In this review, the first of two parts, we first provide an overview of the orthodox
analgesics used commonly against
cancer pain. Then, we examine in more detail the emerging evidence for the potential impact of
analgesic use on
cancer risk and
disease progression. Increasing findings suggest that long-term use of nonsteroidal anti-inflammatory drugs, particularly
aspirin, may reduce
cancer occurrence. However,
acetaminophen may raise the risk of some
hematological malignancies. Drugs acting upon receptors of
gamma-aminobutyric acid (
GABA) and
GABA "mimetics" (eg,
gabapentin) appear generally safe for
cancer patients, but there is some evidence of potential carcinogenicity. Some
barbiturates appear to slightly raise
cancer risks and can affect
cancer cell behavior in vitro. For cannabis, studies suggest an increased risk of
squamous cell carcinoma of the tongue, larynx, and possibly lung.
Morphine may stimulate human microvascular endothelial cell proliferation and angiogenesis; it is not clear whether this might cause harm or produce benefit. The
opioid,
fentanyl, may promote growth in some tumor cell lines.
Opium itself is an emerging risk factor for gastric
adenocarcinoma and possibly
cancers of the esophagus, bladder, larynx, and lung. It is concluded that
analgesics currently prescribed for
cancer pain can significantly affect the
cancer process itself. More futuristically, several
ion channels are being targeted with novel
analgesics, but many of these are also involved in primary and/or secondary
tumorigenesis. Further studies are needed to elucidate possible cellular and molecular effects of orthodox
analgesics and their possible long-term impact, both positive and negative, and thus enable the best possible clinical gain for
cancer patients.