or limited daily calorie consumption for less than a week has the potential to achieve positive metabolic changes while avoiding malnutrition and significant weight loss
IGF-1↑, statistically significant decrease in IGF-1 among participants compliant with fasting compared with regular diet during the middle of therapy
*OXPHOS↑, Healthy cells also use mitochondrial oxidative phosphorylation for metabolism while cancer cells use aerobic glycolysis, also known as the Warburg effect
BG↓, statistically significant decrease in glucose among participants compliant with fasting compared with controls
Insulin↓, statistically significant decrease in insulin among participants compliant with fasting compared with regular diet before the first cycle of chemotherapy (p = .001), as well as during the middle of therapy
RadioS↑, A complete or partial radiographic response was also noted more often among fasting participants compared with normal diet participants

2352- dietFMD,    Glucose restriction reverses the Warburg effect and modulates PKM2 and mTOR expression in breast cancer cell lines
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MCF-7
Warburg↓, n this study, we investigated the role of glucose restriction (GR) and mTOR inhibition in reversing the Warburg effect in MDA-MB 231 and MCF-7 breast cancer cell lines
mTOR↓, Glucose restriction contribute to the reduction of the Warburg effect through mTOR inhibition and regulation of PKM2 kinases.
PKM2↓, Glucose restriction contribute to the reduction of the Warburg effect through mTOR inhibition and regulation of PKM2 kinases.

2152- dietFMD,    Prolonged Nightly Fasting and Breast Cancer Prognosis
- Analysis, BC, NA
eff↑, fasting less than 13 hours per night (lower 2 tertiles of nightly fasting distribution) was associated with an increase in the risk of breast cancer recurrence compared with fasting 13 or more hours per night (hazard ratio, 1.36
Dose↓, Nightly fasting less than 13 hours was not associated with a statistically significant higher risk of breast cancer mortality (hazard ratio, 1.21
Risk↓, Prolonging the length of the nightly fasting interval may be a simple, nonpharmacologic strategy for reducing the risk of breast cancer recurrence

1863- dietFMD,  Chemo,    Effect of fasting on cancer: A narrative review of scientific evidence
- Review, Var, NA
eff↑, recommend combining prolonged periodic fasting with a standard conventional therapeutic approach to promote cancer‐free survival, treatment efficacy, and reduce side effects in cancer patients.
ChemoSideEff↓, lowered levels of IGF1 and insulin have the potential to protect healthy cells from side effects
ChemoSen↑,
Insulin↓, causes insulin levels to drop and glucagon levels to rise
HDAC↓, Histone deacetylases are inhibited by ketone bodies, which may slow tumor development.
IGF-1↓, FGF21 rises during intermittent fasting, and it plays a vital role in lowering IGF1 levels by inhibiting phosphorylated STAT5 in the liver
STAT5↓,
BG↓, Fasting suppresses glucose, IGF1, insulin, the MAPK pathway, and heme oxygenase 1
MAPK↓,
HO-1↓,
ATG3↑, while increasing many autophagy‐regulating components (Atgs, LC3, Beclin1, p62, Sirt1, and LAMP2).
Beclin-1↑,
p62↑,
SIRT1↑,
LAMP2↑,
OXPHOS↑, Fasting causes cancer cells to release oxidative phosphorylation (OXPHOS) through aerobic glycolysis
ROS↑, which leads to an increase in reactive oxygen species (ROS), p53 activation, DNA damage, and cell death in response to chemotherapy.
P53↑,
DNAdam↑,
TumCD↑,
ATP↑, and causes extracellular ATP accumulation, which inhibits Treg cells and the M2 phenotype while activating CD8+ cytotoxic T cells.
Treg lymp↓,
M2 MC↓,
CD8+↑,
Glycolysis↓, By lowering glucose intake and boosting fatty acid oxidation, fasting can induce a transition from aerobic glycolysis to mitochondrial oxidative phosphorylation in cancerous cells, resulting in increased ROS
GutMicro↑, Fasting has been shown to have a direct impact on the gut microbial community's constitution, function, and interaction with the host, which is the complex and diverse microbial population that lives in the intestine
GutMicro↑, Fasting also reduces the number of potentially harmful Proteobacteria while boosting the levels of Akkermansia muciniphila.
Warburg↓, Fasting generates an anti‐Warburg effect in colon cancer models, which increases oxygen demand but decreases ATP production, indicating an increase in mitochondrial uncoupling.
Dose↝, Those patients fasted for 36 h before treatment and 24 h thereafter, having a total of 350 calories per day. Within 8 days of chemotherapy, no substantial weight loss was recorded, although there was an improvement in quality of life and weariness.

1862- dietFMD,    Exceptional tumour responses to fasting-mimicking diet combined with standard anticancer therapies: A sub-analysis of the NCT03340935 trial
- Trial, Var, NA
OS↑, five patients with advanced, poor prognosis solid neoplasms, who achieved complete and long-lasting tumour responses when treated with a combination of cyclic FMD and standard systemic treatments in the context of the NCT03340935 trial.

1861- dietFMD,  Chemo,    Fasting induces anti-Warburg effect that increases respiration but reduces ATP-synthesis to promote apoptosis in colon cancer models
- in-vitro, Colon, CT26 - in-vivo, NA, NA
selectivity↑, Short-term-starvation (STS) was shown to protect normal cells and organs but to sensitize different cancer cell types to chemotherapy
ChemoSen↑, STS potentiated the effects of OXP on the suppression of colon carcinoma growth and glucose uptake in both in vitro and in vivo models.
BG↓, glucose and amino acid deficiency conditions imposed by STS promote an anti-Warburg effect
AminoA↓,
Warburg↓,
OCR↑, characterized by increased oxygen consumption but failure to generate ATP, resulting in oxidative damage and apoptosis.
ATP↓,
ROS↑, a significant increase in O2consumption rate (OCR), indicative of an increased oxidative metabolism, was observed
Apoptosis↑,
GlucoseCon↓, STS was as effective as oxaliplatin (OXP) in reducing the average tumor glucose consumption
PI3K↓, STS and in particular STS+OXP down-regulated the expression of PI3K
PTEN↑, and up-regulated PTEN expression
GLUT1↓, STS induced a profound reduction in GLUT1 , GLUT2 , HKII , PFK1, PK
GLUT2↓,
HK2↓,
PFK1↓,
PKA↓,
ATP:AMP↓, Accordingly, the ATP/AMP ratio, a good indicator of cellular energy charge, was dramatically reduced by the two STS settings
Glycolysis↓, results strongly support the effect of STS on reducing glycolysis and lactate production and increasing respiration at Complexes I-IV resulting in superoxide production/oxidative stress but in reduced ATP generation.
lactateProd↓,

1860- dietFMD,  Chemo,    Fasting-mimicking diet blocks triple-negative breast cancer and cancer stem cell escape
- in-vitro, BC, SUM159 - in-vitro, BC, 4T1
PI3K↑, FMD activates PI3K-AKT, mTOR, and CDK4/6 as survival/growth pathways, which can be targeted by drugs to promote tumor regression.
Akt↑,
mTOR↑,
CDK4↑,
CDK6↑,
hyperG↓, FMD cycles also prevent hyperglycemia and other toxicities caused by these drugs.
TumCG↓, cycles of FMD significantly slowed down tumor growth, reduced tumor size, and caused an increased expression of intratumor Caspase3
TumVol↓,
Casp3↑,
BG↓, confirming our hypothesis that lowering intracellular glucose levels (through reduced extracellular levels or reduced uptake) reduces CSC survival
eff↑, 2DG potentiated the effect of FMD both in terms of delaying tumor progression and in decreasing the number of mammospheres derived by tumor masses,
eff∅, metformin did not show any additive or synergistic antitumor effect when combined with the FMD, thus suggesting that FMD and metformin have redundant effects on blood glucose levels
PKA↓, We have previously shown that prolonged fasting reduces the activity of protein kinase A (PKA) in different types of normal cells
KLF5↓, PKA inhibition resulted in the downregulation of KLF5, a potential therapeutic target for TNBC
p‑GSK‐3β↑, (GSK3β) phosphorylation
Nanog↓, stemness-associated genes NANOG and OCT4, and KLF2 and TBX3,
OCT4↓,
KLF2↓,
eff↑, Combining FMD cycles with PI3K/AKT/mTOR inhibitors results in long-term animal survival and reduces treatment-induced side effects
ROS↑, FMD resulted in an increased expression of pro-apoptotic molecules, such as BIM, and ASK1, a critical cellular stress sensor frequently activated by ROS, whose production was previously shown to be increased by the FMD
BIM↑,
ASK1↑,
PI3K↑, FMD cycles upregulate PI3K-AKT and mTOR pathways and downregulate CCNB-CDK1 while upregulating CCND-CDK4/6 signaling axes
Akt↑,
mTOR↑,
CDK1↓,
CDK4↑,
CDK6↑,
eff↑, combining STS with pictilisib, ipatasertib, and rapamycin, selective inhibitors for PI3K, AKT, and mTOR, respectively, resulted in enhanced cancer cell death and reduction of mammosphere numbers in SUM159 cells

1859- dietFMD,  Chemo,    Fasting-Mimicking Diet Reduces HO-1 to Promote T Cell-Mediated Tumor Cytotoxicity
- in-vitro, BC, 4T1 - in-vivo, Melanoma, B16-BL6
CLP↑, combination of chemotherapy and a fasting-mimicking diet (FMD) increases the levels of bone marrow common lymphoid progenitor cells (CLP) and cytotoxic CD8+ tumor-infiltrating lymphocytes (TILs), leading to a major delay in breast cancer and melanoma
CD8+↑,
TumCG↓,
HO-1↓, In breast tumors, this effect is partially mediated by the down-regulation of the stress-responsive enzyme heme oxygenase-1 (HO-1)
TILs↑, FMD in combination with doxorubicin (DXR) promotes accumulation of tumor-infiltrating lymphocytes (TILs) in the tumor bed

1858- dietFMD,  Chemo,    Effect of short-term fasting on the cisplatin activity in human oral squamous cell carcinoma cell line HN5 and chemotherapy side effects
- in-vitro, HNSCC, HN5
Apoptosis↑, This study revealed that short-term fasting chemotherapy significantly improved HNSCC cell line apoptosis and necrosis.
necrosis↑,

1857- dietFMD,    Fasting cycles retard growth of tumors and sensitize a range of cancer cell types to chemotherapy
- in-vitro, BC, 4T1 - in-vivo, NA, NA
TumCG↓, Cycles of starvation were as effective as chemotherapeutic agents in delaying progression of different tumors and increased the effectiveness of these drugs against melanoma, glioma, and breast cancer cells
ChemoSen↑,
OS↑, In mouse models of neuroblastoma, fasting cycles plus chemotherapy drugs—but not either treatment alone—resulted in long-term cancer-free survival.

1856- dietFMD,  immuno,    Targeting the Gut Microbiome to Improve Immunotherapy Outcomes: A Review
- Review, Var, NA
GutMicro↑, Dietary patterns like the Mediterranean diet, caloric restriction modifications, and specific nutritional components show promise in influencing the tumor microenvironment and gut microbiome for better treatment outcomes

1855- dietFMD,    Impact of modified short-term fasting and its combination with a fasting supportive diet during chemotherapy on the incidence and severity of chemotherapy-induced toxicities in cancer patients - a controlled cross-over pilot study
- Trial, NA, NA
ChemoSideEff↓, total toxicities’ score were significantly reduced. reported significantly fewer chemotherapy-induced side effects, including asthenia, fatigue and gastrointestinal problems such as vomiting and diarrhoea
QoL↑, We also observed significantly fewer chemotherapy postponements post-mSTF, reflecting improved tolerance of chemotherapy
IGF-1↓, On average, Insulin [− 169.4 ± 44.1; 95% CI -257.1 – (− 81.8); P < 0.001] and Insulin-like growth factor 1 levels [− 33.3 ± 5.4; 95% CI -44.1 – (− 22.5); P < 0.001] dropped significantly during fasting.
Insulin↓,

1854- dietFMD,    How Far Are We from Prescribing Fasting as Anticancer Medicine?
- Review, Var, NA
ChemoSideEff↓, ample nonclinical evidence indicating that fasting can mitigate the toxicity of chemotherapy and/or increase the efficacy of chemotherapy.
ChemoSen↑, Fasting-Induced Increase of the Efficacy of Chemotherapy
IGF-1↓,
IGFBP1↑, biological activity of IGF-1 is further compromised due to increased levels of insulin-like growth factor binding protein 1 (IGFBP1)
adiP↑, increased levels of adiponectin stimulate the fatty acid breakdown.
glyC↓, After depletion of stored glycogen, which occurs usually 24 h after initiation of fasting, the fatty acids serve as the main fuels for most tissues
E-cadherin↑, upregulation of E-cadherin expression via activation of c-Src kinase
MMPs↓, decrease of cytokines, chemokines, metalloproteinases, growth factors
Casp3↑, increase of level of activated caspase-3
ROS↑, it is postulated that the beneficial effects of fasting are ascribed to rapid metabolic and immunological response, triggered by a temporary increase in oxidative free radical production
ATP↓, Glucose deprivation leads to ATP depletion, resulting in ROS accumulation
AMPK↑, Additionally, ROS activate AMPK
mTOR↓, Under conditions of glucose deprivation, AMPK inhibits mTORC1
ROS↑, Beyond glucose deprivation, another mechanism increasing ROS levels is the AA (amino acids) starvation
Glycolysis↓, Indeed, in cancer cells, limited glucose sources impair glycolysis, decrease glycolysis-based NADPH production due to reduced utilization of the pentose phosphate pathway [88,89,90,91],
NADPH↓,
OXPHOS↝, and shift the metabolism from glycolysis to oxidative phosphorylation (OXPHOS) (“anti-Warburg effect”), leading to ROS overload [92,93,94,95].
eff↑, Fasting compared to long-term CR causes a more profound decrease in insulin (90% versus 40%, respectively) and blood glucose (50% versus 25%, respectively).
eff↑, FMD have been demonstrated to result in alterations of the serum levels of IGF-I, IGFBP1, glucose, and ketone bodies reminiscent of those observed in fasting
*RAS↓, A plausible explanation of the differential protective effect of fasting against chemotherapy is the attenuation of the Ras/MAPK and PI3K/Akt pathways downstream of decreased IGF-1 in normal cells
*MAPK↓,
*PI3K↓,
*Akt↓,
eff↑, Starvation combined with cisplatin has been shown in vitro to protect normal cells, promoting complete arrest of cellular proliferation mediated by p53/p21 activation in AMPK-dependent and ATM-independent manner
ROS↑, generation of ROS due to paradoxical activation of the AKT/S6K, partially via the AMPK-mTORC1 energy-sensing pathways malignant cells
Akt↑, cancer cells
Casp3↑, combination of fasting and chemotherapy was in part ascribed to enhanced apoptosis due to activation of caspase 3

1852- dietFMD,  Chemo,    Starvation Based Differential Chemotherapy: 
A Novel Approach for Cancer Treatment
- Review, Var, NA
ChemoSideEff↓, Ten volunteers with different types of cancers were starved for 48–140 hours before chemotherapy and five–56 hours after. Overall, all patients showed decreased side effects of chemotherapy.
*toxicity↓, A case report showed that short-term starvation of up to five days followed by chemotherapy is not only safe and feasible, but also helps to ameliorate chemotherapy related side-effects.3
mTOR↓, reduction in mTOR activity
IGF-1↓, Studies reveal that starvation reduces levels of IGF-1 significantly. Short-term starvation of 72 hours reduces circulating IGF-1 by 70%
IGFBP1↑, and increases the level of IGF binding protein (IGFBP-1) an IGF-1 inhibitor, by 11-fold
BG↓, glucose levels were reduced by 41%
ROS↑, Increased metabolic rate as a result of DR causes increased ROS production

1851- dietFMD,  Chemo,    Starvation-dependent differential stress resistance protects normal but not cancer cells against high-dose chemotherapy
- in-vitro, GBM, LN229 - in-vitro, neuroblastoma, SH-SY5Y
selectivity↑, Short-term starved S. cerevisiae or cells lacking proto-oncogene homologs were up to 1,000 times better protected against oxidative stress or chemotherapy drugs than cells expressing the oncogene homolog Ras2
selectivity↑, Finally, short-term starvation provided complete protection to mice but not to injected neuroblastoma cells against a high dose of the chemotherapy drug/pro-oxidant etoposide
ROS↑, promote oxidative stress and DNA damage
DNAdam↑,
BG↓, blood glucose level for both mice and humans is ≈1.0 g/liter but can reach 0.5 g/liter after starvation.

1850- dietFMD,    Fasting-mimicking diet remodels gut microbiota and suppresses colorectal cancer progression
- in-vivo, CRC, NA
TumCP↑, FMD cycles effectively suppressed colorectal cancer growth, reduced cell proliferation and angiogenesis, increased tumor-infiltration lymphocytes especially CD8+T cells
angioG↓,
CD8+↑,
GutMicro↑, FMD stimulated protective gut microbiota, especially Lactobacillus.
eff↑, Additionally, FMD synthesizing with anti-PD-1 therapy effectively inhibited CRC progression.

1849- dietFMD,    The emerging role of fasting-mimicking diets in cancer treatment
- Review, Var, NA
TumCG↓, Accumulating evidence suggests that FMDs attenuate tumor growth by altering the energy metabolism of cancer cells
toxicity∅, FMD reduces risk factors and markers for aging, cardiovascular disease, diabetes, and cancer without serious adverse effects in healthy adults.
BG↓, dramatic downregulation of blood glucose
IGF-1↓, prolonged fasting downregulated IGF-1
mTOR↓, inhibits cellular mTOR activity.
M2 MC↓, In addition, alternate-day fasting inhibited colorectal cancer growth by suppressing adenosine-induced M2 macrophage polarization in the tumor microenvironment
eff↑, large prospective cohort study of breast cancer patients, a longer nightly fasting duration was associated with a decreased risk of breast cancer recurrence, so the FMD may also be beneficial after the eradication of the initial tumo
ChemoSen↑, Combining fasting cycles with chemotherapeutic agents markedly prevented the progression of subcutaneous breast cancer, melanoma, and glioma in mouse models
QoL↑, Fasting for 60 hours seemed to improve the patients' fatigue and quality of life during chemotherapy
RadioS↑, In response to stress, cancer cells engage antioxidant and DNA repair mechanisms in an energy-demanding manner, facilitating cancer cell survival. Thus, restriction of the energy supply would improve the antitumor activity of radiotherapy.
selectivity↑, Recently, short-term starvation was shown to increase the DNA damage induced by a single exposure to high-dose radiation in metastatic cancer cell lines, whereas healthy cells were not affected by starvation medium

1848- dietFMD,  Chemo,    Fasting mimicking diet as an adjunct to neoadjuvant chemotherapy for breast cancer in the multicentre randomized phase 2 DIRECT trial
- Trial, BC, NA
ChemoSideEff↓, Short-term fasting protects tumor-bearing mice against the toxic effects of chemotherapy while enhancing therapeutic efficacy
ChemoSen↑,
eff↑, FMD significantly reinforces the effects of neoadjuvant chemotherapy on the radiological and pathological tumor response in patients with HER2 negative early breast cancer.

1847- dietFMD,  VitC,    Synergistic effect of fasting-mimicking diet and vitamin C against KRAS mutated cancers
- in-vitro, PC, PANC1
TumCG↓, Fasting-mimicking diets delay tumor progression
ChemoSen↑, sensitize a wide range of tumors to chemotherapy
eff↑, vitamin C anticancer activity is limited by the up-regulation of the stress-inducible protein heme-oxygenase-1. The fasting-mimicking diet selectivity reverses vitamin C-induced up-regulation of heme-oxygenase-1
HO-1↓, FMD reverses the effect of vitamin C on HO-1(downregulating HO-1)
Ferritin↓,
Iron↑, consequently increasing reactive iron, oxygen species, and cell death
ROS↑, Vitamin C’s pro-oxidant action is strictly dependent on metal-ion redox chemistry. In particular, free iron was shown to be a key player in vitamin C-induced cytotoxic effects
TumCD↑,
IGF-1↓, effects on the insulin-like growth factor 1 (IGF-1)
eff↓, When cancer cells were grown under STS conditions before and during treatment, vitamin C-mediated toxicity was strongly enhanced
eff↓, Conversely, KRAS-wild-type CRC (SW48, HT29), prostate cancer (PC-3), ovarian cancer (COV362) cell lines and a normal colon cell line (CCD841CoN) were resistant to vitamin C when used both as a single agent and in combination with STS

1846- dietFMD,  VitC,    A fasting-mimicking diet and vitamin C: turning anti-aging strategies against cancer
- Study, Var, NA
TumCG↓, FMDs delay tumor progression
ChemoSen↑, potentiate chemotherapy efficacy
ChemoSideEff↓, while protecting healthy tissues from chemo-associated side effects in different cancer models
ROS↑, presence of metals, and particularly iron, high dose of vitamin C exerts a pro-oxidant action by generating hydrogen peroxide and hydroxyl radicals via Fenton chemistry
Fenton↑,
H2O2↑,
eff↑, we show that FMD cycles potentiate high-dose vitamin C anti-cancer effects in a range of cancer types
HO-1↓, KRAS-mutant cancer cells respond to vitamin C treatment by up-regulating HO-1, and consequently limiting vitamin C pro-oxidant action. FMD is able to revert HO-1 up-regulation
DNAdam↑, increase in free reactive iron and oxygen species causing DNA damage and cell death
eff↑, we found that the nontoxic FMD + vitamin C combination therapy is as effective as oxaliplatin + vitamin C in delaying tumor progression while the triple FMD, vitamin C and chemotherapy combination treatment is the most effective.

1845- dietFMD,    Fasting and fasting mimicking diets in cancer prevention and therapy
- Review, Var, NA
eff↑, Unlike chronic dietary restrictions or water-only fasting, FMDs represent safer and less challenging options for cancer patients.
selectivity↑, FMD cycles increase protection in healthy cells while sensitizing cancer cells to various therapies,
ChemoSen↑, FMD cycles enhance the efficacy of a range of drugs targeting different cancers in mice by stimulating antitumor immunity.

1844- dietFMD,    Unlocking the Potential: Caloric Restriction, Caloric Restriction Mimetics, and Their Impact on Cancer Prevention and Treatment
- Review, NA, NA
Risk↓, CRMs were well tolerated, and metformin and aspirin showed the most promising effect in reducing cancer risk in a selected group of patients.
AMPK↑, the increased AMP levels activate AMPK
Akt↓, This activation results in the inhibition of AKT and mTOR pathways
mTOR↓,
SIRT1↑, energy deficit also activates the SIRT pathways, which downregulates HIF1α, and the Nrf2 pathway
Hif1a↓,
NRF2↓,
SOD↑, enhances antioxidant defenses (e.g., superoxide dismutase SOD1 and SOD2)
ROS↑, Additionally, in prostate cancer (PC) [55] and triple-negative breast cancer (TNBC) [56] cell lines glucose restriction (GR) has been shown to trigger an increase in ROS, leading to cell death.
IGF-1↓, CR decreases poor prognosis markers such as IGF1, pAKT, and PI3K
p‑Akt↓,
PI3K↑,
GutMicro↑, induces changes in the gut microbiome linked to anti-tumor effects
OS↑, Incorporating a nutraceutical regimen like CR or KD with CT has reduced tumor growth and relapse and improved the survival rate
eff↝, type of dietary intervention, with FMD being the first option, followed by KD and CR last. FMD has been considered the most cost-effective and applicable because it does not completely restrict food intake.
ROS↑, findings consistently indicating that dietary restrictions render highly proliferative tumor cells more susceptible to oxidative damage
TumCCA↑, CR has been reported to induce cell cycle arrest in the G0/G1 phases , enabling cells to undergo DNA repair more efficiently and diminishing DNA damage by CRT
*DNArepair↑,
DNAdam↑, In contrast, tumoral cells, which have an altered cell cycle, are unable to repair DNA, leading to cell death

1843- dietFMD,  BTZ,    Cyclic Fasting–Mimicking Diet Plus Bortezomib and Rituximab Is an Effective Treatment for Chronic Lymphocytic Leukemia
- in-vivo, CLL, NA
AntiTum↓, Cyclic fasting–mimicking diet (FMD) is an experimental nutritional intervention with potent antitumor activity in preclinical models of solid malignancies.
Apoptosis↑, murine CLL models had mild cytotoxic effects, which resulted in apoptosis activation mediated in part by lowered insulin and IGF1 concentrations.
IGF-1↓,
eff↑, In CLL cells, fasting conditions promoted an increase in proteasome activity that served as a starvation escape pathway. Pharmacologic inhibition of this escape mechanism with the proteasome inhibitor bortezomib resulted in a strong enhancement
OS↑, combining cyclic fasting/FMD with bortezomib and rituximab, an anti-CD20 antibody, delayed CLL progression and resulted in significant prolongation of mouse survival
eff↑, recent clinical reports have shown that combining cyclic FMD with chemotherapy, endocrine therapies, or immunotherapy improves tumor responses in patients with early-stage neoplasms

1842- dietFMD,    Safety and Feasibility of Fasting-Mimicking Diet and Effects on Nutritional Status and Circulating Metabolic and Inflammatory Factors in Cancer Patients Undergoing Active Treatment
- Trial, Var, NA
Strength∅, The patients’ weight and handgrip remained stable, the phase angle and fat-free mass increased
Weight∅,
IGF-1↓, FMD reduced the serum c-peptide, IGF1, IGFBP3 and leptin levels
IGFBP3↑,
IGFBP1↑, while increasing IGFBP1
eff↑, these modifications persisted for weeks beyond the FMD period.

1841- dietFMD,    Fasting-Mimicking Diet Is Safe and Reshapes Metabolism and Antitumor Immunity in Patients with Cancer
- Trial, Var, NA
BG↓, In 101 patients, the FMD was safe, feasible, and resulted in a consistent decrease of blood glucose and growth factor concentration
AntiCan↑, mediate fasting/FMD anticancer effects in preclinical experiments
IFN-γ↑, enrichment of IFNγ
eff↑, Cyclic FMD Is Safe in Combination with Standard Anticancer Treatments
Dose↝, five-day FMD followed by 16 to 23 days of refeeding
CD14↓, end of five-day FMD, we found a significant decrease of total monocytes (CD14+)
IGF-1↓, Preclinical evidence in tumor-bearing mice suggests that fasting/FMD-induced reduction of blood glucose and insulin/IGF1 concentration
IGFR↓, induced reduction of serum IGF1 levels is associated with the downregulation of total and activated IGF1R at the tumor level
CD8+↑, where five-day fasting/FMD in patients with breast cancer increased total and activated intratumor CD8+ T cells, aDCs, NK cells, and Tem cells,
NK cell↑,

1626- dietSTF,  dietFMD,    When less may be more: calorie restriction and response to cancer therapy
- Review, Var, NA
CRM↑,
ChemoSen↑, CR mimetics as adjuvant therapies to enhance the efficacy of chemotherapy, radiation therapy, and novel immunotherapies.
RadioS↑,
eff↑, CR mimetics as adjuvant therapies to enhance the efficacy of chemotherapy, radiation therapy, and novel immunotherapies.
eff↑, Intermittent fasting has been shown to enhance treatment with both chemotherapy and radiation therapy.
IGF-1↓, Exposure to an energy restricted diet results in reduced systemic glucose and growth factors such as IGF-1
TumCG↓, reduction of IGF-1 levels in CR results in decreased tumor growth and progression
AMPK↑, CR also induces activation of AMP-activated protein kinase (AMPK), (working in opposition to IGF-1)
eff↑, Recent research in our lab showed that combining autophagy inhibition with a CR regimen reduced tumor growth more than either treatment alone [20].
ChemoSen↑, Short-term fasting has been shown to improve chemotherapeutic treatment with etoposide [40], mitoxantrone, oxaliplatin [41], cisplatin, cyclophosphamide, and doxorubicin [42] in transgenic and transplant mouse models
RadioS↑, Alternate day fasting has also been shown to improve the radiosensitivity of mammary tumors in mice
ROS↑, improve the radiosensitivity: likely due to enhanced oxidative stress and DNA damage during short-term fasting on cancer cells.
DNAdam↑,
eff↑, fasting-mimicking diet, in which mice are fed the same amount of food as control mice, albeit with a severely reduced caloric density, showed a similar reduction in tumor growth as short-term starvation
HO-1↓, fasting-mimicking diet were associated with increased autophagy in the cancer cells and reduced heme oxygenase-1 (HO-1) in the microenvironment


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 26

Results for Effect on Cancer/Diseased Cells:
adiP↑,1,   Akt↓,1,   Akt↑,3,   p‑Akt↓,1,   AminoA↓,1,   AMPK↑,3,   angioG↓,1,   AntiCan↑,1,   AntiTum↓,1,   Apoptosis↑,3,   ASK1↑,1,   ATG3↑,1,   ATP↓,2,   ATP↑,1,   ATP:AMP↓,1,   Beclin-1↑,1,   BG↓,8,   BIM↑,1,   Casp3↑,3,   CD14↓,1,   CD8+↑,4,   CDK1↓,1,   CDK4↑,2,   CDK6↑,2,   ChemoSen↑,11,   ChemoSideEff↓,7,   CLP↑,1,   CRM↑,1,   DNAdam↑,5,   Dose↓,1,   Dose↑,1,   Dose↝,2,   E-cadherin↑,1,   eff↓,2,   eff↑,25,   eff↝,2,   eff∅,1,   Fenton↑,1,   Ferritin↓,1,   GlucoseCon↓,1,   GLUT1↓,1,   GLUT2↓,1,   glyC↓,1,   Glycolysis↓,3,   p‑GSK‐3β↑,1,   GutMicro↑,5,   H2O2↑,1,   HDAC↓,1,   Hif1a↓,1,   HK2↓,1,   HO-1↓,5,   hyperG↓,1,   IFN-γ↑,1,   IGF-1↓,11,   IGF-1↑,1,   IGFBP1↑,3,   IGFBP3↑,1,   IGFR↓,1,   Insulin↓,3,   Iron↑,1,   KLF2↓,1,   KLF5↓,1,   lactateProd↓,1,   LAMP2↑,1,   M2 MC↓,2,   MAPK↓,1,   MMPs↓,1,   mTOR↓,5,   mTOR↑,2,   NADPH↓,1,   Nanog↓,1,   necrosis↑,1,   NK cell↑,1,   NRF2↓,1,   OCR↑,1,   OCT4↓,1,   OS↑,4,   OXPHOS↑,1,   OXPHOS↝,1,   P53↑,1,   p62↑,1,   PFK1↓,1,   PI3K↓,1,   PI3K↑,3,   PKA↓,2,   PKM2↓,1,   PTEN↑,1,   QoL↑,2,   QoL∅,1,   RadioS↑,4,   Risk↓,2,   ROS↑,13,   selectivity↑,5,   SIRT1↑,2,   SOD↑,1,   STAT5↓,1,   Strength∅,1,   TILs↑,1,   toxicity↝,1,   toxicity∅,1,   Treg lymp↓,1,   TumCCA↑,1,   TumCD↑,2,   TumCG↓,8,   TumCP↑,1,   TumVol↓,1,   Warburg↓,3,   Weight∅,1,  
Total Targets: 108

Results for Effect on Normal Cells:
Akt↓,1,   DNArepair↑,1,   MAPK↓,1,   OXPHOS↑,1,   PI3K↓,1,   RAS↓,1,   toxicity↓,1,   toxicity∅,1,  
Total Targets: 8

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:79  Target#:%  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

Home Page