PMID- 24595969
OWN - NLM
STAT- MEDLINE
DCOM- 20150923
LR  - 20220408
IS  - 1097-0347 (Electronic)
IS  - 1043-3074 (Linking)
VI  - 37
IP  - 2
DP  - 2015 Feb
TI  - Molecular profiling in primary hyperparathyroidism.
PG  - 299-307
LID - 10.1002/hed.23656 [doi]
AB  - Primary hyperparathyroidism (HPT) is one of the most common endocrine disorders, 
      defined by hypersecretion of parathormone. Primary HPT can be caused by adenoma, 
      hyperplasia, and carcinoma. A great amount of mechanisms contribute to the 
      pathogenesis of this disease, such as genetic predispositions because of the 
      germline-inactivating mutations in the multiple endocrine neoplasia type 1 (MEN1) 
      and HRPT2 tumor suppressor genes. Somatic mutations in these genes were found 
      also in sporadic parathyroid neoplasias. Cell cycle regulators, growth factors, 
      apoptosis-inducing ligands, death receptors, and other transmitter substances 
      have also been implicated in the etiology of primary HPT. Parathyroid carcinoma 
      is often misdiagnosed as parathyroid adenoma and long-term survival is 
      conditioned by the extent of the primary surgical resection, therefore, of great 
      interest is the discovery of definitive diagnostic markers for carcinoma. This 
      article presents current state of knowledge of the molecular pathogenesis of 
      primary HPT.
CI  - (c) 2014 Wiley Periodicals, Inc.
FAU - Segiet, Oliwia Anna
AU  - Segiet OA
AD  - Department of Histology and Embryology, Zabrze, Medical University of Silesia, 
      Katowice, Poland.
FAU - Deska, Mariusz
AU  - Deska M
FAU - Michalski, Marek
AU  - Michalski M
FAU - Gawrychowski, Jacek
AU  - Gawrychowski J
FAU - Wojnicz, Romuald
AU  - Wojnicz R
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20140502
PL  - United States
TA  - Head Neck
JT  - Head & neck
JID - 8902541
RN  - 0 (CASR protein, human)
RN  - 0 (CDC73 protein, human)
RN  - 0 (Cell Cycle Proteins)
RN  - 0 (Intercellular Signaling Peptides and Proteins)
RN  - 0 (MEN1 protein, human)
RN  - 0 (Proto-Oncogene Proteins)
RN  - 0 (Receptors, Calcium-Sensing)
RN  - 0 (Tumor Suppressor Proteins)
RN  - EC 2.7.10.1 (Proto-Oncogene Proteins c-ret)
RN  - EC 2.7.10.1 (RET protein, human)
SB  - IM
MH  - Apoptosis
MH  - Cell Cycle Proteins/metabolism
MH  - Comparative Genomic Hybridization
MH  - Genetic Predisposition to Disease
MH  - Humans
MH  - Hyperparathyroidism, Primary/*genetics/metabolism
MH  - Intercellular Signaling Peptides and Proteins/metabolism
MH  - Loss of Heterozygosity
MH  - Multiple Endocrine Neoplasia Type 1/metabolism
MH  - Multiple Endocrine Neoplasia Type 2a/metabolism
MH  - Mutation
MH  - Proto-Oncogene Proteins/genetics
MH  - Proto-Oncogene Proteins c-ret/genetics
MH  - Receptors, Calcium-Sensing/genetics
MH  - Tumor Suppressor Proteins/genetics
OTO - NOTNLM
OT  - diagnostic markers
OT  - molecular pathogenesis
OT  - parathyroid adenoma
OT  - parathyroid carcinoma
OT  - primary hyperparathyroidism
EDAT- 2014/03/07 06:00
MHDA- 2015/09/24 06:00
CRDT- 2014/03/06 06:00
PHST- 2014/03/01 00:00 [accepted]
PHST- 2014/03/06 06:00 [entrez]
PHST- 2014/03/07 06:00 [pubmed]
PHST- 2015/09/24 06:00 [medline]
AID - 10.1002/hed.23656 [doi]
PST - ppublish
SO  - Head Neck. 2015 Feb;37(2):299-307. doi: 10.1002/hed.23656. Epub 2014 May 2.