PubTransformer

A site to transform Pubmed publications into these bibliographic reference formats: ADS, BibTeX, EndNote, ISI used by the Web of Knowledge, RIS, MEDLINE, Microsoft's Word 2007 XML.

bFGF Polymorphism Is Associated with Disease Progression and Response to Chemotherapy in Multiple Myeloma Patients.

Abstract Vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) play an important role in the initiation of angiogenesis. We aimed to assess whether polymorphisms within the genes coding for these angiogenic activators (VEGF (rs3025039;C>T) and bFGF (rs308395;G>C)) contribute to susceptibility and/or progression in multiple myeloma patients (MM) and to chemotherapy.
PMID
Related Publications

Angiogenic factors in multiple myeloma: higher levels in bone marrow than in peripheral blood.

Polymorphisms within beta-catenin encoding gene affect multiple myeloma development and treatment.

Serum levels of the angiogenic cytokines basic fibroblast growth factor (bFGF), vascular endothelial growth factor (VEGF) and hepatocyte growth factor (HGF) in multiple myeloma.

VEGF and bFGF gene polymorphisms in Polish patients with B-CLL.

VEGF and bFGF gene polymorphisms in patients with non-Hodgkin's lymphoma.

Authors

Mayor MeshTerms
Keywords

VEGF gene polymorphism

bFGF gene polymorphism

disease susceptibility

multiple myeloma

response to immunomodulating therapy

Journal Title anticancer research
Publication Year Start




PMID- 28373444
OWN - NLM
STAT- MEDLINE
DA  - 20170404
DCOM- 20170413
LR  - 20170413
IS  - 1791-7530 (Electronic)
IS  - 0250-7005 (Linking)
VI  - 37
IP  - 4
DP  - 2017 Apr
TI  - bFGF Polymorphism Is Associated with Disease Progression and Response to
      Chemotherapy in Multiple Myeloma Patients.
PG  - 1799-1803
AB  - BACKGROUND/AIM: Vascular endothelial growth factor (VEGF) and basic fibroblast
      growth factor (bFGF) play an important role in the initiation of angiogenesis. We
      aimed to assess whether polymorphisms within the genes coding for these
      angiogenic activators (VEGF (rs3025039;C>T) and bFGF (rs308395;G>C)) contribute
      to susceptibility and/or progression in multiple myeloma patients (MM) and to
      chemotherapy. PATIENTS AND METHODS: One hundred and thirty-two patients with MM
      and 122 controls were genotyped for the VEGF and bFGF alleles by the PCR-RFLP
      technique. Genotyping results were compared regarding progression, risk of
      disease and response to treatment. RESULTS: Patients in stage I-II disease
      (Durie-Salmon criteria) more frequently carried the bFGF -921G allele compared to
      patients in stage III (p=0.053) and healthy controls (OR=2.010, p=0.040).
      Progression after first-line chemotherapy was more frequent among patients
      carrying this variant (p=0.022). CONCLUSION: Our results imply that the course of
      disease in MM patients is associated with a polymorphism within the bFGF gene.
CI  - Copyright(c) 2017, International Institute of Anticancer Research (Dr. George J. 
      Delinasios), All rights reserved.
FAU - Wrobel, Tomasz
AU  - Wrobel T
AD  - Department of Haematology, Blood Neoplasms and Bone Marrow Transplantation,
      Wroclaw Medical University, Wroclaw, Poland.
FAU - Butrym, Aleksandra
AU  - Butrym A
AD  - Department of Physiology, Wroclaw Medical University, Wroclaw, Poland.
FAU - Lacina, Piotr
AU  - Lacina P
AD  - Laboratory of Clinical Immunogenetics and Pharmacogenetics, Hirszfeld Institute
      of Immunology and Experimental Therapy, Polish Academy of Sciences, Wroclaw,
      Poland.
FAU - Rybka, Justyna
AU  - Rybka J
AD  - Department of Haematology, Blood Neoplasms and Bone Marrow Transplantation,
      Wroclaw Medical University, Wroclaw, Poland.
FAU - Gebura, Katarzyna
AU  - Gebura K
AD  - Laboratory of Clinical Immunogenetics and Pharmacogenetics, Hirszfeld Institute
      of Immunology and Experimental Therapy, Polish Academy of Sciences, Wroclaw,
      Poland.
FAU - Mazur, Grzegorz
AU  - Mazur G
AD  - Department and Clinic of Internal and Occupational Diseases, Hypertension and
      Clinical Oncology, Wroclaw Medical University, Wroclaw, Poland.
FAU - Bogunia-Kubik, Katarzyna
AU  - Bogunia-Kubik K
AD  - Laboratory of Clinical Immunogenetics and Pharmacogenetics, Hirszfeld Institute
      of Immunology and Experimental Therapy, Polish Academy of Sciences, Wroclaw,
      Poland [email protected]
AD  - Department and Clinic of Internal and Occupational Diseases, Hypertension and
      Clinical Oncology, Wroclaw Medical University, Wroclaw, Poland.
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PL  - Greece
TA  - Anticancer Res
JT  - Anticancer research
JID - 8102988
RN  - 0 (Biomarkers, Tumor)
RN  - 0 (VEGFA protein, human)
RN  - 0 (Vascular Endothelial Growth Factor A)
RN  - 103107-01-3 (Fibroblast Growth Factor 2)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Antineoplastic Combined Chemotherapy Protocols/*therapeutic use
MH  - Biomarkers, Tumor/*genetics
MH  - Case-Control Studies
MH  - Disease Progression
MH  - Female
MH  - Fibroblast Growth Factor 2/*genetics
MH  - Follow-Up Studies
MH  - Genotype
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Multiple Myeloma/drug therapy/*genetics/pathology
MH  - Neoplasm Staging
MH  - Polymerase Chain Reaction
MH  - Polymorphism, Restriction Fragment Length
MH  - Polymorphism, Single Nucleotide/*genetics
MH  - Prognosis
MH  - Vascular Endothelial Growth Factor A/genetics
OTO - NOTNLM
OT  - *VEGF gene polymorphism
OT  - *bFGF gene polymorphism
OT  - *disease susceptibility
OT  - *multiple myeloma
OT  - *response to immunomodulating therapy
EDAT- 2017/04/05 06:00
MHDA- 2017/04/14 06:00
CRDT- 2017/04/05 06:00
PHST- 2016/12/19 [received]
PHST- 2017/03/08 [revised]
PHST- 2017/03/09 [accepted]
AID - 37/4/1799 [pii]
AID - 10.21873/anticanres.11514 [doi]
PST - ppublish
SO  - Anticancer Res. 2017 Apr;37(4):1799-1803.

<?xml version="1.0" encoding="UTF-8"?>
<b:Sources SelectedStyle="" xmlns:b="http://schemas.openxmlformats.org/officeDocument/2006/bibliography"  xmlns="http://schemas.openxmlformats.org/officeDocument/2006/bibliography" >
</b:Sources>