PMID- 30679158
OWN - NLM
STAT- MEDLINE
DCOM- 20190415
LR  - 20190415
IS  - 1756-1833 (Electronic)
IS  - 0959-8138 (Linking)
VI  - 364
DP  - 2019 Jan 24
TI  - Seven days in medicine: 16-22 January 2019.
PG  - l320
LID - 10.1136/bmj.l320 [doi]
LA  - eng
PT  - Journal Article
DEP - 20190124
PL  - England
TA  - BMJ
JT  - BMJ (Clinical research ed.)
JID - 8900488
SB  - AIM
SB  - IM
MH  - Humans
MH  - Leukemia, Lymphocytic, Chronic, B-Cell/*drug therapy/economics
MH  - Medicine/*standards
MH  - Melanoma/*drug therapy/genetics
MH  - National Health Programs/organization & administration
MH  - Sexual and Gender Minorities/statistics & numerical data
MH  - Surgery, Plastic/legislation & jurisprudence
MH  - Time Factors
MH  - United Kingdom/epidemiology
MH  - World Health Organization/organization & administration
EDAT- 2019/01/27 06:00
MHDA- 2019/04/16 06:00
CRDT- 2019/01/26 06:00
PHST- 2019/01/26 06:00 [entrez]
PHST- 2019/01/27 06:00 [pubmed]
PHST- 2019/04/16 06:00 [medline]
AID - 10.1136/bmj.l320 [doi]
PST - epublish
SO  - BMJ. 2019 Jan 24;364:l320. doi: 10.1136/bmj.l320.

PMID- 30987999
OWN - NLM
STAT- In-Data-Review
LR  - 20190610
IS  - 1538-7445 (Electronic)
IS  - 0008-5472 (Linking)
VI  - 79
IP  - 11
DP  - 2019 Jun 1
TI  - HDAC8 Regulates a Stress Response Pathway in Melanoma to Mediate Escape from BRAF
      Inhibitor Therapy.
PG  - 2947-2961
LID - 10.1158/0008-5472.CAN-19-0040 [doi]
AB  - Melanoma cells have the ability to switch to a dedifferentiated, invasive
      phenotype in response to multiple stimuli. Here, we show that exposure of
      melanomas to multiple stresses including BRAF-MEK inhibitor therapy, hypoxia, and
      UV irradiation leads to an increase in histone deacetylase 8 (HDAC8) activity and
      the adoption of a drug-resistant phenotype. Mass spectrometry-based
      phosphoproteomics implicated HDAC8 in the regulation of MAPK and AP-1 signaling. 
      Introduction of HDAC8 into drug-naive melanoma cells conveyed resistance both in 
      vitro and in vivo. HDAC8-mediated BRAF inhibitor resistance was mediated via
      receptor tyrosine kinase activation, leading to MAPK signaling. Although HDACs
      function at the histone level, they also regulate nonhistone substrates, and
      introduction of HDAC8 decreased the acetylation of c-Jun, increasing its
      transcriptional activity and enriching for an AP-1 gene signature. Mutation of
      the putative c-Jun acetylation site at lysine 273 increased transcriptional
      activation of c-Jun in melanoma cells and conveyed resistance to BRAF inhibition.
      In vivo xenograft studies confirmed the key role of HDAC8 in therapeutic
      adaptation, with both nonselective and HDAC8-specific inhibitors enhancing the
      durability of BRAF inhibitor therapy. Our studies demonstrate that HDAC8-specific
      inhibitors limit the adaptation of melanoma cells to multiple stresses including 
      BRAF-MEK inhibition. SIGNIFICANCE: This study provides evidence that HDAC8 drives
      transcriptional plasticity in melanoma cells in response to a range of stresses
      through direct deacetylation of c-Jun.Graphical Abstract:
      http://cancerres.aacrjournals.org/content/canres/79/11/2947/F1.large.jpg.
CI  - (c)2019 American Association for Cancer Research.
FAU - Emmons, Michael F
AU  - Emmons MF
AD  - The Department of Tumor Biology, The Moffitt Cancer Center and Research
      Institute, Tampa, Florida.
FAU - Faiao-Flores, Fernanda
AU  - Faiao-Flores F
AD  - The Department of Tumor Biology, The Moffitt Cancer Center and Research
      Institute, Tampa, Florida.
FAU - Sharma, Ritin
AU  - Sharma R
AUID- ORCID: https://orcid.org/0000-0001-8365-9916
AD  - The Department of Molecular Oncology, The Moffitt Cancer Center and Research
      Institute, Tampa, Florida.
FAU - Thapa, Ram
AU  - Thapa R
AD  - Department of Bioinformatics and Biostatistics, The Moffitt Cancer Center and
      Research Institute, Tampa, Florida.
FAU - Messina, Jane L
AU  - Messina JL
AUID- ORCID: https://orcid.org/0000-0002-0332-0224
AD  - The Department of Cutaneous Oncology, The Moffitt Cancer Center and Research
      Institute, Tampa, Florida.
FAU - Becker, Jurgen C
AU  - Becker JC
AUID- ORCID: https://orcid.org/0000-0001-9183-653X
AD  - Department of Translational Skin Cancer Research, German Cancer Consortium
      (DKTK), University Hospital Essen, Essen, Germany.
FAU - Schadendorf, Dirk
AU  - Schadendorf D
AUID- ORCID: https://orcid.org/0000-0003-3524-7858
AD  - Department of Translational Skin Cancer Research, German Cancer Consortium
      (DKTK), University Hospital Essen, Essen, Germany.
FAU - Seto, Edward
AU  - Seto E
AD  - George Washington University, Washington, D.C.
FAU - Sondak, Vernon K
AU  - Sondak VK
AD  - The Department of Cutaneous Oncology, The Moffitt Cancer Center and Research
      Institute, Tampa, Florida.
FAU - Koomen, John M
AU  - Koomen JM
AUID- ORCID: https://orcid.org/0000-0002-3818-1762
AD  - The Department of Molecular Oncology, The Moffitt Cancer Center and Research
      Institute, Tampa, Florida.
FAU - Chen, Yian A
AU  - Chen YA
AD  - Department of Bioinformatics and Biostatistics, The Moffitt Cancer Center and
      Research Institute, Tampa, Florida.
FAU - Lau, Eric K
AU  - Lau EK
AD  - The Department of Tumor Biology, The Moffitt Cancer Center and Research
      Institute, Tampa, Florida.
AD  - The Department of Cutaneous Oncology, The Moffitt Cancer Center and Research
      Institute, Tampa, Florida.
FAU - Wan, Lixin
AU  - Wan L
AD  - The Department of Molecular Oncology, The Moffitt Cancer Center and Research
      Institute, Tampa, Florida.
FAU - Licht, Jonathan D
AU  - Licht JD
AUID- ORCID: https://orcid.org/0000-0002-3942-1369
AD  - The University of Florida Health Cancer Center, Gainesville, Florida.
FAU - Smalley, Keiran S M
AU  - Smalley KSM
AD  - The Department of Tumor Biology, The Moffitt Cancer Center and Research
      Institute, Tampa, Florida. keiran.smalley@moffitt.org.
AD  - The Department of Cutaneous Oncology, The Moffitt Cancer Center and Research
      Institute, Tampa, Florida.
LA  - eng
GR  - P30 CA076292/CA/NCI NIH HHS/United States
GR  - P50 CA168536/CA/NCI NIH HHS/United States
GR  - R21 CA198550/CA/NCI NIH HHS/United States
GR  - R21 CA216756/CA/NCI NIH HHS/United States
PT  - Journal Article
DEP - 20190415
PL  - United States
TA  - Cancer Res
JT  - Cancer research
JID - 2984705R
PMC - PMC6548652
MID - NIHMS1527336
EDAT- 2019/04/17 06:00
MHDA- 2019/04/17 06:00
CRDT- 2019/04/17 06:00
PMCR- 2020/06/01 00:00
PHST- 2019/01/03 00:00 [received]
PHST- 2019/03/01 00:00 [revised]
PHST- 2019/04/10 00:00 [accepted]
PHST- 2020/06/01 00:00 [pmc-release]
PHST- 2019/04/17 06:00 [pubmed]
PHST- 2019/04/17 06:00 [medline]
PHST- 2019/04/17 06:00 [entrez]
AID - 0008-5472.CAN-19-0040 [pii]
AID - 10.1158/0008-5472.CAN-19-0040 [doi]
PST - ppublish
SO  - Cancer Res. 2019 Jun 1;79(11):2947-2961. doi: 10.1158/0008-5472.CAN-19-0040. Epub
      2019 Apr 15.

PMID- 30987979
OWN - NLM
STAT- In-Data-Review
LR  - 20190419
IS  - 1538-7445 (Electronic)
IS  - 0008-5472 (Linking)
VI  - 79
IP  - 8
DP  - 2019 Apr 15
TI  - Concurrent Targeting of Glutaminolysis and Metabotropic Glutamate Receptor 1
      (GRM1) Reduces Glutamate Bioavailability in GRM1(+) Melanoma.
PG  - 1799-1809
LID - 10.1158/0008-5472.CAN-18-1500 [doi]
AB  - Aberrant glutamatergic signaling has been implicated in altered metabolic
      activity in many cancer types, including malignant melanoma. Previously, we have 
      illustrated the role of metabotropic glutamate receptor 1 (GRM1) in neoplastic
      transformation of melanocytes in vitro and spontaneous metastatic melanoma in
      vivo. In this study, we showed that autocrine stimulation constitutively
      activates the GRM1 receptor and its downstream mitogenic signaling.
      GRM1-activated (GRM1(+)) melanomas exhibited significantly increased expression
      of glutaminase (GLS), which catalyzes the first step in the conversion of
      glutamine to glutamate. In cultured GRM1(+) melanoma cell lines, CB-839, a
      potent, selective, and orally bioavailable inhibitor of GLS, suppressed cell
      proliferation, while riluzole, an inhibitor of glutamate release, promoted
      apoptotic cell death in vitro and in vivo. Combined treatment with CB-839 and
      riluzole treatment proved to be superior to single-agent treatment, restricting
      glutamate bioavailability and leading to effective suppression of tumor cell
      proliferation in vitro and tumor progression in vivo. Hyperactivation of GRM1 in 
      malignant melanoma is an oncogenic driver, which acts independently of canonical 
      melanoma proto-oncogenes, BRAF or NRAS. Overall, these results indicate that
      expression of GRM1 promotes a metabolic phenotype that supports increased
      glutamate production and autocrine glutamatergic signaling, which can be
      pharmacologically targeted by decreasing glutamate bioavailability and the
      GLS-dependent glutamine to glutamate conversion. SIGNIFICANCE: These findings
      demonstrate that targeting glutaminolytic glutamate bioavailability is an
      effective therapeutic strategy for GRM1-activated tumors.
CI  - (c)2019 American Association for Cancer Research.
FAU - Shah, Raj
AU  - Shah R
AD  - Susan Lehman Cullman Laboratory for Cancer Research, Ernest Mario School of
      Pharmacy, Department of Chemical Biology, Rutgers University, Piscataway, New
      Jersey.
AD  - Joint Graduate Program in Toxicology, Rutgers University, Piscataway, New Jersey.
FAU - Singh, Simar J
AU  - Singh SJ
AD  - St. George's University, School of Medicine, Grenada, West Indies.
FAU - Eddy, Kevinn
AU  - Eddy K
AD  - Susan Lehman Cullman Laboratory for Cancer Research, Ernest Mario School of
      Pharmacy, Department of Chemical Biology, Rutgers University, Piscataway, New
      Jersey.
FAU - Filipp, Fabian V
AU  - Filipp FV
AUID- ORCID: https://orcid.org/0000-0001-9889-5727
AD  - Cancer Systems Biology, Institute of Computational Biology, Helmholtz Zentrum
      Munchen, Munchen, Germany. suziec@pharmacy.rutgers.edu
      fabian.filipp@helmholtz-muenchen.de.
AD  - School of Life Sciences Weihenstephan, Technical University Munchen, Freising,
      Germany.
FAU - Chen, Suzie
AU  - Chen S
AD  - Susan Lehman Cullman Laboratory for Cancer Research, Ernest Mario School of
      Pharmacy, Department of Chemical Biology, Rutgers University, Piscataway, New
      Jersey. suziec@pharmacy.rutgers.edu fabian.filipp@helmholtz-muenchen.de.
AD  - Joint Graduate Program in Toxicology, Rutgers University, Piscataway, New Jersey.
AD  - Rutgers Cancer Institute of New Jersey, New Brunswick, New Jersey.
LA  - eng
GR  - I01 BX003742/BX/BLRD VA/United States
GR  - T32 ES007148/ES/NIEHS NIH HHS/United States
GR  - K99 CA154887/CA/NCI NIH HHS/United States
GR  - R25 GM115293/GM/NIGMS NIH HHS/United States
GR  - R00 CA154887/CA/NCI NIH HHS/United States
PT  - Journal Article
DEP - 20190415
PL  - United States
TA  - Cancer Res
JT  - Cancer research
JID - 2984705R
PMC - PMC6469683
MID - NIHMS1522822
EDAT- 2019/04/17 06:00
MHDA- 2019/04/17 06:00
CRDT- 2019/04/17 06:00
PMCR- 2020/04/15 00:00
PHST- 2018/05/15 00:00 [received]
PHST- 2018/12/15 00:00 [revised]
PHST- 2019/02/21 00:00 [accepted]
PHST- 2020/04/15 00:00 [pmc-release]
PHST- 2019/04/17 06:00 [entrez]
PHST- 2019/04/17 06:00 [pubmed]
PHST- 2019/04/17 06:00 [medline]
AID - 79/8/1799 [pii]
AID - 10.1158/0008-5472.CAN-18-1500 [doi]
PST - ppublish
SO  - Cancer Res. 2019 Apr 15;79(8):1799-1809. doi: 10.1158/0008-5472.CAN-18-1500. Epub
      2019 Apr 15.

PMID- 30992297
OWN - NLM
STAT- Publisher
LR  - 20190604
IS  - 1078-0432 (Print)
IS  - 1078-0432 (Linking)
DP  - 2019 Apr 16
TI  - Developments in the Space of New MAPK Pathway Inhibitors for BRAF-Mutant
      Melanoma.
LID - 10.1158/1078-0432.CCR-18-0836 [doi]
AB  - The characterization of the MAPK signaling pathway has led to the development of 
      multiple promising targeted therapy options for a subset of patients with
      metastatic melanoma. The combination of BRAF and MEK inhibitors represents an
      FDA-approved standard of care in patients with metastatic and resected
      BRAF-mutated melanoma. There are currently three FDA-approved BRAF/MEK inhibitor 
      combinations for the treatment of patients with BRAF-mutated melanoma. Although
      there have been significant advances in the field of targeted therapy, further
      exploration of new targets within the MAPK pathway will strengthen therapeutic
      options for patients. Important clinical and translational research focuses on
      mechanisms of resistance, predictive biomarkers, and challenging patient
      populations such as those with brain metastases or resected melanoma.
CI  - (c)2019 American Association for Cancer Research.
FAU - Cohen, Justine V
AU  - Cohen JV
AD  - Division of Medical Oncology, Department of Medicine, Massachusetts General
      Hospital Cancer Center, Center for Melanoma, Harvard Medical School, Boston,
      Massachusetts.
FAU - Sullivan, Ryan J
AU  - Sullivan RJ
AD  - Division of Medical Oncology, Department of Medicine, Massachusetts General
      Hospital Cancer Center, Center for Melanoma, Harvard Medical School, Boston,
      Massachusetts. rsullivan7@mgh.harvard.edu.
LA  - eng
GR  - R01 CA193970/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Review
DEP - 20190416
PL  - United States
TA  - Clin Cancer Res
JT  - Clinical cancer research : an official journal of the American Association for
      Cancer Research
JID - 9502500
EDAT- 2019/04/18 06:00
MHDA- 2019/04/18 06:00
CRDT- 2019/04/18 06:00
PHST- 2018/10/01 00:00 [received]
PHST- 2019/01/28 00:00 [revised]
PHST- 2019/04/12 00:00 [accepted]
PHST- 2019/04/18 06:00 [pubmed]
PHST- 2019/04/18 06:00 [medline]
PHST- 2019/04/18 06:00 [entrez]
AID - 1078-0432.CCR-18-0836 [pii]
AID - 10.1158/1078-0432.CCR-18-0836 [doi]
PST - aheadofprint
SO  - Clin Cancer Res. 2019 Apr 16. pii: 1078-0432.CCR-18-0836. doi:
      10.1158/1078-0432.CCR-18-0836.

PMID- 30998207
OWN - NLM
STAT- In-Process
LR  - 20190509
IS  - 1952-4013 (Electronic)
IS  - 1167-1122 (Linking)
VI  - 29
IP  - 1
DP  - 2019 Feb 1
TI  - Erythema multiforme-like rash upon anti-melanoma therapy with BRAF and MEK
      inhibitors.
PG  - 107-108
LID - 10.1684/ejd.2019.3511 [doi]
FAU - Gran, Franziska
AU  - Gran F
AD  - Department of Dermatology, Venereology and Allergology, University Hospital
      Wurzburg, Wurzburg, Germany.
FAU - Goebeler, Matthias
AU  - Goebeler M
AD  - Department of Dermatology, Venereology and Allergology, University Hospital
      Wurzburg, Wurzburg, Germany.
FAU - Gesierich, Anja
AU  - Gesierich A
AD  - Department of Dermatology, Venereology and Allergology, University Hospital
      Wurzburg, Wurzburg, Germany.
LA  - eng
PT  - Journal Article
PL  - France
TA  - Eur J Dermatol
JT  - European journal of dermatology : EJD
JID - 9206420
EDAT- 2019/04/19 06:00
MHDA- 2019/04/19 06:00
CRDT- 2019/04/19 06:00
PHST- 2019/04/19 06:00 [entrez]
PHST- 2019/04/19 06:00 [pubmed]
PHST- 2019/04/19 06:00 [medline]
AID - ejd.2019.3511 [pii]
AID - 10.1684/ejd.2019.3511 [doi]
PST - ppublish
SO  - Eur J Dermatol. 2019 Feb 1;29(1):107-108. doi: 10.1684/ejd.2019.3511.

PMID- 30986476
OWN - NLM
STAT- Publisher
LR  - 20190426
IS  - 1097-6787 (Electronic)
IS  - 0190-9622 (Linking)
DP  - 2019 Apr 12
TI  - Patient satisfaction with patient-provider interactions at time of diagnosis
      among early stage melanoma survivors - a cross-sectional survey.
LID - S0190-9622(19)30600-0 [pii]
LID - 10.1016/j.jaad.2019.04.014 [doi]
FAU - Zaffran, Kailey
AU  - Zaffran K
AD  - Division of Epidemiology and Community Health, School of Public Health,
      University of Minnesota, Minneapolis, MN, USA.
FAU - Lazovich, DeAnn
AU  - Lazovich D
AD  - Division of Epidemiology and Community Health, School of Public Health,
      University of Minnesota, Minneapolis, MN, USA; Masonic Cancer Center, University 
      of Minnesota, Minneapolis, MN, USA.
FAU - Boull, Christina
AU  - Boull C
AD  - Department of Dermatology, Medical School, University of Minnesota, Minneapolis, 
      MN, USA.
FAU - Vogel, Rachel I
AU  - Vogel RI
AD  - Masonic Cancer Center, University of Minnesota, Minneapolis, MN, USA; Division of
      Gynecologic Oncology, Department of Obstetrics, Gynecology and Women's Health,
      Medical School, University of Minnesota, Minneapolis, MN, USA. Electronic
      address: isak0023@umn.edu.
LA  - eng
GR  - P30 CA077598/CA/NCI NIH HHS/United States
GR  - UL1 TR000114/TR/NCATS NIH HHS/United States
PT  - Journal Article
DEP - 20190412
PL  - United States
TA  - J Am Acad Dermatol
JT  - Journal of the American Academy of Dermatology
JID - 7907132
EDAT- 2019/04/16 06:00
MHDA- 2019/04/16 06:00
CRDT- 2019/04/16 06:00
PHST- 2019/02/13 00:00 [received]
PHST- 2019/03/29 00:00 [revised]
PHST- 2019/04/02 00:00 [accepted]
PHST- 2019/04/16 06:00 [entrez]
PHST- 2019/04/16 06:00 [pubmed]
PHST- 2019/04/16 06:00 [medline]
AID - S0190-9622(19)30600-0 [pii]
AID - 10.1016/j.jaad.2019.04.014 [doi]
PST - aheadofprint
SO  - J Am Acad Dermatol. 2019 Apr 12. pii: S0190-9622(19)30600-0. doi:
      10.1016/j.jaad.2019.04.014.

PMID- 30985445
OWN - NLM
STAT- In-Data-Review
LR  - 20190612
IS  - 1537-4513 (Electronic)
IS  - 1524-9557 (Linking)
VI  - 42
IP  - 6
DP  - 2019 Jul/Aug
TI  - Racial and Socioeconomic Disparities in the Delivery of Immunotherapy for
      Metastatic Melanoma in the United States.
PG  - 228-235
LID - 10.1097/CJI.0000000000000264 [doi]
AB  - Immunotherapy for metastatic melanoma has rapidly expanded, but racial and/or
      socioeconomic factors often impact the type of therapies delivered for cancer
      care. This study addressed a crucial public health priority by evaluating
      disparities in administration of immunotherapy for metastatic melanoma. The
      National Cancer Database was queried for newly diagnosed metastatic melanoma.
      Patients were dichotomized based on receipt of immunotherapy based on National
      Cancer Database coding. Multivariable logistic regression ascertained factors
      associated with immunotherapy delivery. Subgroup analysis evaluated the
      interaction between race, insurance status, and income. Secondarily, Cox
      multivariate and propensity-matched Kaplan-Meier analyses assessed overall
      survival based on immunotherapy receipt. Of 15,941 patients meeting the selection
      criteria, 2448 (15.4%) received immunotherapy, and 13,493 (84.6%) did not.
      Temporal trends showed that utilization of immunotherapy was 8%-12% of patients
      between 2004 and 2010, with utilization increasing to 29.7% of patients in 2014. 
      Immunotherapy was more likely administered to younger and healthier patients, at 
      academic centers, and in the absence of chemotherapy and brain metastases (P<0.05
      for all). African Americans, along with patients with Medicaid and lower incomes 
      were less likely to receive immunotherapy (P<0.05 for all). As expected,
      immunotherapy was associated with improved overall survival (median 16.3 vs. 8.3 
      mo, P<0.001). Although immunotherapy for metastatic melanoma is markedly
      escalating, not all populations experience this rise equally. Because
      immunotherapy utilization is expected to amplify even further in the future,
      these public health and economic issues are essential to identify and address
      appropriately, and have implications on public health policy, pharmaceutical and 
      insurance companies, and value-based oncology. Methods to address these
      inequalities are also discussed.
FAU - Haque, Waqar
AU  - Haque W
AD  - Departments of Radiation Oncology, Houston Methodist Hospital, Houston, TX.
FAU - Verma, Vivek
AU  - Verma V
AD  - Radiation Oncology, Allegheny General Hospital, Pittsburgh, PA.
FAU - Butler, Edward Brian
AU  - Butler EB
AD  - Departments of Radiation Oncology, Houston Methodist Hospital, Houston, TX.
FAU - Teh, Bin S
AU  - Teh BS
AD  - Departments of Radiation Oncology, Houston Methodist Hospital, Houston, TX.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Immunother
JT  - Journal of immunotherapy (Hagerstown, Md. : 1997)
JID - 9706083
EDAT- 2019/04/16 06:00
MHDA- 2019/04/16 06:00
CRDT- 2019/04/16 06:00
PHST- 2019/04/16 06:00 [pubmed]
PHST- 2019/04/16 06:00 [medline]
PHST- 2019/04/16 06:00 [entrez]
AID - 10.1097/CJI.0000000000000264 [doi]
PST - ppublish
SO  - J Immunother. 2019 Jul/Aug;42(6):228-235. doi: 10.1097/CJI.0000000000000264.

PMID- 30943338
OWN - NLM
STAT- MEDLINE
DCOM- 20190419
LR  - 20190419
IS  - 1533-4406 (Electronic)
IS  - 0028-4793 (Linking)
VI  - 380
IP  - 14
DP  - 2019 Apr 4
TI  - Machine Learning in Medicine.
PG  - 1347-1358
LID - 10.1056/NEJMra1814259 [doi]
FAU - Rajkomar, Alvin
AU  - Rajkomar A
AUID- ORCID: 0000-0001-5750-5016
AD  - From Google, Mountain View, CA (A.R., J.D.); and the Department of Biomedical
      Informatics, Harvard Medical School, Boston (I.K.).
FAU - Dean, Jeffrey
AU  - Dean J
AD  - From Google, Mountain View, CA (A.R., J.D.); and the Department of Biomedical
      Informatics, Harvard Medical School, Boston (I.K.).
FAU - Kohane, Isaac
AU  - Kohane I
AD  - From Google, Mountain View, CA (A.R., J.D.); and the Department of Biomedical
      Informatics, Harvard Medical School, Boston (I.K.).
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - N Engl J Med
JT  - The New England journal of medicine
JID - 0255562
SB  - AIM
SB  - IM
MH  - *Decision Making, Computer-Assisted
MH  - Humans
MH  - *Machine Learning
MH  - Male
MH  - *Medical Informatics
MH  - Medical Records Systems, Computerized
MH  - Melanoma/diagnosis
MH  - Middle Aged
MH  - Skin Neoplasms/diagnosis
MH  - Workflow
EDAT- 2019/04/04 06:00
MHDA- 2019/04/20 06:00
CRDT- 2019/04/04 06:00
PHST- 2019/04/04 06:00 [entrez]
PHST- 2019/04/04 06:00 [pubmed]
PHST- 2019/04/20 06:00 [medline]
AID - 10.1056/NEJMra1814259 [doi]
PST - ppublish
SO  - N Engl J Med. 2019 Apr 4;380(14):1347-1358. doi: 10.1056/NEJMra1814259.

PMID- 30995246
OWN - NLM
STAT- In-Data-Review
LR  - 20190505
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 14
IP  - 4
DP  - 2019
TI  - Critical role of miR-10b in B-RafV600E dependent anchorage independent growth and
      invasion of melanoma cells.
PG  - e0204387
LID - 10.1371/journal.pone.0204387 [doi]
AB  - Recent high-throughput-sequencing of cancer genomes has identified oncogenic
      mutations in the B-Raf genetic locus as one of the critical events in
      melanomagenesis. B-Raf encodes a serine/threonine kinase that regulates the
      MAPK/ERK kinase (MEK) and extracellular signal-regulated kinase (ERK) protein
      kinase cascade. In normal cells, the activity of B-Raf is tightly regulated and
      is required for cell growth and survival. B-Raf gain-of-function mutations in
      melanoma frequently lead to unrestrained growth, enhanced cell invasion and
      increased viability of cancer cells. Although it is clear that the invasive
      phenotypes of B-Raf mutated melanoma cells are stringently dependent on
      B-Raf-MEK-ERK activation, the downstream effector targets that are required for
      oncogenic B-Raf-mediated melanomagenesis are not well defined. miRNAs have
      regulatory functions towards the expression of genes that are important in
      carcinogenesis. We observed that miR-10b expression correlates with the presence 
      of the oncogenic B-Raf (B-RafV600E) mutation in melanoma cells. While expression 
      of miR-10b enhances anchorage-independent growth of B-Raf wild-type melanoma
      cells, miR-10b silencing decreases B-RafV600E cancer cell invasion in vitro.
      Importantly, the expression of miR-10b is required for B-RafV600E-mediated
      anchorage independent growth and invasion of melanoma cells in vitro. Taken
      together our results suggest that miR-10b is an important mediator of oncogenic
      B-RafV600E activity in melanoma.
FAU - Datar, Ila
AU  - Datar I
AD  - Case Comprehensive Cancer Center, Case Western Reserve University, Cleveland, OH,
      United States of America.
FAU - Kalpana, Gardiyawasam
AU  - Kalpana G
AD  - Department of Cancer Biology, College of Medicine and Life Sciences, University
      of Toledo, Health Science Campus, Toledo, OH, United States of America.
FAU - Choi, Jungmin
AU  - Choi J
AD  - Department of Genetics, Yale School of Medicine, New Haven, CT, United States of 
      America.
FAU - Basuroy, Tupa
AU  - Basuroy T
AD  - Department of Cancer Biology, College of Medicine and Life Sciences, University
      of Toledo, Health Science Campus, Toledo, OH, United States of America.
FAU - Trumbly, Robert
AU  - Trumbly R
AD  - Department of Cancer Biology, College of Medicine and Life Sciences, University
      of Toledo, Health Science Campus, Toledo, OH, United States of America.
FAU - Chaitanya Arudra, Sri Krishna
AU  - Chaitanya Arudra SK
AD  - Department of Pathology, Sanford Hospital, Bismarck, ND, United States of
      America.
FAU - McPhee, Michael D
AU  - McPhee MD
AD  - ProMedica Cancer Institute, Toledo, OH, United States of America.
FAU - de la Serna, Ivana
AU  - de la Serna I
AD  - Department of Cancer Biology, College of Medicine and Life Sciences, University
      of Toledo, Health Science Campus, Toledo, OH, United States of America.
FAU - Yeung, Kam C
AU  - Yeung KC
AUID- ORCID: http://orcid.org/0000-0002-1415-484X
AD  - Department of Cancer Biology, College of Medicine and Life Sciences, University
      of Toledo, Health Science Campus, Toledo, OH, United States of America.
LA  - eng
PT  - Journal Article
DEP - 20190417
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
PMC - PMC6469749
COIS- The authors have declared that no competing interests exist.
EDAT- 2019/04/18 06:00
MHDA- 2019/04/18 06:00
CRDT- 2019/04/18 06:00
PHST- 2018/09/05 00:00 [received]
PHST- 2019/03/19 00:00 [accepted]
PHST- 2019/04/18 06:00 [entrez]
PHST- 2019/04/18 06:00 [pubmed]
PHST- 2019/04/18 06:00 [medline]
AID - 10.1371/journal.pone.0204387 [doi]
AID - PONE-D-18-26080 [pii]
PST - epublish
SO  - PLoS One. 2019 Apr 17;14(4):e0204387. doi: 10.1371/journal.pone.0204387.
      eCollection 2019.