PMID- 36889765
OWN - NLM
STAT- MEDLINE
DCOM- 20230310
LR  - 20230310
IS  - 1550-8080 (Electronic)
IS  - 0091-7370 (Linking)
VI  - 53
IP  - 1
DP  - 2023 Jan
TI  - Review: Mammalian Target of Rapamycin (mTOR) Pathway Is Critical in Developing 
      Most Renal Cell Tumors.
PG  - 3-13
AB  - OBJECTIVE: Various renal cell carcinomas (RCC) are derived from different 
      segments of the renal tubular origin, which determines their morphological and 
      immunohistochemical phenotype and their molecular signaling pathway as a 
      therapeutic target. Most of these tumors utilize the mammalian target of 
      rapamycin (mTOR) pathway to activate pathways involving metabolic and nutritional 
      supplies. METHODS: Overexpressed mTOR signals are reported in more than 90% of 
      the most common types of RCC. Many new renal tumor entities have been reported in 
      recent years. RESULTS: Among them, somatic mutations in tuberous sclerosis 
      complex (TSC) result in loss of its normal inhibitory control over mTOR, thus 
      promoting mTOR-associated proliferative activities in several new renal 
      neoplastic entities including RCC with fibromyomatous stroma (RCCFMS), 
      eosinophilic vacuolated tumor, eosinophilic solid & cystic RCC, and low-grade 
      oncocytic tumor. CONCLUSIONS: This short review provides a comprehensive 
      correlation of tumor morphology and immunohistochemical phenotype with renal 
      tubular differentiation and their shared mTOR. These essential pieces of 
      knowledge are vital in the diagnosis and clinical management of renal cell 
      neoplasms.
CI  - (c) 2023 by the Association of Clinical Scientists, Inc.
FAU - Zhang, Kevin J
AU  - Zhang KJ
AD  - Division of Hematology and Oncology, Beth Israel Deaconess Medical Center, 
      Boston, MA, USA Ping.Zhang@beaumont.edu.
FAU - Qu, Zhenhong
AU  - Qu Z
AD  - Division of Pathology, Beaumont Health, Royal Oak, MI, USA.
FAU - Pszenica, Elan
AU  - Pszenica E
AD  - William Beaumont School of Medicine, Oakland University, Rochester, MI, USA.
FAU - Hafron, Jason M
AU  - Hafron JM
AD  - Department of Urology, Beaumont Health, Royal Oak, MI, USA.
FAU - Zhang, Ping L
AU  - Zhang PL
AD  - Division of Pathology, Beaumont Health, Royal Oak, MI, USA.
FAU - Brown, Robert E
AU  - Brown RE
AD  - Department of Pathology, University of Texas Health Science Center at 
      Houston-UTHealth Medical School, Houston, TX, USA Robert.Brown@uth.tmc.edu.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Ann Clin Lab Sci
JT  - Annals of clinical and laboratory science
JID - 0410247
RN  - 0 (Tuberous Sclerosis Complex 2 Protein)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - EC 2.7.1.1 (MTOR protein, human)
SB  - IM
MH  - Humans
MH  - *Carcinoma, Renal Cell/genetics/pathology
MH  - Tuberous Sclerosis Complex 2 Protein/genetics
MH  - Mutation
MH  - *Kidney Neoplasms/pathology
MH  - TOR Serine-Threonine Kinases/metabolism
OTO - NOTNLM
OT  - mTOR
OT  - mutations
OT  - renal cell neoplasm
OT  - treatment resistance
OT  - tuberous sclerosis complex
EDAT- 2023/03/09 06:00
MHDA- 2023/03/11 06:00
CRDT- 2023/03/08 20:33
PHST- 2023/03/08 20:33 [entrez]
PHST- 2023/03/09 06:00 [pubmed]
PHST- 2023/03/11 06:00 [medline]
AID - 53/1/3 [pii]
PST - ppublish
SO  - Ann Clin Lab Sci. 2023 Jan;53(1):3-13.