PMID- 20337574
OWN - NLM
STAT- MEDLINE
DCOM- 20110124
LR  - 20211020
IS  - 1873-4286 (Electronic)
IS  - 1381-6128 (Print)
IS  - 1381-6128 (Linking)
VI  - 16
IP  - 16
DP  - 2010 Jun
TI  - The natural tumor suppressor protein maspin and potential application in non 
      small cell lung cancer.
PG  - 1877-81
AB  - The grim prognosis of lung cancer, that has an overall 10-15% survival at 5 
      years, remains in the US the leading cause of cancer mortality, provides a 
      compelling rationale for studying the molecular basis of this malignancy. 
      Surmising the common, general association with smoking, lung cancers differ at 
      the microscopic, anatomical, epidemiological and clinical level and harbor 
      complex genetic and epigenetic alterations. Currently, lung cancer is divided 
      into small cell lung carcinoma (SCLC) and non small cell lung carcinoma (NSCLC) 
      for the purpose of clinical management. (NSCLC) constitutes 80-85% of lung 
      cancers and is further divided into histological subtypes such as adenocarcinoma, 
      squamous cell carcinoma, and large cell carcinoma, etc. The ultimate goal for 
      lung cancer research is to develop a strategy to block the tumor progression and 
      improve the prognosis of lung cancer. This goal can realistically be achieved 
      only when the biological complexity of this disease is taken into account. To 
      this end, identification and understanding of molecular markers that are 
      mechanistically involved in tumor progression is needed. Our recent studies 
      suggest histological subtype-dependent distinct correlations between the 
      expression and/or subcellular localization of tumor suppressive maspin with the 
      progression and prognosis of NSCLC. Maspin is an epithelial specific member of 
      the serine protease inhibitor (serpin) superfamily but recently identified as an 
      endogenous inhibitor of histone deacetylase 1 (HDAC1). This novel biochemical 
      activity coincides with a consensus emerged recently from the evidence that 
      nuclear maspin confers better differentiated epithelial phenotypes, decreased 
      tumor angiogenesis, increased tumor sensitivity to drug-induced apoptosis, and a 
      more favorable prognosis. In the current review, we discuss the evidence that 
      maspin may be a marker that stratifies the progression and prognosis of different 
      subtypes of NSCLC.
FAU - Lonardo, Fulvio
AU  - Lonardo F
AD  - Department of Pathology, Wayne State University School of Medicine, Barbara Ann 
      Karmanos Cancer Institute, Detroit, MI 48201, USA.
FAU - Li, Xiaohua
AU  - Li X
FAU - Kaplun, Alexander
AU  - Kaplun A
FAU - Soubani, Ayman
AU  - Soubani A
FAU - Sethi, Seema
AU  - Sethi S
FAU - Gadgeel, Shirish
AU  - Gadgeel S
FAU - Sheng, Shijie
AU  - Sheng S
LA  - eng
GR  - CA084176/CA/NCI NIH HHS/United States
GR  - CA127735/CA/NCI NIH HHS/United States
GR  - R01 CA127735/CA/NCI NIH HHS/United States
GR  - R01 CA084176-07/CA/NCI NIH HHS/United States
GR  - R01 CA084176/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Review
PL  - United Arab Emirates
TA  - Curr Pharm Des
JT  - Current pharmaceutical design
JID - 9602487
RN  - 0 (Antineoplastic Agents)
RN  - 0 (Biomarkers, Tumor)
RN  - 0 (Histone Deacetylase Inhibitors)
RN  - 0 (SERPIN-B5)
RN  - 0 (Serpins)
RN  - EC 3.5.1.98 (Histone Deacetylase 1)
SB  - IM
MH  - Animals
MH  - Antineoplastic Agents/*chemistry/metabolism/pharmacology
MH  - Biomarkers, Tumor/chemistry/*metabolism
MH  - Carcinoma, Non-Small-Cell Lung/diagnosis/drug therapy/*metabolism/physiopathology
MH  - Disease Progression
MH  - Drug Design
MH  - Histone Deacetylase 1/antagonists & inhibitors/chemistry/metabolism
MH  - Histone Deacetylase Inhibitors/*chemistry/metabolism/pharmacology
MH  - Humans
MH  - Lung Neoplasms/diagnosis/drug therapy/*metabolism/physiopathology
MH  - Prognosis
MH  - Protein Transport
MH  - Serpins/*chemistry/*metabolism
PMC - PMC2908495
MID - NIHMS218467
EDAT- 2010/03/27 06:00
MHDA- 2011/01/25 06:00
PMCR- 2010/07/22
CRDT- 2010/03/27 06:00
PHST- 2010/03/13 00:00 [received]
PHST- 2010/03/22 00:00 [accepted]
PHST- 2010/03/27 06:00 [entrez]
PHST- 2010/03/27 06:00 [pubmed]
PHST- 2011/01/25 06:00 [medline]
PHST- 2010/07/22 00:00 [pmc-release]
AID - BSP/CPD/E-Pub/00074 [pii]
AID - 10.2174/138161210791208974 [doi]
PST - ppublish
SO  - Curr Pharm Des. 2010 Jun;16(16):1877-81. doi: 10.2174/138161210791208974.