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2cannabis Lecture Cancer
2cannabis Lecture Cancer
ข้อเท็จจริงทางการแพทย์
ข้อควรระวัง.. ??
ทำไมต้องมีงานวิจัย เรื่องนี้.??
ยาหรือการรักษามาตรฐานที่จะนำมาใช้ทางการแพทย์
95%
แหล่งข้อมูลที่นำมาศึกษา
รายงานล่าสุดถึงปี 2018
(1999-2018)
การทบทวนอย่างเป็นระบบ
การวิเคราะห์เชิงเปรียบเทียบ
รายงานวิจัยแบบสุ่ม
รายงานวิจัยแบบการสังเกต
ศักยภาพของกัญชา ทางการแพทย์(1)
Whiting PF. Cannabinoids for medical use : a systematic review and meta-analysis. JAMA 2015;313(24):2456-73.
ยาลดอาการคลื่นไส้อาเจียน
สารสกัดกัญชา กับการรักษามะเร็ง
อัตราการอยู่รอดชีพ 5 ปี ในมะเร็งชนิดต่างๆ
ด้วยการรักษาปัจจุบัน
99.3% 90.9%
43.2%
26.3%
มะเร็งเต้านม มะเร็งลำไส้ใหญ่
80-100% 87.5%
nasopharynx
5-yr survival rate
5-yr survival rate
5-25%
มะเร็งกระเพาะอาหาร มะเร็งหลังโพรงจมูก
75-100% 91-96%
3-yr survival rate 5-yr survival rate
20-33%
1.3%
มะเร็งตับ มะเร็งปากมดลูก
ศักยภาพของกัญชา ทางการแพทย์(2)
LNCaP prostate cancer cells, serum- ↑thymidine incorporation seen with max effect at 0.125-0.25 Sánchez MG et al. (2003)
Δ9-THC μM Δ9-THC, thereafter tailing off at 0.5 and 1 μM. Similar effect FEBS Lett.2003;555:561-6.
free, 48 h incubation seen with R(+)-methAEA and HU-210
50 and 100 nM, but not 250 nM Δ9-THC ↑thymidine
incorporation and cell viability (MTT assay, 72 h). 100 nM Δ9-
THC ↑ Akt phosphorylation, Erk phosphorylation, Raf-1
PC3 prostate cancer cells, serum- Δ9-THC translocation, and EGFR production (48 h). Experiments with Sánchez MG et al. (2003)
free, 48-72 h rimonabant and SR144528 and suggest involvement of both Cell Signal.2003;15:851-9.
CB1 and CB2 receptors. Similar results seen with 100 nM R(+)-
methAEA.
Capan2 ↑ cell viability (Cell titer 96 assay) at 0.5 & 1 μM Δ9-
Panc1, Capan2, BxPc3, Mia-PaCa2 Δ9-THC THC; Panc at 1μM alone. No significant effect of 0.5 or 1 μM Δ9- Carracedo A et al. (2006)
pancreatic cancer cell lines; 0-0.1% THC on MiaPaCa2 and BxPc3 cell viability. All four cell lines
fetal bovine serum, 66 h show complete loss of cell viability after incubation with 3 and 4 Cancer Res.2006;66:6748-55.
μM Δ9-THC .
At concentration range 0.1 nM to 1 μM, no effects of Δ9-THC
AV40-transformed human trabecular Δ9-THC on cell viability (WST-1 assay). Significant ↓ cell migration Ramer R & Hinz B (2010)
meshwork cell line, serum-free, 24 h (Boyden chamber, wound-healing assay) with 0.01, 0.1, and 1 Biochem Pharmacol.
or 72 h μM Δ9-THC. Effect Δ9-THC on migration accompanied by ↑ 2010;80:846-57.
COX-2 activity.
Presence f serum, 24 & 48 h: no effect on cell viability
Δ9-THC (propidium iodide staining) at either time point for THC in range Richardson SJ et al. (2007)
Granta 519 mantle cell lymphoma 1.6-310 nM, ↓ at 6.3 μM. Absence of serum, 24 h, no effect of Leuk Lymphoma.
line, 24 & 48 h, 0 or 10% serum 31 nM Δ9-THC upon cell proliferation. The cells expressed CB1 2007;48:1855-7.
receptors.
0.1 and 0.3 μM Δ9-THC ↑ thymidine incorporation (U373-MG
U373-MG glioblastoma cell line; NCI- cells, 18 h) and cell viability (MTT assay, NCI-H292, 24 h). Effect Hart S et al. (2004)
H292 lung carcinoma cell line, serum- Δ9-THC blocked by EGFR inhibitor AG1478. No apoptosis seen at 0.1-1 Cancer Res.2004;64:1943-50.
free, 6-24 h μM THC, but a significant increase at 4-10 μM THC (NCI-H292, 6
h).
SF126 glioblastoma cell line; 0.1% fetal Δ9-THC ↑ Cell viability (MTT assay) at 0.1 μM Δ9-THC, thereafter McAllister SD et al.
bovine serum, 72 h inhibition ( IC50 value 0.6 μM). (2005)
J Neurooncol.
2005;74:31-40.
Glioma cells from biopsies from three Δ9-THC No obvious effect on cell viability (trypan blue exclusion) at 0.5 Guzmám M et al.
patients with recurrent glioblastoma μM, but large reduction at 2.5 μM. Biopsies expressed both CB1 (2006)
multiforme; 0.5% fetal bovine serum, and CB2 receptors, and the effect of 2.5 μM Δ9-THC was Br J Cancer.
48 h blocked by a combination or rimonabant + SR144528. 2006;95:197-203.
THC-”sensitive” (Gos3, U87, A172, Δ9-THC Possible ↑ cell viability (MTT assay) for some cell lines (e.g., T98), Lorente M et al.
SW1783, U118) and “resistant” (U373, not for others (e.g., SW1088) at 0.5 μM Δ9-THC. “Sensitive” (2011)
T98, SW1088, CCF, LN405) glioma cell lines were completely inhibited at 3 μM (IC50 <2.5 μM), all Cell Death Differ.
lines, serum-free, 72 h “resistant” lines except LN405 (40% reduction) at 4 μM (IC50 2011;18:959-73.
>2.5 μM).
CaCo-2 and HCT116 colon CBD Cell viability: no effect 0.01-10 μM CBD (neutral red uptake Aviello G et al. (2012)
adenocarcinoma cells, serum-free, 24 assay); no effect at 0.01-1 μM, modest reduction at 10 μM CBD J Mol Med (Berl).
h (MTT assay). Thymidine incorporation: Caco-2 cells show ↓ at 2012;90:925-34.
0.1, 1, and 10 μM, HCT116 cells only at 10 μM CBD
Caco-2 colorectal adenocarcinoma CBD Serum-dependent effects in proliferating cells. At 1% serum, an Macpherson T et al.
cells, 1% or 5% serum, 72 h increased cell viability (XTT assay) was seen at <1 μM CBD, ↓ at (2014)
higher concentration. At 5% serum, only the inhibition was seen. In Vitro Cell Dev Biol
The curves for assays undertaken using physiological O2 Anim. 2014;50:427-26.
concentrations were leftward shifted compared with those at
atmospheric O2 concentrations. No effect of CBD were noted
on post-confluent cells. In presence of 0.5 mM butyrate and 8%
serum, 0.16 μM CBD ↑ cell proliferation (CyQuant assay),
Whereas it was blocked by 10 μM CBD.
Human primary lung carcinoma cells CBD Concentration-dependent ↓ cell viability (WST-1 assay); Ramer R et al. (2013)
from a brain metastasis, serum-free, 48 significant effects seen at all concentrations tested (1 nM – 3 Mol Cancer Ther.
h μM; IC50 0.12 μM). Maximum effect (∼70% reduction in viability ) 2013;12:69-82.
seen at 1 μM. Effect of 3 μM reduced by COX-2 and PPARγ
inhibitors. CBD less potent in A549 and H460 lung carcinoma
cell (IC50 3.5 and 2.8 μM, respectively).
DLD-1 and HCT 116 epithelial colon CBD No significant effect on cell viability (MTT assay) at 0.3, 1 μM, ↓ Romano B et al.
adenocarcinoma cells, serum-free, 24 at 5 μM (and 3 μM for DLD-1 cells). (2014)
h Phytomedicine.
2014;21:631-9.
Source: Fowler CJ (Clin Phamacol Ther.2015;95(6):587-96.)
Effects of Δ9-THC and CBD at submicromolar concentrations upon cell viability, motility, and invasivity in human immortalized cell lines (Cont.)
SF126, U251, and U87 glioblastoma, 72 h Δ9-THC, CBD Cell viability (MTT assay): IC50 values 2.5-3.3 μM (Δ9-THC) Marcu JP et al. (2010)
and 0.6-1.2 μM (CBD). In U251 cells, two-way ANOVAs Mol Cancer Ther.2010;9:180-9.
indicated significant interactions CBD + Δ9-THC for
combination of IC20 and IC80 concentration. 1.7 μM Δ9-
THC + 0.4 μM CBD: ↑ annexin-positive cells, reduced by
SR144528, blocked by α-tocopherol. Combination also
↑ reactive oxygen species. Cell invasion (Boyden
chamber): U251 cell IC50 values ∼85 nM (Δ9-THC), ∼130
nM (CBD). No synergistic effects reported for
combination of 100 nM.
U87MG glioma, serum-free, 72 h Δ9-THC, CBD IC50 values for inhibition of cell viability (MTT assay) 1.2 Torres S et al. (2011)
μM (Δ9-THC) and 1.5 μM (CBD). No significant increase Mol Cancer Ther.2011;10:90-103.
in cell viability seen at low concentrations. Combination
of 0.9 μM THC + 0.9 μM CBD ↓ cell viability ∼20%,
whereas compounds per se had no significant effect.
Similar result for SW1783 cells and for combination of Δ9-
THC with tomozolomide (25-75 μM). Effect of Δ9-THC /
CBD combination not seen in cells where autophagy or
apoptosis is compromised.
Human T98G, U87MG, and mouse GL261 THC, CBD and No obvious effect (mean values in the rage 90-115% of Scott KA et al. (2014)
glioma cells, 5% serum, 48 h botanical control) of the compounds at 0.5 or 1 μM upon cell Mol Cancer Ther.
preparations proliferation (resazurin reduction assay). The compounds 2014;13:2955-67.
were inhibitory at higher concentrations
Source: Fowler CJ (Clin Phamacol Ther.2015;95(6):587-96.)
ศักยภาพของกัญชา ทางการแพทย์(2)
‘ควรมีการพัฒนางานวิจัยทั้งทางระดับหลอดทดลอง
สัตว์ทดลองและมนุษย์ เพื่อหาสัดส่วนของ
สารสกัดกัญชาที่เหมาะสมต่อการรักษามะเร็ง’
สารสกัดกัญชา กับอาการปวดจากมะเร็ง
ศักยภาพของกัญชา ทางการแพทย์(3)
ควรพัฒนางานวิจัยเพื่อจะหาข้อสรุป รวมทั้งหาสัดส่วนสารสกัดกัญชาที่เหมาะสม