PMID- 26288396
OWN - NLM
STAT- MEDLINE
DCOM- 20160817
LR  - 20220408
IS  - 1543-2165 (Electronic)
IS  - 0003-9985 (Linking)
VI  - 140
IP  - 4
DP  - 2016 Apr
TI  - New Markers for Separating Benign From Malignant Mesothelial Proliferations: Are 
      We There Yet?
PG  - 318-21
LID - 10.5858/arpa.2015-0240-SA [doi]
AB  - CONTEXT: The separation of benign from malignant mesothelial proliferations is 
      crucial to patient care but is frequently morphologically difficult. OBJECTIVE: 
      To briefly review adjunctive tests claimed to be useful in this setting and to 
      examine in detail 2 new tests: p16 fluorescence in situ hybridization (FISH) and 
      BRCA1-associated protein 1 (BAP1) immunohistochemistry. DESIGN: Literature review 
      with emphasis on p16 FISH and BAP1 immunohistochemistry. RESULTS: Glucose 
      transporter-1, p53, insulin-like growth factor 2 messenger RNA-binding protein 3 
      (IMP-3), desmin, and epithelial membrane antigen have all been claimed to mark 
      either benign or malignant mesothelial processes, but in practice they at best 
      provide statistical differences in large series of cases, without being useful in 
      an individual case. Homozygous deletion of p16 by FISH or loss of BAP1 has only 
      been reported in malignant mesotheliomas and not in benign mesothelial 
      proliferations. BAP1 appears to be lost more frequently in epithelial than mixed 
      or sarcomatous mesotheliomas. Homozygous deletion of p16 by FISH is seen in 
      pleural epithelial, mixed, and sarcomatous mesotheliomas, but it is much less 
      frequent in peritoneal mesothelioma. The major drawback to both these tests is 
      limited sensitivity; moreover, failure to find p16 deletion or BAP1 loss does not 
      make a mesothelial process benign. CONCLUSIONS: In the context of a mesothelial 
      proliferation, the finding of homozygous deletion of p16 by FISH or loss of BAP1 
      by immunohistochemistry is, thus far, 100% specific for malignant mesothelioma. 
      The limited sensitivity of each test may be improved to some extent by running 
      both tests.
FAU - Churg, Andrew
AU  - Churg A
FAU - Sheffield, Brandon S
AU  - Sheffield BS
FAU - Galateau-Salle, Francoise
AU  - Galateau-Salle F
AD  - From the Department of Pathology, Vancouver General Hospital and University of 
      British Columbia, Vancouver, British Columbia, Canada (Drs Churg and Sheffield); 
      and Service Anatomie Pathologique, Centre National Referent MESOPATH, CHU du 
      Caen, Caen, France (Dr Galateau-Salle). Dr Galateau-Salle is now with the 
      Department of Pathology, Centre Leon Berard, Lyon, France.
LA  - eng
PT  - Journal Article
DEP - 20150819
PL  - United States
TA  - Arch Pathol Lab Med
JT  - Archives of pathology & laboratory medicine
JID - 7607091
RN  - 0 (BAP1 protein, human)
RN  - 0 (Biomarkers, Tumor)
RN  - 0 (CDKN2A protein, human)
RN  - 0 (Cyclin-Dependent Kinase Inhibitor p16)
RN  - 0 (Mucin-1)
RN  - 0 (Neoplasm Proteins)
RN  - 0 (Tumor Suppressor Proteins)
RN  - EC 3.4.19.12 (Ubiquitin Thiolesterase)
SB  - IM
MH  - Biomarkers, Tumor/*genetics/metabolism
MH  - Cell Proliferation
MH  - Cyclin-Dependent Kinase Inhibitor p16
MH  - Diagnosis, Differential
MH  - Epithelium/pathology
MH  - Female
MH  - Gene Deletion
MH  - Humans
MH  - Immunohistochemistry
MH  - In Situ Hybridization, Fluorescence
MH  - Lung Neoplasms/*pathology
MH  - Mesothelioma/*pathology
MH  - Mesothelioma, Malignant
MH  - Mucin-1/genetics/metabolism
MH  - Neoplasm Proteins/genetics/metabolism
MH  - Peritoneal Neoplasms/*pathology
MH  - Pleura/pathology
MH  - Pleural Neoplasms/*pathology
MH  - Tumor Suppressor Proteins/genetics/metabolism
MH  - Ubiquitin Thiolesterase/genetics/metabolism
EDAT- 2015/08/20 06:00
MHDA- 2016/08/18 06:00
CRDT- 2015/08/20 06:00
PHST- 2015/08/20 06:00 [entrez]
PHST- 2015/08/20 06:00 [pubmed]
PHST- 2016/08/18 06:00 [medline]
AID - 10.5858/arpa.2015-0240-SA [doi]
PST - ppublish
SO  - Arch Pathol Lab Med. 2016 Apr;140(4):318-21. doi: 10.5858/arpa.2015-0240-SA. Epub 
      2015 Aug 19.