Prognostic markers for bladder cancer: International Consensus Panel on bladder tumor markers. 2005

Tomonori Habuchi, and Michael Marberger, and Michael J Droller, and George P Hemstreet, and H Barton Grossman, and Jack A Schalken, and Bernd J Schmitz-Dräger, and William M Murphy, and Aldo V Bono, and Peter Goebell, and Robert H Getzenberg, and Stefan H Hautmann, and Edward Messing, and Yves Fradet, and Vinata B Lokeshwar
Department of Urology, Kyoto University, Kyoto, Japan.

The International Consensus Panel on cytology and bladder tumor markers evaluated markers that have the ability to predict tumor recurrence, progression, development of metastases, or response to therapy or patient survival. This article summarizes those findings. The panel mainly reviewed articles listed in PubMed on various prognostic indicators for bladder cancer. Based on these studies, most of which were case-control retrospective studies, various prognostic indicators were classified into 6 groups: (1) microsatellite-associated markers, (2) proto-oncogenes/oncogenes, (3) tumor suppressor genes, (4) cell cycle regulators, (5) angiogenesis-related factors, and (6) extracellular matrix adhesion molecules. The panel concluded that although certain markers, such as Ki-67 and p53, appear to be promising in predicting recurrence and progression of bladder cancer, the data are still heterogeneous. The panel recommends that identifying definitive criteria for test positivity, a clearly defined patient population, standardization of techniques used to evaluate markers, and clearly specified endpoints and statistical methods will help to bring accurate independent prognostic indicators into the clinical management of patients with bladder cancer.

UI MeSH Term Description Entries
D009857 Oncogenes Genes whose gain-of-function alterations lead to NEOPLASTIC CELL TRANSFORMATION. They include, for example, genes for activators or stimulators of CELL PROLIFERATION such as growth factors, growth factor receptors, protein kinases, signal transducers, nuclear phosphoproteins, and transcription factors. A prefix of "v-" before oncogene symbols indicates oncogenes captured and transmitted by RETROVIRUSES; the prefix "c-" before the gene symbol of an oncogene indicates it is the cellular homolog (PROTO-ONCOGENES) of a v-oncogene. Transforming Genes,Oncogene,Transforming Gene,Gene, Transforming,Genes, Transforming
D001749 Urinary Bladder Neoplasms Tumors or cancer of the URINARY BLADDER. Bladder Cancer,Bladder Neoplasms,Cancer of Bladder,Bladder Tumors,Cancer of the Bladder,Malignant Tumor of Urinary Bladder,Neoplasms, Bladder,Urinary Bladder Cancer,Bladder Cancers,Bladder Neoplasm,Bladder Tumor,Cancer, Bladder,Cancer, Urinary Bladder,Neoplasm, Bladder,Neoplasm, Urinary Bladder,Tumor, Bladder,Tumors, Bladder,Urinary Bladder Neoplasm
D002869 Chromosome Aberrations Abnormal number or structure of chromosomes. Chromosome aberrations may result in CHROMOSOME DISORDERS. Autosome Abnormalities,Cytogenetic Aberrations,Abnormalities, Autosome,Abnormalities, Chromosomal,Abnormalities, Chromosome,Chromosomal Aberrations,Chromosome Abnormalities,Cytogenetic Abnormalities,Aberration, Chromosomal,Aberration, Chromosome,Aberration, Cytogenetic,Aberrations, Chromosomal,Aberrations, Chromosome,Aberrations, Cytogenetic,Abnormalities, Cytogenetic,Abnormality, Autosome,Abnormality, Chromosomal,Abnormality, Chromosome,Abnormality, Cytogenetic,Autosome Abnormality,Chromosomal Aberration,Chromosomal Abnormalities,Chromosomal Abnormality,Chromosome Aberration,Chromosome Abnormality,Cytogenetic Aberration,Cytogenetic Abnormality
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D016147 Genes, Tumor Suppressor Genes that inhibit expression of the tumorigenic phenotype. They are normally involved in holding cellular growth in check. When tumor suppressor genes are inactivated or lost, a barrier to normal proliferation is removed and unregulated growth is possible. Antioncogenes,Cancer Suppressor Genes,Emerogenes,Genes, Cancer Suppressor,Genes, Growth Suppressor,Genes, Metastasis Suppressor,Growth Suppressor Genes,Metastasis Suppressor Genes,Tumor Suppressor Genes,Anti-Oncogenes,Genes, Onco-Suppressor,Oncogenes, Recessive,Tumor Suppressing Genes,Anti Oncogenes,Anti-Oncogene,Antioncogene,Cancer Suppressor Gene,Emerogene,Gene, Cancer Suppressor,Gene, Growth Suppressor,Gene, Metastasis Suppressor,Gene, Onco-Suppressor,Gene, Tumor Suppressing,Gene, Tumor Suppressor,Genes, Onco Suppressor,Genes, Tumor Suppressing,Growth Suppressor Gene,Metastasis Suppressor Gene,Onco-Suppressor Gene,Onco-Suppressor Genes,Oncogene, Recessive,Recessive Oncogene,Recessive Oncogenes,Suppressor Gene, Cancer,Suppressor Gene, Growth,Suppressor Gene, Metastasis,Suppressor Genes, Cancer,Suppressor Genes, Growth,Suppressor Genes, Metastasis,Tumor Suppressing Gene,Tumor Suppressor Gene
D042501 Angiogenic Proteins Intercellular signaling peptides and proteins that regulate the proliferation of new blood vessels under normal physiological conditions (ANGIOGENESIS, PHYSIOLOGICAL). Aberrant expression of angiogenic proteins during disease states such as tumorigenesis can also result in PATHOLOGICAL ANGIOGENESIS. Angiogenic Peptide,Angiogenic Protein,Angiogenic Peptides,Peptide, Angiogenic,Protein, Angiogenic
D018797 Cell Cycle Proteins Proteins that control the CELL DIVISION CYCLE. This family of proteins includes a wide variety of classes, including CYCLIN-DEPENDENT KINASES, mitogen-activated kinases, CYCLINS, and PHOSPHOPROTEIN PHOSPHATASES as well as their putative substrates such as chromatin-associated proteins, CYTOSKELETAL PROTEINS, and TRANSCRIPTION FACTORS. Cell Division Cycle Proteins,Cell-Cycle Regulatory Proteins,cdc Proteins,Cell Cycle Regulatory Proteins
D019656 Loss of Heterozygosity The loss of one allele at a specific locus, caused by a deletion mutation; or loss of a chromosome from a chromosome pair, resulting in abnormal HEMIZYGOSITY. It is detected when heterozygous markers for a locus appear monomorphic because one of the ALLELES was deleted. Allelic Loss,Heterozygosity, Loss of,Allelic Losses,Heterozygosity Loss

Related Publications

Tomonori Habuchi, and Michael Marberger, and Michael J Droller, and George P Hemstreet, and H Barton Grossman, and Jack A Schalken, and Bernd J Schmitz-Dräger, and William M Murphy, and Aldo V Bono, and Peter Goebell, and Robert H Getzenberg, and Stefan H Hautmann, and Edward Messing, and Yves Fradet, and Vinata B Lokeshwar
September 2006, Aktuelle Urologie,
Tomonori Habuchi, and Michael Marberger, and Michael J Droller, and George P Hemstreet, and H Barton Grossman, and Jack A Schalken, and Bernd J Schmitz-Dräger, and William M Murphy, and Aldo V Bono, and Peter Goebell, and Robert H Getzenberg, and Stefan H Hautmann, and Edward Messing, and Yves Fradet, and Vinata B Lokeshwar
March 1990, Der Urologe. Ausg. A,
Tomonori Habuchi, and Michael Marberger, and Michael J Droller, and George P Hemstreet, and H Barton Grossman, and Jack A Schalken, and Bernd J Schmitz-Dräger, and William M Murphy, and Aldo V Bono, and Peter Goebell, and Robert H Getzenberg, and Stefan H Hautmann, and Edward Messing, and Yves Fradet, and Vinata B Lokeshwar
September 2000, Urologic oncology,
Tomonori Habuchi, and Michael Marberger, and Michael J Droller, and George P Hemstreet, and H Barton Grossman, and Jack A Schalken, and Bernd J Schmitz-Dräger, and William M Murphy, and Aldo V Bono, and Peter Goebell, and Robert H Getzenberg, and Stefan H Hautmann, and Edward Messing, and Yves Fradet, and Vinata B Lokeshwar
May 2021, Urologic oncology,
Tomonori Habuchi, and Michael Marberger, and Michael J Droller, and George P Hemstreet, and H Barton Grossman, and Jack A Schalken, and Bernd J Schmitz-Dräger, and William M Murphy, and Aldo V Bono, and Peter Goebell, and Robert H Getzenberg, and Stefan H Hautmann, and Edward Messing, and Yves Fradet, and Vinata B Lokeshwar
December 2005, Urology,
Tomonori Habuchi, and Michael Marberger, and Michael J Droller, and George P Hemstreet, and H Barton Grossman, and Jack A Schalken, and Bernd J Schmitz-Dräger, and William M Murphy, and Aldo V Bono, and Peter Goebell, and Robert H Getzenberg, and Stefan H Hautmann, and Edward Messing, and Yves Fradet, and Vinata B Lokeshwar
April 2003, Seminars in oncology,
Tomonori Habuchi, and Michael Marberger, and Michael J Droller, and George P Hemstreet, and H Barton Grossman, and Jack A Schalken, and Bernd J Schmitz-Dräger, and William M Murphy, and Aldo V Bono, and Peter Goebell, and Robert H Getzenberg, and Stefan H Hautmann, and Edward Messing, and Yves Fradet, and Vinata B Lokeshwar
January 1992, Journal of insurance medicine (New York, N.Y.),
Tomonori Habuchi, and Michael Marberger, and Michael J Droller, and George P Hemstreet, and H Barton Grossman, and Jack A Schalken, and Bernd J Schmitz-Dräger, and William M Murphy, and Aldo V Bono, and Peter Goebell, and Robert H Getzenberg, and Stefan H Hautmann, and Edward Messing, and Yves Fradet, and Vinata B Lokeshwar
March 2011, Annals of oncology : official journal of the European Society for Medical Oncology,
Tomonori Habuchi, and Michael Marberger, and Michael J Droller, and George P Hemstreet, and H Barton Grossman, and Jack A Schalken, and Bernd J Schmitz-Dräger, and William M Murphy, and Aldo V Bono, and Peter Goebell, and Robert H Getzenberg, and Stefan H Hautmann, and Edward Messing, and Yves Fradet, and Vinata B Lokeshwar
January 2002, Journal of B.U.ON. : official journal of the Balkan Union of Oncology,
Tomonori Habuchi, and Michael Marberger, and Michael J Droller, and George P Hemstreet, and H Barton Grossman, and Jack A Schalken, and Bernd J Schmitz-Dräger, and William M Murphy, and Aldo V Bono, and Peter Goebell, and Robert H Getzenberg, and Stefan H Hautmann, and Edward Messing, and Yves Fradet, and Vinata B Lokeshwar
May 2019, Scientific reports,
Copied contents to your clipboard!