PMID- 22679120
OWN - NLM
STAT- MEDLINE
DCOM- 20121031
LR  - 20211203
IS  - 1540-1413 (Electronic)
IS  - 1540-1405 (Linking)
VI  - 10
IP  - 6
DP  - 2012 Jun 1
TI  - Systemic therapy for advanced carcinoid tumors: where do we go from here?
PG  - 785-93
AB  - Carcinoid tumors are relatively indolent, but the treatment of advanced disease 
      remains a challenge. Liver-directed therapies are a consideration in patients 
      with liver-dominant disease. Somatostatin analogs (SSTa) are routinely used to 
      control hormone-mediated symptoms (carcinoid syndrome), but the identification of 
      systemic agents with antitumor efficacy has proven difficult. Aside from 
      octreotide for small bowel carcinoid (which is associated with delayed 
      progression), no treatment has proven antitumor activity. Chemotherapy seems to 
      be of limited value. The role of interferon is also controversial; it is 
      typically used after failure of octreotide. Peptide receptor radionuclide therapy 
      may have activity in patients with SST receptor-expressing tumors, but randomized 
      controlled trials are lacking. Advances in the understanding of the mechanisms 
      underlying tumor progression have led to the identification of several potential 
      therapeutic targets (including the vascular endothelial growth factor [VEGF] and 
      mammalian target of rapamycin [mTOR] signaling pathways), but none has been 
      definitively validated in carcinoid. Everolimus is associated with a trend toward 
      improved progression-free survival in patients with progressive carcinoid, but is 
      not approved for this indication. Therefore, a serious unmet need remains for 
      additional therapeutic strategies for patients with advanced disease. Several 
      avenues are under study, including the use of novel SSTa; VEGF and mTOR 
      inhibitors; and agents that interfere with insulin growth factor 1 receptor and 
      AKT signaling. Moving forward, optimizing patient selection based on clinical 
      features or biomarkers holds promise for identifying individuals most likely to 
      benefit from therapy.
FAU - Paulson, A Scott
AU  - Paulson AS
AD  - University of California, San Francisco, UCSF Helen Diller Family Comprehensive 
      Cancer Center, San Francisco, CA 94115, USA.
FAU - Bergsland, Emily K
AU  - Bergsland EK
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - J Natl Compr Canc Netw
JT  - Journal of the National Comprehensive Cancer Network : JNCCN
JID - 101162515
RN  - 0 (Protein Kinase Inhibitors)
RN  - 0 (Vascular Endothelial Growth Factor A)
RN  - 51110-01-1 (Somatostatin)
RN  - 9008-11-1 (Interferons)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
MH  - Antineoplastic Combined Chemotherapy Protocols/therapeutic use
MH  - Carcinoid Tumor/*drug therapy/*pathology
MH  - Humans
MH  - Interferons/therapeutic use
MH  - Neoplasm Staging
MH  - Protein Kinase Inhibitors/therapeutic use
MH  - Somatostatin/analogs & derivatives/therapeutic use
MH  - TOR Serine-Threonine Kinases/antagonists & inhibitors
MH  - Vascular Endothelial Growth Factor A/antagonists & inhibitors
EDAT- 2012/06/09 06:00
MHDA- 2012/11/01 06:00
CRDT- 2012/06/09 06:00
PHST- 2012/06/09 06:00 [entrez]
PHST- 2012/06/09 06:00 [pubmed]
PHST- 2012/11/01 06:00 [medline]
AID - 10/6/785 [pii]
AID - 10.6004/jnccn.2012.0078 [doi]
PST - ppublish
SO  - J Natl Compr Canc Netw. 2012 Jun 1;10(6):785-93. doi: 10.6004/jnccn.2012.0078.