Research Focus:
It is becoming increasingly clear that in
addition to gene alterations in cancer cells, clinical behavior of malignant
tumors is profoundly affected by host environment, including several
pathophysiological conditions, such as chronic inflammation, infections,
diabetes and obesity.
Our lab is focusing on the pathologic interactions
between tumor cells and their microenvironment. Detailed understanding of the
molecular events fueling these interactions is necessary for development of
effective therapies, as well as for personalization of cancer treatment based
on host environment (in addition to tumor genetics).
In particular, we are interested in
pursuing the following avenues of investigation:
1. Mechanisms
through which chronic inflammation contributes to cancer progression and resistance
to therapy:
a) tumor-associated
macrophages and their mode of action in malignancy;
b) role of
inflammatory microenvironment in conferring aggressiveness and therapy
resistance in breast / pancreatic cancer;
c) modulation
of clinical behavior of the tumor by chronic infection (head&neck cancer,
pancreatic carcinoma).
2. Complex
relationships between heparanase enzyme (critical determinant of tumor-host
interactions) and heparan sulfate
proteoglycans
(heparanase substrate and at the same time regulator of its activity), as
important biological mechanism of cancer progression.
3. Impact of obesity / diabetes on patho-biologic characteristics of malignant
tumors (breast, pancreas), and their response to treatment.
4. Control of tumor-microenvironment crosstalk in hormonally regulated cancers (i.e., breast, prostate).
