Begell House Inc.
Critical Reviews™ in Oncogenesis
CRO
0893-9675
13
1
2007
Molecular Mechanisms of Apoptosis in Prostate Cancer
1-38
10.1615/CritRevOncog.v13.i1.10
Petra I.
Lorenzo
Department of Molecular Biosciences, University of Oslo, Postboks 1041, Blindern, 0316 Oslo, Norway
Yke J.
Arnoldussen
Department of Molecular Biosciences, University of Oslo, Postboks 1041, Blindern, 0316 Oslo, Norway
Fahri
Saatcioglu
Department of Molecular Biosciences, University of Oslo, Postboks 1041, Blindern, 0316 Oslo, Norway
Prostate cancer is the most frequently diagnosed noncutaneous cancer in men in Western countries. As in the normal prostate, the initial stages of prostate cancer progression depend on androgens that increase proliferation and inhibit apoptosis. Androgen-deprivation therapy is the major course of treatment in recurrent and metastatic prostate cancer. However, in most cases prostate cancer progresses to an apoptosis-resistant androgen-independent stage for which there is no available therapy. It is therefore important to understand the molecular mechanisms underlying prostate cancer progression, and how prostate cancer cells evade apoptotic mechanisms that give rise to their uncontrolled growth behavior. Here, we have reviewed the most important signaling pathways implicated in prostate cancer apoptosis and cell growth and how they may be deregulated during prostate cancer progression.
Aberrant Receptor Signaling and Trafficking as Mechanisms in Oncogenesis
39-74
10.1615/CritRevOncog.v13.i1.20
Tor Erik
Rusten
Centre for Cancer Biomedicine, University of Oslo, and Department of Biochemistry, Institute for Cancer Research, the Norwegian Radium Hospital, Montebello, 0310 Oslo, Norway
Kaisa
Haglund
Centre for Cancer Biomedicine, University of Oslo, and Department of Biochemistry, Institute for Cancer Research, the Norwegian Radium Hospital, Montebello, 0310 Oslo, Norway
Harald
Stenmark
Rikshospitalet-Radiumhospitalet Comprehensive Cancer Centre, University of Oslo, and Department of Biochemistry, Institute for Cancer Research, the Norwegian Radium Hospital, Montebello, 0310 Oslo, Norway
Intracellular signaling pathways activated through cell surface receptors are essential for cell proliferation, differentiation, survival, and migration. Dysregulation of such signaling through mutations, chromosome rearrangements, aberrant gene expression, or epigenetic changes is a key factor in oncogenesis. Prominent examples of receptor signaling pathways that are dysregulated in cancers include those initiated by receptor tyrosine kinases, WNT, TGFβ, and Notch receptors. In this review we will discuss these signaling pathways and how their dysfunction may contribute to oncogenesis. We will also highlight the important role of endocytic membrane trafficking in receptor signaling and tumor suppression.
Epigenetic Transgenerational Actions of Vinclozolin on the Development of Disease and Cancer
75-82
10.1615/CritRevOncog.v13.i1.30
Michael K.
Skinner
Center for Reproductive Biology, School of Molecular Biosciences, Washington State University, Pullman WA 99164-4231, USA
Matthew D.
Anway
Center for Reproductive Biology, School of Molecular Biosciences, Washington State University, Pullman WA 99164-4231, USA
Exposure to an environmental endocrine disruptor (e.g., vinclozolin) during embryonic gonadal sex determination appears to alter the male germ line epigenome and subsequently promotes transgenerational adult onset disease. The epigenetic mechanism involves the induction of new imprinted-like genes/DNA sequences in the germ line that appear to transmit disease phenotypes. The disease phenotypes include testis abnormalities, prostate disease, kidney disease, immune abnormalities, and tumor development. This epigenetic transgenerational disease mechanism provides a unique perspective from which to view inheritable adult onset disease states, such as cancer, and ultimately offers new insights into novel diagnostic and therapeutic strategies.
NEW DOCTORIAL CANCER RESEARCH:[18F] Fluoroerythronitroimidazole, Tumor Hypoxia and Positron Emission Tomography/951-29-3265-2
85-87
10.1615/CritRevOncog.v13.i1.40
Tove
Gronroos
Turku PET Centre, Department of Clinical Physiology and Nuclear Medicine and Department of Oncology and Radiotherapy, University of Turku, Turku, Finland
With the re-launch of Critical Reviews in Oncogenesis, a special section called "New Doctorial Cancer Research" is introduced. Here, we provide new Ph.Ds. with the opportunity to present themselves and their work, preferentially followed by a commentary of a senior scientist with knowledge of the study, and as such, attention is also drawn to the work of the research group. In the current issue of CRO we present six new Ph.Ds. Keep this opportunity in mind when new Ph.Ds. have fulfilled their dissertations. Instructions for submission to the "New Doctorial Cancer Research" section can be found in the general Instructions to Authors of CRO (www.begellhouse.com).
Molecular Cytogenetic Analysis of Archival and Fresh Solid Tumor Samples, 82-8072-229-7
89-92
10.1615/CritRevOncog.v13.i1.50
Petter
Brandal
Department of Cancer Genetics, Rikshospitalet-Radiumhospitalet Medical Center, Montebello, Oslo, Norway