world cancer report - iarc

USA and the percentage is much lower in
developing countries (Fig. 5.44).
In the absence of extrahepatic disease,
resection with negative pathologic margins
is the mainstay of treatment for
malignant liver neoplasms. In patients in
whom a small liver remnant is anticipated,
portal vein embolization is used to
increase the size of the future liver remnant
[11]. The fact that most hepatocellular
carcinomas occur in a cirrhotic liver
excludes many patients from consideration
for surgical resection, due to the risk
of liver failure. Other techniques used
alone or as an adjuvant to resection
include radiofrequency ablation and
cryoablation. Liver transplantation has
been performed in non-resectable
patients, although use of this procedure
has declined due to a number of factors,
including the frequency of death from
tumour recurrence, especially in the
transplanted liver, and organ shortages.
Hepatocellular carcinoma is largely radiotherapy
resistant [10]. Nonsurgical treatments
include hepatic artery infusion of
drugs or thrombotic agents (port or
pump), chemoembolization and percutaneous
alcohol or acetic acid injection,
although side-effects are many and benefit
to the unresectable patient is doubtful
[4,11]. Hepatic intra-arterial iodine 131labelled
lipiodol (iodized poppy seed oil)
shows promise for the future [4,12].
Recent results suggest that a chemother-
206 Human cancers by organ site
Fig. 5.44 Five-year relative survival after diagnosis
of liver cancer.
apy regimen combining cisplatin, doxorubicin,
interferon and 5-fluorouracil may
elicit a response, although previously no
agent, either singly or in combination, has
been found to improve survival. Hormone
therapy is also disappointing, although
results with octreotide are more hopeful
than with tamoxifen. Metastatic hepatocellular
cancer commonly spreads to the
lungs and bones. Response to chemother-
Hepatocellular carcinoma
Familial
CDKN 2A, APC and BRCA2
Sporadic
HBV genome integration
p53
CDKN2A
M6P/IGF2R
SMAD gene family members
Cyclin D and Cyclin A
Altered MET function?
Intrahepatic cholangiocarcinoma
KRAS
p53
c-erbB2
MET oncogene
E-cadherin, α-cadherin, β-cadherin
BCL2
Telomerase
Table 5.7 Genes involved in the development of
liver cancer.
apy and local regional therapy is poor [12].
The liver is also a frequent site of metastases
from cancers at other sites, of which
the most common is colorectal cancer.
The poor prognosis and lack of effective
therapies for hepatocellular cancer suggest
that the development of prevention
programmes is of critical importance
(Hepatitis B vaccination, p144).