AMERICAN CANNABIS NURSES ASSOCIATION

OVERVIEW
SIGMOID/RECTUM 70%
8%

DESCENDING
5%
6%
11%

TRANSVERSE
11%
5%
70%

ASCENDING 6%

IMAGE SOURCE: NATIONAL CANCER INSTITUTE (1)

CECUM 8%

NDQ COLORECTAL CANCER

Last Revised: April 23, y

AMERICAN CANNABIS NURSES ASSOCIATION

Last Revised: April 23, y

COLORECTAL CANCER
NURSING DATA QUERY (NDQ)

CRC INCIDENCE BY
ANATOMICAL LOCATION

TRADITIONAL TREATMENT
METHODS

ABLATION
CHEMOTHERAPY
CRYOSURGERY
LOCAL EXCISON
RADIATION
RADIOFREQUENCY

Colorectal cancer can (CRC) occur at any anatomical

location in the colon or the rectum through mutations
in the genetic material of mucosal cells (2). These
mutations disrupt apoptosis, leading to tumor
initiation, progression, or metastasis. Tumors may
present with cells that are well differentiated,
moderately differentiated, or poorly differentiated
(3). 75-95% of colorectal cancer is unrelated to
genetics, making it difficult to identify at-risk
populations.
Recent research shows that the endocannabinoid
system plays an important role in the bodys defense
against colon cancer, and that cannabinoids have
significant anti-tumor effects both in vitro and in vivo
(4).

SURGICAL RESECTION

THERAPEUTIC CANNABINOIDS
Botanicals
Cannabidiol (CBD), Delta-9 Tetrahydrocannabinol (THC)
Extracts
Nabiximols (Sativex)
Chemicals
Dronabinol (Marinol),
Nabilone (Cesamet)
SOURCE: NATURE (8)

* In binding assays, Nabiximols

showed greater affinity than pure CBD
for both CB1 and CB2 receptors, with pure CBD having very little affinity (5)

NDQ COLORECTAL CANCER

AMERICAN CANNABIS NURSES ASSOCIATION

CANNABINOID
RECEPTOR ACTIVATION
Upon receptor binding,
cannabinoid receptor
agonists inhibit cell
proliferation through
inhibition of cAMP-

Last Revised: April 23, y

ACTION/MECHANISM
CBD, THC, and Nabiximols cause anti-tumor effects by
various mechanisms, including: induction of apoptosis,
inhibition of tumor angiogenesis invasion, and inhibition of
metastasis (4). Cannabinoids appear to kill tumor cells but
do
not

dependent protein kinase,

which activates mitogenactivated protein kinases
(MAPK).
Stimulation of ceramide
synthesis via activation of
serine pamitoyltranferase
(SPT) up-regulates p8,
leading to the subsequent
induction of apoptosis.
Cannabinoid receptor
agonists also activate
MAPKs and PI3K/Akt
pathways; sustained

SOURCE: CANCER RESEARCH REVIEWS (7)

activation of ERK1/2 leads

to the induction of cyclin
kinase inhibitor
p27/KIP1with modulation of

affect the non-cancerous somatic cells, and may even

protect them from cell death (6).

cell cycle regulatory

molecules, resulting in G1
arrest and apoptosis (7).

ADMINISTRATION
PO: Tinctures, Tonics, Oils, Teas, Edibles, Oral Spray
Inhaled: Smoked botanical substance, Vaporized botanical
substance
Topical:
*CBD and THC must be in decarboxylated form

CONTRAINDICATION/PRECAUTIONS
NDQ COLORECTAL CANCER

AMERICAN CANNABIS NURSES ASSOCIATION

Last Revised: April 23, y

CBD: sevofluorane
THC: psychological disorders,
Nabiximols: breastfeeding, psychological disorders, sevofluorane

ADVERSE REACTIONS/SIDE EFFECTS

CBD: P450 inhibition
THC: dizziness, drowsiness, diarrhea, nausea, paranoia, disorientation
Nabiximols: same as THC plus: severe psychological events, suicidal ideation, seizure,
cardiac arrhythmias

ACCESSIBILITY BY STATE
CBD: Alabama, Alaska, Arizona, California, Colorado, Connecticut, Delaware, Florida,
Hawaii, Illinois, Iowa, Kentucky, Maine, Maryland, Massachusetts, Michigan, Minnesota*,
Mississippi, Montana, Nevada, New Hampshire, New Jersey, New Mexico, New York*,
North Carolina, Oregon, Rhode Island, South Carolina, Tennessee, Utah, Vermont,
Washington (also, Washington, DC), Wisconsin
THC: Alaska, Arizona, California, Colorado, Connecticut, Delaware, Hawaii, Illinois,
Maine, Maryland, Massachusetts, Michigan, Minnesota*, Montana, Nevada, New
Hampshire, New Jersey, New Mexico, New York*, Oregon, Rhode Island, Vermont,
Washington (also, Washington, DC)
Chemicals: All U.S. States (Not considered a Schedule I drug)

REFERENCES
1. National Cancer Institute. (n.d.). Colon and rectal cancer.
http://cancer.gov/cancertopics/types/colon-and-rectal.
2. Walden, P. (2011). The facts about colorectal cancer. Nursing Made Incredibly Easy, Volume 9 Issue 5 - p 3644 doi: 10.1097/01.NME.0000403191.78471.05

NDQ COLORECTAL CANCER

AMERICAN CANNABIS NURSES ASSOCIATION

Last Revised: April 23, y

3. Lowe1, S. & Lin, A. (2000) Apoptosis in cancer. Carcinogenesis, 21 (3): 485-495. doi:
10.1093/carcin/21.3.485
4. National Cancer Institute: (n.d) PDQ Cannabis and cannabinoids. Bethesda, MD: National
Cancer Institute. Available at: http://www.cancer.gov/cancertopics/pdq/cam/cannabis/
healthprofessional. Accessed 02/19/2015
5. Romano B, Borrelli F, Pagano E, Cascio MG, Pertwee RG, Izzo AA. (2014). Inhibition of
colon carcinogenesis by a standardized Cannabis sativa extract with high content of
cannabidiol. Phytomedicine 21(5):631-9. doi: 10.1016/j.phymed.2013.11.006.
6. Freimuth N1, Ramer R, Hinz B. (2010). Antitumorigenic effects of cannabinoids beyond
apoptosis. J Pharmacol Experimental Therepeutics (2):336-44. doi: 10.1124/jpet.
109.157735. Epub 2009 Nov 4.
7. Sarfaraz S., Adhami VM., Syed DN., Afaq F., Mukhtar H. (2008). Cannabinoids for cancer
treatment: progress and promise. Cancer Research 68: 339-342
8. Di Marzo, V., Bifulco, M., De Petrocellis, L. (2004). The endocannabinoid system and its
therapeutic exploitation. Nature Reviews Drug Discovery 3, 771-784 doi:10.1038/nrd1495

NDQ COLORECTAL CANCER