Comprehensive Review
The “Emigration, Migration, and Immigration” of Prostate Cancer

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Abstract

In the vast majority of cases, cancer continues to be an incurable disease when it has spread beyond the primary organ. Most cancer research and therapy design to date has focused on chemotherapy directed at killing the replicating tumor cells. Little attention has been placed on targeting the microenvironments of the primary tumor site, the circulating tumor cells, or the metastatic or secondary (target) tumor site and how cancer cells move among them. To develop these targets, a better understanding of metastasis and the mechanisms underlying the spread of tumors is required. This review describes the steps of metastasis using a paradigm of emigration to migration to immigration, with prostate cancer as a model system.

References (91)

  • CH Chay et al.

    A functional thrombin receptor (PAR1) is expressed on bone-derived prostate cancer cell lines

    Urology

    (2002)
  • M Jakobisiak et al.

    Natural mechanisms protecting against cancer

    Immunol Lett

    (2003)
  • A Zlotnik et al.

    Chemokines: a new classification system and their role in immunity

    Immunity

    (2000)
  • S Karmakar et al.

    Integrin receptors and ECM proteins involved in preferential adhesion of colon carcinoma cells to lung cells

    Cancer Lett

    (2003)
  • P Nangia-Makker et al.

    Carbohydrate-binding proteins in cancer, and their ligands as therapeutic agents

    Trends Mol Med

    (2002)
  • SK Khaldoyanidi et al.

    MDA-MB-435 human breast carcinoma cell homo- and heterotypic adhesion under flow conditions is mediated in part by Thomsen-Friedenreich antigen-galectin-3 interactions

    J Biol Chem

    (2003)
  • PV Hauschka et al.

    Growth factors in bone matrix. Isolation of multiple types by affinity chromatography on heparin- Sepharose

    J Biol Chem

    (1986)
  • C Woodham-Smith

    The Great Hunger: Ireland, 1845-1849

    (1995)
  • J Ewing

    Metastasis

  • IJ Fidler

    The pathogenesis of cancer metastasis: the ‘seed and soil’ hypothesis revisited

    Nat Rev Cancer

    (2003)
  • PH Sugarbaker

    Metastatic inefficiency: The scientific basis for resection of liver metastases from colorectal cancer

    J Surg Oncol

    (1993)
  • LM Kalikin et al.

    In vivo visualization of metastatic prostate cancer and quantitation of disease progression in immunocompromised mice

    Cancer Biol Ther

    (2003)
  • TJ Rosol et al.

    Animal models of bone metastasis

    Cancer

    (2003)
  • HJ Varghese et al.

    Activated ras regulates the proliferation/apoptosis balance and early survival of developing micrometastases

    Cancer Res

    (2002)
  • GN Naumov et al.

    Persistence of solitary mammary carcinoma cells in a secondary site: a possible contributor to dormancy

    Cancer Res

    (2002)
  • MD Cameron et al.

    Temporal progression of metastasis in lung: cell survival, dormancy, and location dependence of metastatic inefficiency

    Cancer Res

    (2000)
  • D Glaves et al.

    Haematogenous dissemination of cells from human renal adenocarcinomas

    Br J Cancer

    (1988)
  • L Norton

    A Gompertzian model of human breast cancer growth

    Cancer Res

    (1988)
  • J Folkman

    Toward an understanding of angiogenesis: search and discovery

    Perspect Biol Med

    (1985)
  • LT Furcht

    Critical factors controlling angiogenesis: cell products, cell matrix, and growth factors

    Lab Invest

    (1986)
  • R Pardal et al.

    Applying the principles of stem-cell biology to cancer

    Nat Rev Cancer

    (2003)
  • IK Park et al.

    BMI1, stem cells, and senescence regulation

    J Clin Invest

    (2004)
  • LA Liotta et al.

    The microenvironment of the tumour-host interface

    Nature

    (2001)
  • MJ Bissell et al.

    Putting tumors in context

    Nat Rev Cancer

    (2001)
  • J Grego-Bessa et al.

    Notch and epithelial- mesenchyme transition in development and tumor progression: another turn of the screw

    Cell Cycle

    (2004)
  • T Pralhad et al.

    Concept, mechanisms and therapeutics of angiogenesis in cancer and other diseases

    J Pharm Pharmacol

    (2003)
  • I Stamenkovic

    Extracellular matrix remodelling: the role of matrix metalloproteinases

    J Pathol

    (2003)
  • SJ Welsh et al.

    Hypoxia inducible factor as a cancer drug target

    Curr Cancer Drug Targets

    (2003)
  • A Giaccia et al.

    HIF-1 as a target for drug development

    Nat Rev Drug Discov

    (2003)
  • GL Semenza

    Targeting HIF-1 for cancer therapy

    Nat Rev Cancer

    (2003)
  • S Stacker et al.

    The role of tumor lymphangiogenesis in metastatic spread

    FASEB J

    (2002)
  • MJ Hendrix et al.

    Vasculogenic mimicry and tumour-cell plasticity: lessons from melanoma

    Nat Rev Cancer

    (2003)
  • N Sharma et al.

    Prostatic tumor cell plasticity involves cooperative interactions of distinct phenotypic subpopulations: role in vasculogenic mimicry

    Prostate

    (2002)
  • L Weiss

    Biomechanical destruction of cancer cells in the heart: a rate regulator for hematogenous metastasis

    Invasion Metastasis

    (1988)
  • L Weiss et al.

    Mechanism of mechanical trauma to Ehrlich ascites tumor cells in vitro and its relationship to rapid intravascular death during metastasis

    Int J Cancer

    (1989)

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