Hepatitis B Virus infection have close

association and the occurrence of liver

cancer.
HBV is endemic in countries of the Far East
and Africa.
Those who are infected with HBV have a
greater than 200-fold increased risk of
developing liver cancer compared with
uninfected individuals in the same areas.
 It is likely that the effect of HBV is indirect and
possibly multifactorial:
1. By causing chronic liver cell injury and
accompanying regenerative hyperplasia, HBV
expand the pool of cycling cells at risk for
subsequent genetic changes.
2. HBV encodes a regulatory element called HBx
protein.

Mitotically active hepatocytes, surrounded by an

altered environment, are presumably prone to
genetic instability and cancer development.
 HTLV-1 is associated with a form of T-cell
leukemia/lymphoma.
Endemic in certain parts of Japan and the
Caribbean basin but is found sporadically
elsewhere, including the United States.
The genomic structure of HTLV-1 reveals the
gag, pol, env, and long terminal repeat (LTR)
region typical of other retroviruses, but in
contrast to other leukemia viruses, it contains
another region, referred to as tax. It seems that
the secrets of its transforming activity are
locked in the TAX gene.
 The main steps that lead to the development of
adult T-cell leukemia/lymphoma may be
summarized as follows.
HTLV-1 Infection

Stimulate TAX
Proliferation

Expansion of polyclonal cell population

*Incrased risk of mutation & genetic instability

Monoclonal neoplastic T-cell population emerge

Malignant cells
 Helicobacter Pylori is the causative agent of
gastric carcinomas and gastric.
In most cases H. Pylori is present in 90% of
patient in chronic gastritis.
Infection leads gastric ulcers, and in smaller
proportion of cases, gastric carcinomas, and
gastric lymphomas may develop.
 The causing agent is :
CagA (cytotoxin associated gene A) which injects
the CagA protein into the host cells.
VacA which encodes a vacoulating toxin that causes
apoptosis.
 Gastric lymphomas arise in mucosa-associated lymphoid
tissue (MALT)

B cells that give rise to the tumors normally reside in the marginal zones of
lymphoid follicles (marginal zone lymphomas)

Cronic infection with H. pylori leads to formation of

lymphoid infiltrates

B cells actively proliferate and may acuire genetic

abnormalities

Tumor growth is initially dependent on immune stimulation by H. pylori, but

at later stages it no longer requires the presence of the bacterium.