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The enormous burden of liver cancer on society becomes clear by considering the fact
that approximately 625,000 new cases of this cancer are diagnosed globally each year.
Distressingly, the number of deaths is approximately the same at 598,000 per year. Liver
cancer, therefore, is the third most common cause of death from cancer. Survival rates
for liver cancer are only 3–5% globally. In the United States, 19,160 new cases of liver
cancer and 16,780 deaths were reported for 2007. The major risk factors for this cancer
include prior infection with hepatitis B and C viruses, with the former more prevalent.
Dietary exposure to fungus Aspergillus fumigatus (aflatoxins) also contributes to the
incidence of liver cancer in many parts of the world. Tobacco use is the most serious
preventable cause of cancer, as its use causes cancer of the lung, throat, mouth, liver,
pancreas, urinary bladder, stomach, kidney, as well as other types. Alcohol-induced liver
injury is another major risk factor for hepatocellular carcinoma (HCC).
In view of these devastating statistics, the urgency of deciphering the molecular mechanism
underlying this disease, perfecting reliable diagnostic methods, understanding
risk factors, developing effective targeted drugs, improving other treatments, assessing
the effectiveness of therapies, and providing improved care for post-treatment patients,
becomes apparent. This volume provides up-to-date information on the above-mentioned
aspects of liver cancer; specifically, details of the methodologies used are included. The
other seven volumes in this series provide similar information on other types of cancers.
This series of handbooks has taken the unique approach of discussing cancer diagnosis,
treatment, and prognosis in the same volume. It is pointed out that this vast subject
cannot be fully discussed by only one author. This is the primary reason for inviting a
large number of oncologists/clinicians/surgeons to write each of the eight volumes of
this series of handbooks. Another advantage of involving more than one author is to
present different points of view on a specific controversial aspect of cancer. I hope these
goals were accomplished in this and other published volumes of this series.

M.A. Hayat

This book serves as a tribute to the work of the many investigators who have
attempted to understand the role of the androgen receptor (AR) in the development
and progression of prostate cancer. The relationship between prostate cancer and
androgen status was initially appreciated in the late 1800s, and then awareness
reawakened in the 1940s (Huggins and Hodges 2002) by the studies of Charles
Huggins and colleagues, for which the Nobel prize was awarded in 1966. Androgen
deprivation therapy by surgical or medical means using methods that remove the
source of testicular androgens or inhibit the production of testicular androgens,
respectively, produced remission in most, but not all, men. Moreover, clinical
studies have cast doubt on whether ‘‘combined androgen blockade’’ (Labrie et al.
1982) is any more effective than androgen deprivation monotherapy (Prostate
Cancer Trialists’ Collaborative Group, 1995), except when an antiandrogen is
used to block testosterone flair in men with bulky metastatic disease. Nonetheless,
responses to androgen deprivation therapy vary widely. In order to explain this
clinical variation, it was proposed initially that prostate cancer consists of ‘‘androgen-
dependent’’ and ‘‘androgen-independent’’ cells (Carter and Isaacs 1988; Isaacs
and Coffey 1981). The argument went as follows:
The relative distribution of prostate cancer cells between these two phenotypes determine
whether there is a clinical response to androgen deprivation therapy and the duration of any
response. If the tumor consists of androgen-dependent cells entirely, androgen deprivation
therapy would prove curative since all androgen-dependent cells would undergo apoptosis
upon androgen deprivation. If a prostate cancer is composed exclusively of androgenindependent
cells, then no clinical response to androgen deprivation therapy would occur
and that patient would ‘‘resist’’ androgen deprivation therapy and succumb to his prostate
cancer as if androgen deprivation therapy had never been administered. Almost, if not,
all patients fall between these two extremes and exhibit clinical remissions, which may be
complete and sustained if the androgen-dependent cells far outnumber the androgenindependent
cells. Because apoptosis does not occur in as high a proportion of cells as
predicted, a third phenotype of prostate cancer cell was proposed, the androgen-sensitive
cell (Pollack et al. 1983; Grossman 1986). The ‘‘androgen-sensitive’’ cell is responsive to
androgen deprivation therapy by becoming quiescent until such time that androgens
become available. Thus, the extent of regression of prostate cancer after androgen
deprivation therapy is influenced by the relative proportion of androgen-dependent,
androgen-sensitive and androgen-independent cells. The eventual emergence of the
‘‘androgen-independent phenotype’’ is predicted by the proportion of androgen-independent
cells.

James L. Mohler and Donald J. Tindall

Cancer Treatment and Research: Coagulation in Cancer, 1st Edition
By David Green, Hau C. Kwaan

* Publisher: Springer
* Number Of Pages: 320
* Publication Date: 2009-04-24
* ISBN-10 / ASIN: 0387799613
* ISBN-13 / EAN: 9780387799612
* Binding: Hardcover
* Format: PDF

Steven T. Rosen, M.D., Series Editor
Editors
David Green, MD, PhD
Professor of Medicine Emeritus
Division of Hematology/Oncology
Feinberg School of Medicine
Northwestern University
Chicago, Illinois 60611-2927
USA

In a series of updated reviews, the contributors to this book describe the effects of cancer on coagulation and coagulation on cancer. In the first chapter, Monroe and Hoffman present
their current concept of hemostasis, with an emphasis on the cell-based mechanism they recently delineated
The treatment of the cancer patient presents certain challenges not present
in patients without malignancies. These include the risk of bleeding due to chemotherapy-induced thrombocytopenia, recurrent and refractory venous thromboembolism, and concerns about maintaining the quality of life of patients with advanced disease. In the final chapter of this section, there is an examination of the effects of anticoagulants on cancer.
The final section of the book discusses bleeding problems in cancer, beginning with a review of cancer-associated thrombocytopenia by Eklund. A diagnostic algorithm for assessing thrombocytopenia in the cancer patient is presented, and the use of platelet transfusions for patients with decreased platelet production, as proposed by the American Society of Clinical Oncology