Remission Cancer Research Results
Remission, Remission: Click to Expand ⟱
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Remission of the cancer
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Scientific Papers found: Click to Expand⟱
Dose↓, The patient was given 9 doses of KAT (200 mg) over a period of 6 months
Remission↑, After treatment, the patient loses cancer and the tissue regenerates from 5% to 30%
OS↑, remission
Dose↓, Electron microscopy of AgNP solution revealed bimodal nanoparticle size
distribution: 3 and 12 nm.
BioAv↝, basal **silver ion** concentrations of 32 ng/g, rising to 46 ng/g 1 hour after ingesting 60 mL of AgNP solution.
toxicity↓, no toxicities were observed and he had complete radiographic resolution of his cancer
Remission↑,
other↝, patient serum was analyzed and intact nanoparticles were not identified. Thus, we could not isolate the circulating AgNP form
other↝, Analysis of urine showed no AgNP or detectable nanoparticle fragments
other↝, AgNP solution was also exposed to simulated gastric fluid, in which they aggregated into larger nanoparticles according to UV-Vis absorption.
Dose↝, GDH: based on repeat setup, estimated PPM is 20PPM assuming 67% effecient. 1.2mg/60mL (he took 160mL/day
BioAv↝, GDH: chatAI computed the estimated bioavailability at 7%
Remission↑, Complete remission was achieved in all 77 patients in the ATRA–arsenic trioxide group who could be evaluated (100%) and in 75 of 79 patients in the ATRA–chemotherapy group (95%)
OS↑, Two-year event-free survival rates were 97% in the ATRA–arsenic trioxide group and 86% in the ATRA–chemotherapy group
toxicity↓, As compared with ATRA–chemotherapy, ATRA–arsenic trioxide was associated with less hematologic toxicity and fewer infections but with more hepatic toxicity.
lipid-P↓, Statins exhibit “pleiotropic” properties that are independent of their lipid-lowering effects.
TumCG↓, preclinical evidence suggests that statins inhibit tumor growth and induce apoptosis in specific cancer cell types.
Apoptosis↑,
ChemoSen↑, statins show chemo-sensitizing effects by impairing Ras family GTPase signaling.
RAS↓,
HMG-CoA↓, Statins are potent, competitive inhibitors of hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase (HMGCR).
HMGCR↓,
LDL↓, Statins reduce blood plasma cholesterol levels by decreasing de novo cholesterol biosynthesis and by inducing changes in low density lipoprotein (LDL) receptor expression [2].
toxicity↓, Due to the well-established safety profile of statins, such studies are less expensive than the development of novel drugs.
Risk↓, statin use in cancer patients was associated with reduced cancer-related mortality. The risk of cancer death was significantly lower in postmenopausal women
P21↑, Other proposed mechanisms leading to an increase of p21 levels include the release of promoter-associated histone deacetylase and inhibition of histone deacetylase
HDAC↓,
Bcl-2↓, Statins trigger the intrinsic apoptosis pathway and decrease Bcl-2 protein expression [[154], [155], [156]], increase Bax and BIM protein expression [[156], [157], [158], [159]], and activate several caspases
BAX↑,
BIM↑,
Casp↑,
cl‑PARP↑, thereby increasing cleaved PARP-1 levels.
MMP↓, different tumor cell lines (breast, brain, and lung) showed that simvastatin-induced apoptosis is dependent on decreasing mitochondrial membrane potential and increasing reactive oxygen species (ROS) production
ROS↑,
angioG↓, Statins inhibit angiogenesis and metastasis
TumMeta↓,
PTEN↑, n breast cancer xenografts, simvastatin prevented tumor growth by reducing Akt phosphorylation and BclXL transcription, while simultaneously increasing the transcription of pro-apoptotic/anti-proliferative PTEN
eff↑, In mice, the administration of a combination of celecoxib and atorvastatin was more effective than each individual treatment, and effectively prevented prostate cancer progression from androgen dependent to androgen independent
OS↑, Long-term statin use may improve survival in GBM patients treated with temozolomide chemotherapy
Remission↑, statin use during or after chemotherapy is not associated with improved disease-free-, recurrence-free-, or overall survival in stage II colon cancer patients
Dose↝, Bicalutamide 150 mg orally daily was started and tolerated well, causing only grade 1 fatigue and grade 1 hot flashes (CTCAE criteria v4.03).
Remission↑, After 4 months of treatment, the patient achieved a complete clinical response according to RECIST criteria which is ongoing 12 months after starting treatment.
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Case Report, |
lymphoma, |
NA |
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Remission↑, Refusing all suggested chemotherapies, the patient began self-administering dichloroacetate (DCA) 900 mg daily with a PET scan showing complete remission four months later.
p‑PDKs↓, DCA has been shown to block this phosphorylation by PDK at the mitochondrial membrane level and decrease glycolysis in favor of glucose oxidation
Glycolysis↓,
i-Ca+2↓, This return to a normal metabolism of glucose allows for major changes including a decrease in Ca++ intracellularly, and stabilization of the mitochondria allowing a reactivation of caspases in cancer cells leading to apoptosis
toxicity↓, A reversible, minimal nerve damage can be considerably reduced by a daily thiamine intake of several hundred milligrams for humans. thiamine amount varies from 50 mg/day to 100 mg/day depending on whether it is administered orally or injected
Dose∅, A Non-Hodgkin′s lymphoma patient taking 10 mg/kg [750 mg] of dichloroacetate daily of his own accord, had a complete remission of his Non-Hodgkin′s lymphoma cancer after four months
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vitro+vivo, |
Melanoma, |
NA |
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Case Report, |
Melanoma, |
NA |
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P-gp↓, disulfiram blocks the P-glycoprotein extrusion pump, inhibits the transcription factor nuclear factor-κB, sensitizes tumors to chemotherapy, reduces angiogenesis, and inhibits tumor growth in mice.
NF-kB↓,
ChemoSen↑,
angioG↓,
TumCG↓,
TumMeta↓, The combination of oral zinc gluconate and disulfiram at currently approved doses for alcoholism also induced >50% reduction in hepatic metastases and produced clinical remission in a patient with stage IV metastatic ocular melanoma, who has continu
Remission↑,
toxicity↓, who has continued on oral zinc gluconate and disulfiram therapy for 53 continuous months with negligible side effects.
ATF2↓, Disulfiram and Metals Inhibit ATF/CREB DNA Binding and Cyclin A Expression
CREB↓,
cycA1/CCNA1↓,
TumCG↓, Disulfiram and Zn2+ Inhibit Melanoma Growth and Angiogenesis in Mice
angioG↓,
Dose↝, 250 mg/d disulfiram with the largest meal of the day. This dose was increased to 500 mg/d after 1 month. Zinc gluconate (50 mg chelated elemental Zn2+, ) was also given thrice daily but not concurrent with disulfiram administration.
toxicity↝, On starting the protocol, the patient suffered grade 1 (National Cancer Institute Common Toxicity Criteria, version 2.0) diarrhea, nausea, depression, and malaise. Except for nausea, these side effects resolved within 2 months of continued treatment.
Remission↑, complete molecular remission 20 years
after a diagnosis of chronic lymphocytic leukemia
ALC↓, (31%) patients experiencing a sustained ≥20% reduction in ALC
Remission↑, One patient treated at the phase II dose level of the phase I trial achieved a partial remission
Remission↑, patient has remained asymptomatic for more than 15 years
OS↑, first published case report of "spontaneous" recovery from secondary autoimmune hemolytic anemia in an adult.
Remission↑, In 2015, more than three years after the documented remission, the patient remains well at age 52.
eff↑, The timing of this second remission, shortly after an increase in dose of epigallocatechin-3-gallate to 4 g daily, is provocative, as is the concurrent use of curcumin.
Dose↝, He takes epigallocatechin-3-gallate (1200 mg) daily and maintains his self-directed lifestyle regimen.
other↝, Figure 1, equivalent electrical circuit
ROS↑, Another aspect to consider is the fact that PEF application has been shown to result in reactive oxygen species (ROS) production not only in cells71,72 but also in the medium surrounding the cells
Temp∅, Provided the number of pulses and the PRF are not too high, allowing for interpulse heat dissipation, in most cases, thermal effects can even be neglected.
CellMemb↑, he main primary effect of nsPEFs is the permeabilization of both the cell membrane82 and organelle membranes, followed by calcium entry,83 loss of resting membrane potential,62,84 increased cellular K+ efflux,84 activation of VGCC ion channels
Ca+2↑, In addition to apoptosis, nsPEFs are known to trigger calcium mobilization.
Apoptosis↑, The apoptosis is characterized by several morphological changes in the cell, due to energy-dependent biochemical mechanisms, leading to cell death
TumCD↑,
MMP↓, , while the dissipation of ψ (mitochondria membrane potential) occurs at a higher level (around 40 kV/cm)
necrosis↑, A severe dysregulation of Ca2+ stimulates a cell death by necrosis, while a milder dysregulation provokes a cell death by apoptosis.103
TumVol↓, As a result, tumor shrinkage of 90% could be observed within 2 weeks, and the repetition of a second treatment at that time could result in complete regressions.
Remission↑,
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
Remission↑, Complete Remission
TumAuto↓, Hydroxychloroquine has been shown to inhibit autophagy. Autophagy is a process of self-cannibalization in which injured cancer cells ingest pieces of themselves, such as organelles and macromolecules, to conserve energy, and, therefore, thrive.
Remission↑, have now enjoyed a complete response with my latest CA19-9 of just 15 U/mL and no evidence of active disease on my most recent CT scan.
Remission↑, tumor remission rate in the MLT group was significantly higher than that in the control group
OS↑, MLT group had an overall survival rate of 28.24% (n=294/1,041), which was greatly increased compared with the control group (RR =2.07; 95% CI, 1.55–2.76; P<0.00001; I2=55%)
neuroP↑, MLT could effectively reduce the incidence of neurotoxicity
VEGF↓, by the downregulation of vascular endothelial growth factor (VEGF)
KISS1↑, MLT could suppress the metastasis of triple-negative breast cancer by inducing KISS1 expression
TumCP↓, MLT can significantly inhibit the proliferation of cancer cells
ChemoSideEff↓, while reducing the incidence of side effects in chemotherapy or radiotherapy
radioP↑, In the 20 randomized trials included, MLT was beneficial to reduce multiple side effects of radiotherapy and chemotherapy
Dose∅, mostly 20 mg/day and taken orally and taken at night, respectively
*ROS↓, Preclinical experimental research has confirmed that MLT was capable of scavenging ROS and repairing damaged DNA to exert antitumor effects
DNArepair↑,
ROS↑, The mechanisms of MLT exerting antitumor effect might involve with other pathways, such as antiangiogenesis and pro-oxidant
Dose∅, dosage of melatonin used in the 8 included RCTs was 20 mg orally, once a day.
Remission↑, Melatonin significantly improved the complete and partial remission (16.5 vs. 32.6%; RR = 1.95, 95% CI, 1.49-2.54; P < 0.00001)
OS↑, as well as 1-year survival rate (28.4 vs. 52.2%; RR = 1.90; 95% CI, 1.28-2.83; P = 0.001)
radioP↑, dramatically decreased radiochemotherapy-related side effects
Remission↑, Improved effect was found for complete response, partial response, and stable disease with RRs of 2.33 (95% CI = 1.29-4.20), 1.90 (1.43-2.51), and 1.51 (1.08-2.12), respectively
angioG↓, Since chemotherapy administered with metronomic schedules inhibits angiogenesis, we treated a 64-year-old man with advanced HCC with metronomic capecitabine.
TumVol↓, After only two months of treatment the HCC nodules disappeared on ultrasonography
Remission↑, After more than three years the patient is still in treatment with minimal toxicity and maintains a complete remission.
AntiCan↑, Sodium Bicarbonate “Kills” Cancer Cells
e-pH↑, The utilization of sodium bicarbonate to neutralize the acidity and increase the tumor pHe might control cancer cells progression
TumMeta↓, Sodium bicarbonate reduces the formation of spontaneous metastases and the rate of lymph node involvement in mouse models of metastatic breast cancer.
TumCI↓, administration of 200 mM bicarbonate to 4-week-old TRAMP mice (weaning at 3 weeks) effectively perturbs the in situ evolution of cancer to a microinvasive disease
TumCG↓, sodium bicarbonate significantly controls tumor growth and improves CD8+ T-cell infiltration.
CD8+↑,
NK cell↑, Natural killer (NK) cell activity is also increased in a B-cell lymphoma mouse model following the systemic administration of a buffer therapy.
Remission↑, began a self-administered course of vitamins, supplements, and 60 g of bicarbonate mixed in water daily. As of this submission, he has remained well with stable tumor for 10 months.
eff↑, Therefore, sodium bicarbonate could be used as an adjuvant therapy to enhance the efficacy of conventional treatments.
ChemoSen↑, Surprisingly, extracellular alkalization induced a 2- to 3-fold increase in the efficacy of doxorubicin
ChemoSen↓, it greatly reduces the efficacy of some weak acidic chemotherapeutics, such as chlorambucil.
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in-vivo, |
BC, |
NA |
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in-vitro, |
BC, |
MCF-7 |
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in-vitro, |
Nor, |
MCF10 |
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CardioT↓, SFN (4 mg/kg, 5 days/week) protected against mortality and cardiac dysfunction induced by DOX
*GSH↑, Rats Hearts: SFN and DOX co-treatment reduced MDA and 4-HNE adduct formation and also prevented DOX-induced depletion of GSH levels
*ROS↓, SFN reduces DOX-induced oxidative stress in the heart of non-tumor bearing rats.
*NRF2↑, activates Nrf2 in rat hearts during DOX treatment
NRF2∅, SFN does not interfere with DOX toxicity or Nrf2 activity in breast cancer cell lines
HDAC↓, SFN acts synergistically with DOX to inhibit HDAC and DNMT activity, decrease ERα detection and increase caspase-3 activity
DNMTs↓,
Casp3↑,
ER-α36↓, ERα levels in MCF-7, MDA-MB-231
Remission↑, SFN+DOX treatment (with a total DOX dose of 20 mg/kg) was able to eradicate the tumors in all rats by day 35 after tumor implantation
eff↑, SFN (4 mg/kg oral; 5 days/week for 5 weeks) with DOX (total of 10 or 20 mg/kg i.p. administered over 4 weeks) and showed that in combination with SFN, the dosage of DOX could be < by 50% while still eliciting the same anti-cancer effects as DOX alone
ROS↑, Increased generation of reactive oxygen species (ROS), an altered redox status, and aerobic glycolysis for energy production distinguish highly proliferative cancer cells from normal healthy cells
selectivity?, ROS production... distinguish highly proliferative cancer cells from normal healthy cells
TumVol↓, tumors were reduced over 25% in diameter
Remission↑, The effective rate was 63.3%, remission rate 36.9%, survival rate of one year 47.3%.
OS↑,
QoL↑, After treatment the life quality of patients were greatly improved
Weight↑, The patients got better appetite and their body weights were increased
*toxicity∅, It had no harmful effects on peripheral blood picture, heart, kidney and liver. Shikonin mixture is safe and effective for later-stage cancer
OS↑, patient showed improvement after receiving high dose IV vitamin C infusions for three months by decreasing tumor marker levels Alkaline Phosphatase (ALP)
Remission↑, remission acheived, still alive
ROS↑, high-dose vitamin C can act as a prooxidant, conferring selective toxic effects on cancer cells.
Dose↝, Twenty grams of vitamin C in 250 mL normal saline was initially administered via an ante-cubital vein twice a week in September 2011. To neutralize acidic pH (3.5-5.0) of vitamin C, it was mixed with NaHCO3, resulting in pH 6.2
Dose↝, high-dose vitamin C administration was continued for more than a year. In July 2013, she finally decided to undergo TACE
TumCG↓, Hepatocellular carcinoma regressed completely after the fourth TACE treatment (
Remission↑, describe a case of regression of multiple pulmonary metastases after treatment with high-dose vitamin C, which enabled a subsequent trial of TACE, eventually leading to complete remission
Showing Research Papers: 1 to 24 of 24
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 24
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
lipid-P↓, 1, NRF2∅, 1, ROS↑, 5,
Mitochondria & Bioenergetics ⓘ
MMP↓, 2,
Core Metabolism/Glycolysis ⓘ
CREB↓, 1, Glycolysis↓, 1, HMG-CoA↓, 1, LDL↓, 1, p‑PDKs↓, 1,
Cell Death ⓘ
Apoptosis↑, 2, ATF2↓, 1, BAX↑, 1, Bcl-2↓, 1, BIM↑, 1, Casp↑, 1, Casp3↑, 1, necrosis↑, 1, TumCD↑, 1,
Transcription & Epigenetics ⓘ
KISS1↑, 1, other↝, 4,
Autophagy & Lysosomes ⓘ
TumAuto↓, 1,
DNA Damage & Repair ⓘ
DNArepair↑, 1, DNMTs↓, 1, cl‑PARP↑, 1,
Cell Cycle & Senescence ⓘ
cycA1/CCNA1↓, 1, P21↑, 1,
Proliferation, Differentiation & Cell State ⓘ
HDAC↓, 2, HMGCR↓, 1, PTEN↑, 1, RAS↓, 1, TumCG↓, 5,
Migration ⓘ
Ca+2↑, 1, i-Ca+2↓, 1, ER-α36↓, 1, TumCI↓, 1, TumCP↓, 1, TumMeta↓, 3,
Angiogenesis & Vasculature ⓘ
angioG↓, 4, VEGF↓, 1,
Barriers & Transport ⓘ
CellMemb↑, 1, P-gp↓, 1,
Immune & Inflammatory Signaling ⓘ
NF-kB↓, 1, NK cell↑, 1,
Cellular Microenvironment ⓘ
e-pH↑, 1, Temp∅, 1,
Drug Metabolism & Resistance ⓘ
BioAv↝, 2, ChemoSen↓, 1, ChemoSen↑, 3, Dose↓, 2, Dose↝, 6, Dose∅, 3, eff↑, 6, selectivity?, 1,
Clinical Biomarkers ⓘ
ALC↓, 1, BMD↑, 1,
Functional Outcomes ⓘ
AntiCan↑, 1, CardioT↓, 1, ChemoSideEff↓, 1, cognitive↑, 1, neuroP↑, 1, OS↑, 9, QoL↑, 1, radioP↑, 2, Remission↑, 24, Risk↓, 1, toxicity↓, 5, toxicity↝, 1, TumVol↓, 3, Weight↑, 1,
Infection & Microbiome ⓘ
CD8+↑, 1,
Total Targets: 70
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
GSH↑, 1, NRF2↑, 1, ROS↓, 2,
Functional Outcomes ⓘ
toxicity∅, 1,
Total Targets: 4
Scientific Paper Hit Count for: Remission, Remission
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
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