- Joe Tippens, från Oklahoma, diagnostiserades 2016 med avancerad småcellig lungcancer
- I januari 2017 hade den spridit sig genom hela kroppen
- Joe hade en förväntad livslängd på tre månader, men hans läkare anmälde honom till en klinisk studie som de hoppades skulle kunna ge honom upp till ett år längre
- En veterinär föreslog att han provade ett avmaskningsläkemedel för hundar, Fenbendazol, som har visat anticancer egenskaper i studier
- I maj 2017 var all cancer inte längre synlig på Joe’s röntgenbilder
- Nu, två år senare, är han fortfarande cancerfri och medicinska forskare planerar att börja studera Joe’s fal
Bloggen: ‘Cancer Treatments – from Research to Application’ har en mycket detaljerade sammanställning kring Fenbendazol och dess anticancer egenskaper:
I denna studie utförd på möss visade man på synergier mellan Metformin och intermitent fasta, men att Metformin endast hade tumörhämmande effekt, men endast när det administrerades vid hypogklikemi (mycket lågt blodsocker).
Glioblastom multiforme (GBM) är den vanligaste, mest aggressiva och dödliga typen av hjärntumör. Spridningsgrad-IV har en dålig prognos eftersom de nuvarande terapeutiska alternativen (kirurgi, strålbehandling och kemoterapi) inte helt kan utrota tumörceller. Tillvägagångssättet för behandling av glioblastom har inte heller förändrats mycket under det senaste decenniet, och Temozolomid (TMZ) är fortfarande standardbehandling. Motståndsmekanismer för TMZ och andra kemoterapeutiska medel uppstår lätt.
Bristen på effektiva alternativ är ett problem som dock kan motverkas genom ”läkemedelsompositionering” (drug repurposing) kända och vanliga droger för andra sjukdomar. Detta tillvägagångssätt tar hänsyn till de tillgängliga farmakokinetiska, farmakodynamiska, toxicitets- och säkerhetsuppgifterna och möjliggör en mycket snabbare och billigare läkemedels- och produktutvecklingsprocess.
Denna studier omfattar en mycket utförlig granskning av vetenskapliglitteratur och syftar till att lista läkemedel med potential för ”ompositionering”, baserat på deras förmåga att påverka glioblastomceller genom olika mekanismer. Några av dessa droger har redan gått in i kliniska prövningar och visar gynnsamma resultat och väcker hopp för deras potentiella tillämpning inom glioblastoma behandling.
ScienceDirect: Repurposing drugs for glioblastoma: From bench to bedside
|Drug||Main achievements||New IC50||Ref.|
|Chloroquine||Chloroquine treatments (10 and 25 μΜ) halved proliferation of primary cultures from GBM specimens and cell lines (U 373 and U 87). Chloroquine inhibited MMP-2 activity and GBM invasion; In an MTT assay, U251, LN229, and U87 glioma cell lines were treated with increasing concentrations of chloroquine for 48 hours (10‑100 μM).||30 μΜ (U251, LN229, U87)
40 μΜ (U251‑TMZR, LN229‑ TMZR, U87‑ TMZR)
|Hydroxichloroquine||Hydroxichloroquine killed glioma cells that were highly resistant to temozolomide, proving its cytotoxicity. Quinoline-based antimalarial compounds are cytotoxic to glioma cells.||–|||
|Mefloquine||Mefloquine effectively killed U251 cells at much lower concentrations than chloroquine. Mefloquine killed U 251 and U 251-TMZ resistant cells in a concentration dependent manner.||10 μΜ (U251, LN229, U87)
15 μΜ (U251‑ TMZR, LN229‑ TMZR, U87‑ TMZR)
|Quinacrine||Quinoline-based antimalarial compounds are cytotoxic to glioma cells. In an MTT assay, the U251 and U251-TMZR glioma cell lines were treated with increasing concentrations of quinacrine (10‑100 μΜ) for 48 hours. In a subcutaneous human xenograft U87 glioma model, nude mice were treated with 50 mg/kg of quinacrine and tumors were harvested after 24 hours. Quinacrine significantly reduced tumor progression.||5 μΜ (U251, LN229, U87)
8 μΜ (U251‑TMZR, LN229‑TMZR, U87‑TMZR)
|Pyrvinium pamoate||GBM samples with a CD133 high fraction are much more sensitive to pyrvinium treatment than those with a CD133 low fraction. CD133+ cells decline upon treatment with 200 nmol/L with pyrvinium for 48 hours in both primary (BT428) and recurrent (BT 566) GBM samples. Treated cells with pyrvinium at its IC80 levels for 3 days were intracranially injected in immunodeficient mice, that later displayed no evidence of tumor formation.||239.8 nmol/L (BT241), 122.5 nmol/L (BT486)|||
|Mebendazole||Oral administration of mebendazole at 50 mg/kg from day 5 after tumor implantation in C57BL/6 mice slowed tumor growth. 100 mg/Kg daily led to toxicities. 60919 GBM cells were incubated with 0.1 or 1 μM of mebendazole, and 1μM of mebendazole clearly reduced the polymerization of tubulin; this activity of mebendazole was also verified at 0.1 or 0.2 μM after 72 h||0.24 μM (GL261),
1μM (060919 GBM)
|Acyclovir||Acyclovir at high concentrations (up to 500 mg/mL) inhibited growth in tissue culture of the human glioblastoma cell lines T98G, SNB-19, and U 373 by as much as 68.3%.||–|||
|Ritonavir||In vitro, ritonavir induced a G1-block at the 100-μM dose in GL15 cells. Rats were treated daily with 40 mg/kg, IP, until their death but there was no control over tumor growth, most likely because the therapeutic dose was not reached in the tumor.||–||[7,8]|
|Atazanavir||50 μmol/L atazanavir induced inhibitory effects in both U 251 and LN229 cells.||–|||
|Ribavirin||Ribavirin treatment (30 μM) leads to a significant decrease in all glioma cell growth. Ribavirin treatment in vivo significantly enhances chemo-radiotherapy efficacy and improves survival of rats and mice orthotopically implanted with gliosarcoma tumors or glioma stem‑like cells, respectively.||53.6 μM (A 172)
27.9 μM (AM-38)
55.0 μM (T98G)
59.7 μM (U87)
664.2 μM (U 138)
257.7 μM (U 251)
76.9 μM (YH-13)
|Itraconazole||2-80 μM of itraconazole led to cytotoxicity in U87 and C6 cells. Nude mice with U87 subcutaneous tumor xenografts were treated with 75 mg/kg, twice daily, by gavage for 3 weeks. Itraconazole inhibited the proliferation of glioblastoma cells both in vitro and in vivo.||–|||
|Ciprofloxacin||Ciprofloxacin induced tumor cell death in a dose-dependent manner. IC50 reduced to 22.8 μM for ciprofloxacin in the presence of 62.5 μM of temozolomide.||259.3 μM (A 172)||[12,13]|
|Salinomycin||Salinomycin significantly reduced the cell viability of GL261 neurospheres and GL261 adherent cells in a dose-dependent manner. The inhibitory effect was more effective than that of 1-(4-amino-2-methyl-5-pyrimid l)-methyl-3-(2-chloroethyl)-3-nitrosourea hydrochloride and vincristine. Salinomycin depleted GL261 neurospheres from tumorspheres and induced cell apoptosis. In addition, it prolonged the median survival time of glioma-bearing mice.||–|||
|Minocycline||50 μM of minocycline reduced cell viability of U 87, U 251 and C6 glioma cells. Alone, it did not affect cell viability of normal cells (SVGP12 and rat primary astrocytes).
Mice that were injected with C6 cells and treated with minocycline (20 or 100 mg/kg, IP) in saline, daily, during 10 days had a slower tumor growth rate when compared to control group.
|30 μM (C6)|||
|Doxycycline||Doxycycline exerted mild anti-proliferative effects after high‑concentration treatments (20, 25, 30, and 35 µg/ml) on glioma cell lines U 251HF, U 87 and LN229.||–|||
|Tigecycline||Tigecycline inhibited glioma cell growth in a concentration-dependent way. 10 μM of tigecycline alone did not affect cell viability of normal cells (SVGp12 and rat primary astrocytes).
Tigecycline effectively inhibited tumor growth in the xenograft tumor model of U87 glioma cell, after the administration of tigecycline (100 mg/kg in DMSO), daily, for 10 days.
|Chlorpromazine||A significant decrease in cell viability was observed in cells treated for 24h with high concentration of chlorpromazine (≥20 μM). Overall survival significantly improved for U 251-TMZRorthotopic mouse brain tumor models, but not for the U 251 group, after treatment with 5 or 7 mg/Kg, IP for three times a week for 2 weeks and 5 days after tumor implantation.||18.8-27.7 μM (C6)
15 μM (SH-SY5Y)
|Thioridazine||GBM8401 cells were treated with at concentrations ranging from 5 to 15 μM for 24h. GBM8401 cells were treated concentrations of 10 and 20 μM for 24 h. Thioridazine induces autophagy in GBM8401 and U 87 cells, and has cytotoxic effect at 7.5 μM. U 87 cells were subcutaneously implanted into mice. Thioridazine (5 mg/kg/day, 5 days/week, IP) significantly reduced tumor size. Flow cytometry of propidium iodide-stained glioma cells treated with thioridazine, fluphenazine, or perphenazine (6–50 µM) resulted in a concentration-dependent increase of fragmented DNA up to 94% vs 3% in controls by all agents, with thioridazine being the most potent.||13.7 μM (C6)
11 μM (SH-SY5Y)
|Fluphenazine||Fluphenazine, from 0-24 μM, induced a marked and concentration-dependent decrease in cell viability in glioma C6 cells. Flow cytometry of propidium iodide-stained glioma cells treated with thioridazine, fluphenazine, or perphenazine (6–50 µM) resulted in a concentration-dependent increase of fragmented DNA up to 94% vs 3% in controls by all agents.||19-24.5 μM (C6)
15 μM (SH-SY5Y)
|Perphenazine||Perphenazine, from 0-24 μM, induced a marked and concentration-dependent decrease in cell viability in glioma C6 cells. Flow cytometry of propidium iodide-stained glioma cells treated with thioridazine, fluphenazine, or perphenazine (6–50 µM) resulted in a concentration-dependent increase of fragmented DNA up to 94% vs 3% in controls by all agents.||15.8 μM (C6)
15 μM (SH-SY5Y)
|Olanzapine||Treatment with olanzapine (up to 100 μM) inhibits the proliferation of established glioblastoma cell lines and enhances the antiproliferative effect of temozolomide on U 87 and A 172 cells.||27.9 μM (A172)
49.1 μM (U87)
|Penfluridol||With increasing concentrations, penfluridol significantly suppressed the growth of several glioblastoma cell lines in a concentration and time-dependent manner. Penfluridol (10 mg/kg by oral gavage, daily) led to a 65% suppression of glioblastoma tumor growth (U 87) in mice.||2–5 μM (GBM43, GBM10, GBM44, GBM28, GBM14, T98G, U 251, U 87, SJ‑GBM2, CHLA-200)|||
|Quetiapine||Relatively high doses of quetiapine (>25 μM) may inhibit cell proliferation by retarding cell cycle in the G2-M phase. In xenograft tumor model in nude mice, quetiapine (20mg/kg, IP) alone or combined with temozolomide, significantly suppressed tumor growth, displaying a synergistic antitumor effect with TMZ.||–|||
|Lithium||Inhibition of migration was dose-dependent, with a near complete blockade at 20 mM lithium for X12 (human biopsy) and U 87 glioma cells. A reduction in viability of about 20% was seen after 48 h of 20 mM lithium treatment in U 87 cells. Lithium concentrations above 5 mM can affect the proliferation, apoptosis and migration of glioma cells via GSK-3 inhibition. Combination with 1.2 mM Lithium potentiated TMZ-induced cell death in TP53wt glioma cells. TMZ combined with Lithium prevented tumor growth in vivo and increased mice median survival times.||–||[27,28]|
|Donepezil||Treatment of Hs683 cells with 2.5 μM donepezil for 72 h blocked a large majority of Hs683 cells in division, as also observed for T98G and U373 cells. Mice with orthotopically implanted Hs683 cells and treated with donepezil + TMZ (2 mg/kg + 40 mg/kg, per os, thrice a week, respectively) had a significant increase in survival, while treatment with donepezil alone (2 mg/kg per os, thrice a week) did not show significant benefits.||–||[29,30]|
|Memantine||Memantine (up to 600 μM) had an antiproliferative effect on T98G cells, but not on U 251 cells.||400 μM (T98G)|||
|Paroxetine||Paroxetine induced a dose-dependent decrease in cell viability. Concentrations of SSRIs that induced apoptosis are higher than those achieved with the current therapeutic use of these drugs||12–30 μM (C6)|||
|Fluoxetine||25-50 μM fluoxetine application decreased the viability of various glioma cell lines. The concentrations of SSRIs that induced apoptosis are higher than those achieved with the current therapeutic use of these drugs.||12–30 μM (C6)||[23,32,33]|
|Sertraline||Sertraline alone (up to 10 μM) displayed cytotoxicity in U 87 cells. When combined with imatinib or temozolomide, the antiproliferative effect was markedly improved.||3.1-6.8 μM (U 87)|||
|Fluvoxamine||The inhibitory effect of fluvoxamine on actin polymerization was concentration dependent. 20-30 μM was enough to inhibit lamellipodia formation and migration and invasion of U 87 and U 251 cells in vitro. Therapeutic doses of fluvoxamine were sufficient to prevent invasion of GBM cells (A 172, U 87, and U 251). Daily administration of fluvoxamine (50 mg/kg) inhibited GBM cell invasion and prolonged survival in mice bearing GBM tumors.||30 μM|||
|Imipramine||Exposure to imipramine 60 μM for 7 days strongly reduced the ability of U 87 and C6 cells, but not primary cultured rat astrocytes, to form colonies, due to cell death; 10 μM imipramine inhibited mitochondrial activity at a rate dependent on the oxygen content in the atmosphere (from 6% in hypoxia, 11% in average hypoxia, and 19% in hypoxia‑reoxygenation to 26% in 20% oxygen).||–||[35–37]|
|Amitriptyline||10 μM amitriptyline inhibited mitochondrial activity on TG98 cells at a rate dependent on the oxygen content in the atmosphere (from 6% in hypoxia, 11% in average hypoxia, and 19% in hypoxia-reoxygenation to 39% in 20% oxygen). Low-dose amitriptyline(0.14-0.5 mM) has emerged as a potential strategy for inducing inhibition of cellular respiration in tumor cells.||–||[38,39]|
|Escitalopram||Significant decreases in the proliferation of C6 glioma cells were detected with the increase in the escitalopram concentration and incubation period. Comparing to controls, cell proliferation after 24 h of incubation were 97.7, 85.9, 74.5 and 67.9% for 25, 50, 100 and 200 μM escitalopram, respectively. After 48 h, it was found to be 96.5, 68.0, 50.7 and 39.9% for 25, 50, 100 and 200 μM concentrations, respectively. Results indicate escitalopram induced citotoxitcity and apoptotic events in C6 glioma cells.||106.97 μM (C6)|||
|Levetiracetam||40, 80, 160, and 360 μg/mL reduced T98G cell numbers to a certain degree relatively to the number of control cells (at 72h); 80, 160, and 360 μg/mL reduced A 172 cell numbers by 20.2%, 23.5%, and 24.8% relatively to the number of control cells.||–|||
|Valproic acid||5 to 20 mM induced G2/M cell cycle arrest and increased the production of ROS (in U 87, GBM8401, and DBTRG-05MG GBM‑derived cell lines); it inhibited MTT dehydrogenase activity at concentrations over 800 µM (in those 3 GBM cell lines); Epilepsy patients generally accumulate total plasma concentrations in the range of 0.3-0.7 mM, when treated orally with 15-20 mg/kg valproic acid per day (lower concentrations of around 40-200 µM at a daily treatment are observed in the brain indicating valproic acid brain/plasma ratios in the range of 0.07 to 0.28); a dose escalation study in GBM patients defined 60 mg/kg valproic acidper day as maximal tolerable dose which gave rise to median plasma concentrations of about 0.85 mM and a maximal plasma concentration not exceeding 1.4 mM.||1.4 mM (T98G)
1.0 mM (U 251)
1.3 mM (U 87)
|Propofol||5 and 10 μg/ml significantly inhibited the proliferation of U 373 glioma cells at 48 and 72 h.||–|||
|Disulfiram||Classically TMZ resistant cells (SF188 cells) were sensitive to 500 nM, a sufficient concentration to suppress growth in monolayer by approx. 100% over 72 hours; U 251 cells treated with 200 nM were suppressed in growth by 80% and 500 nM doses completely eliminated the cells; IC90 value reported for disulfiram in SF188 cells was 100 nM.||–||[45,46][|
|Dimethyl fumarate||It is rapidly metabolized to MMF and has a Cmax in plasma of ∼15 μM, with an approximate steady state tissue and plasma concentration of 5 μM. GBM cells were treated with MMF (5 μM), enhancing toxicity of velcade and carfilzomib.||–|||
|Digitoxin||Non-cytotoxicity concentration (20 nmol/l) can induce TRAIL‑mediated apoptosis of GSCs; While digitoxin was capable of inhibiting HIF-1α expression in GSC at clinically achievable concentrations (10–25 nM), it required higher concentration than those used for cardiac therapy (2–3 nM);
Increased cell death at a concentration of 10 nM, while 1–5 nM did not reproduce a significant effect.
|Atorvastatin||10− 4 M significantly decreased cell viability of U 87 and microglia; 10 μM reduced the invasion and migration of U 87 spheroid cells after 58h.||–||[50–52]|
|Lovastatin||There were 26, 51, 58 and 71% cell death induced by 1, 5, 20, and 40 μM lovastatin alone in M059K GBM cells, respectively; A significant increase in cell population at G0/G1 phase was observed when cells were treated with 20 μM lovastatin, indicating that lovastatin was able to arrest the cells at G0/G1 stage.||–||[50,53,54]|
|Simvastatin||10 μM was a cytotoxic concentration of simvastatin; 10 μM significantly reduced the number of U 251 and U 87) colonies perfield (pro-apoptotic effect); the survival rates (C6 glioma cells) on exposure to 2.5, 5, 10, and 20 μM of simvastatin were 96.17, 53.82, 1.76 and 0.49%, respectively, at 72 h; the survival rates of U 251 cells on exposure to 2.5, 5, 10, and 20 μM of simvastatin were 65.57, 57.59, 25.11 and 21.87%, respectively, at 72 h;||–||[50,53,55]|
|Mevastatin,ﬂuvastatin||5 μM was the cytotoxic concentration of mevastatin and fluvastatin; the survival rates of C6 cells on exposure to 1, 2.5, 5, and 10 μM of fluvastatin were 69.70, 54.71, 9.71 and 0.88%, respectively, at 72 h; the survival rates of C6 cells on exposure to 1, 2.5, 5, and 10 μM of mevastatin were 83.82, 58.23, 4.41, and 0.52, respectively, at 72 h; the survival rates of U 251 cells on exposure to 1, 2.5, 5, and 10 μM of mevastatin were 81.44, 58.41, 31.81 and 16.93%, respectively, at 72 h; the survival rates of U 251 cells on exposure to 1, 2.5, 5, and 10 μM of fluvastatin were 63.37, 53.71, 25.45 and 24.08%, respectively, at 72 h.||0.922 μM (A 172)||[50,53]|
|Cerivastatin||50 nM induced mild morphological changes in U251 cells; 10 μM stimulated the G1 phase arrest; low concentrations (10 and 50 nM) dose-dependently inhibited the formation of focal adhesion plaques; disorganized phalloidin staining of actin stress fibers was also noted; at concentrations from 10 to 100 nM, cerivastatin drastically reduced FAK phosphorylation at Py397; 1 mg kg−1cerivastatin per day intraperitoneally significantly delayedsubcutaneous U 87 tumor growth (average tumour size decreased by 50.2%).||0.098 μM (A 172)||[50,56]|
|Pitavastatin||The IC50 was less than 10 μM in most of U 87 human GBM cells tested (range of 1.260 to 55.63 μM); The ability of pitavastatin to cross the BBB is predicted to be limited as the –log BB was calculated as ‑0.6499; 1 mg kg−1 pitavastatin per day intraperitoneally significantly delayed subcutaneous U 87 tumor growth (tumor size decreased by 74.3%).||0.334 μM (A172 cells)
21.2, 7.30 and 4.80 μM (U87, 2-, 3- and 4-day treatments, respectively)
|Mibefradil||2.5–5 μmol/L significantly inhibited cell growth and enhanced the inhibition of GSC growth by TMZ; mibefradil (24 mg/kg bodyweight) was administered per oral gavage (GSC-based xenograft mouse model) every 6 hours for 4 days and resulted insignificant inhibition of tumor growth.||–||[59,60]|
|Captopril||MMP-2 and MMP-9 activity was reduced to half at captopril concentrations of 30–50 nM, levels easily clinically achieved in humans.||–|||
|Metformin||10 mM significantly decreased GBM cell proliferation (U 87, U 251, LN18 and SF767); metformin EC50, as CLIC1 inhibitor, was 2.1 mM, while IAA94 (a well-characterized CLIC1 inhibitor) showed EC50 32 μM (in U 87 cells); metformin time-dependently decreased U 87 cell viability (EC50: 23, 6.6 and 1.7 mM after 24, 48 and 72 hours); metformin dose-dependently reduced CSC viability (EC50: 3.9, 11.3, and 8.0 mM for GBM CSC, after 48 hours of treatment); metformin inhibited CLIC1 conductance in wt GBM CSCs with an EC50 (2.3 mM) similar to U 87 cells; metformin (200-1000 μM) significantly inhibited CSC CLIC1 current during high frequency stimulation (7 days); prolonged treatment (up to 15 days) with low doses of metformin (10‑300μM) significantly reduced CSC viability.||–||[62,63]|
|Repaglinide||10 μM inhibited LN229 cell migration (at a much lower concentration compared to its IC50). Repaglinide (1.04 mg/kg) was administrated daily via intraperitoneal injection after GBM cell implantation, resulting in a significant increase in the median survival time (38 days) of mice.||200 μM (LN229)|||
|Pioglitazone||100-200 μM significantly reduced the cellular viability of glioma cells (U 251, T98G, and U 87) in a concentration- and time-dependent manner; 100 μM pioglitazone inhibited U 251 cell migration by reduction of MMP-2 expression; 50 μM reduced significantly the metabolic activity of G144 cell lines; 10 μM promoted only a slight decrease of the metabolic activity in GliNS2 cell line. IC90 value reported for pioglitazone was reported to be 158 μM in U 87 cells.||85 μM (U 87)||[65,66]|
|Rosiglitazone||5–20 μM decreased survival of glioma cells (C6 and U 251) without affecting primary astrocytes; 50 μM had a small effect on the growth of A 172 and U 87 cells; 50 μM produced only a slight and reversible block in the G2/M phase (M059K cells) at 24 h, which was lost by 48 h.||20-30 μM (M059K and M059J)||[67,68]|
|Ciglitazone||20 μM was toxic for glioma cells and primary astrocytes; 10 μM was cytoprotective for primary astrocytes but toxic to glioma cells.||–|||
|Phenformin||100 μM significantly decreased the proliferation of HF2414 GSCs and their self renewal (such effect was also observed at a concentration of 50 μM); phenformin (100 μM) inhibited the expression of the stemness markers OCT4, SOX2 and CD44; phenformin (1 mg/ml) administered orally in mice harboring GSC-derived xenografts for 4 weeks significantly decreased tumor growth (similar results were obtained when phenformin (50 mg/kg/day) was administered by intraperitoneal injection).||–|||
|Sulfasalazine||Concentrations over 0.5 mM reduced NF-κB activity for prolonged incubation (48 and 72 h); even at low doses (0.25 mM), sulfasalazine was able to suppress glioma growth by over 60%;||–|||
|Aprepitant||Maximum inhibition was reached with aprepitant at 70 μM when no living cells were observed after 48 h of co-culture (GAMG glioma cell line); 15 μM exerted a growth inhibition 6.71 % in that cell line; the IC50 of aprepitant for non-tumor cells is 90 µM, more than two-fold higher than for tumor cells.||32 µM (GAMG)|||
|Cimetidine||Significantly decreased growth rates of both U 373 GBM and 9L gliosarcoma cells at concentrations equal or higher than 100 mM; 100 and 1000 nM cimetidine significantly decreased the migration levels of both cell lines; doses between 100 and 0.1 mM induced no modification in either cell cycle kinetics or apoptotic features.||–||[72,73]|
|Estradiol||In the range of 0.1–25 μM, estradiol decreased cell viability in a concentration-dependent manner.||3.5 μM (C6)
3.8 μM (T98G)
|Celecoxib||In U 87 cells, celecoxib (8 and 30 μM) significantly induced DNA damage and inhibited DNA synthesis, corresponding with p53 activation.||–|||
|Amlexanox||150 μM caused a significant increase in G0/G1 and decrease in the S and G2/M populations of glioma cells, reducing as well the migration capability of cells; amlexanox intraperitoneally injected, every day for 21 days, in subcutaneous glioma model using U 87 cells, resulted in inhibitory effect on tumor growth and significantly decreased the tumor volume.||120 μM (U 87)
140 μM (U 251)
|Ivermectin||1 μM, 5 μM, and 10 μM inhibited proliferation of U 87 and T98G cells in a dose-dependent manner: 1 μM, 5 μM, and 10 μM (with ED50 of ∼5 μM); ivermectin at 10 μM completely abolished the ability of HBMEC to form tubular structures; the serum concentration of the ivermectin 15 mg/kg administered orally was∼33 μM; ivermectin (40 mg/kg) given intraperitoneally during 3 weeks in SCID mouse resulted in notorious inhibition of U 87 and T98G tumors growth. EC50 value for ivermectin was reported to be 5 μM.||–|||
Möss med bukspottkörtelcancer som behandlades med Cannabidiol (CBD), en naturligt förekommande beståndsdel av medicinsk cannabis, tillsammans med kemoterapi, överlevde nästan tre gånger längre än de som endast behandlades med kemoterapi, visar en ny studie.
I en studie som leddes av Moffitt Cancer Center fann man att kvinnor som tog en lågdos aspirin varje dag hade en 23 procent lägre risk för äggstockscancer jämfört med kvinnor som inte tog aspirin.
Man fann också att kvinnor som var regelbundet använde antiinflammatoriska läkemedel (NSAID), som ibuprofen eller naproxen, under en längre tid hade en högre risk att utveckla äggstockscancer.
Regelbunden användning av aspirin kan hjälpa till vid behandling av vissa cancerformer, visar en genomgång av 71 medicinska studier.
Studien som granskade ett mycket stort antal patienter visade att patienter som tog aspirin hade 20-30% större chans att vara i livet jämfört med patienter som inte tog läkemedlet.
Spridningen av cancer till andra delar av kroppen reducerades också väsentligt hos patienter som använde aspirin.