Bcl-2 Expression in Oral Squamous Cell Carcinoma

:  Apoptosis is a genetically regulated process involved in tissue size regulation, morphogenesis, and elimination of genetically damaged cells. A pallet of genes is involved in the control of apoptosis, such as bcl‐2 family whose oncogenic potential has been demonstrated in oral tumorigenesis. Diff...

Full description

Saved in:
Bibliographic Details
Published inAnnals of the New York Academy of Sciences Vol. 1095; no. 1; pp. 19 - 25
Main Authors POPOVIĆ, B., JEKIĆ, B., NOVAKOVIĆ, I., LUKOVIĆ, L.J., TEPAVČEVIĆ, Z., JURIŠIĆ, V., VUKADINOVIĆ, M., MILAŠIN, J.
Format Journal Article
LanguageEnglish
Published Malden, USA Blackwell Publishing Inc 01.01.2007
Subjects
Online AccessGet full text
ISSN0077-8923
1749-6632
DOI10.1196/annals.1397.003

Cover

Abstract :  Apoptosis is a genetically regulated process involved in tissue size regulation, morphogenesis, and elimination of genetically damaged cells. A pallet of genes is involved in the control of apoptosis, such as bcl‐2 family whose oncogenic potential has been demonstrated in oral tumorigenesis. Different members of bcl‐2 family may promote or inhibit apoptosis by synthesizing anti‐ and proapoptotic proteins. One of antiapoptotic proteins, bcl‐2, with a crucial role in apoptosis regulation was the object of our study. By means of immunohistochemistry we estimated the level of overexpression of bcl‐2 proteins in a series of the 26 formalin fixed, paraffin‐embedded samples of oral squamous cell carcinoma (OSCC). Analyzed tumors originated from different sites of oral cavity; 7/26 belonged to stage II, 14/26 to stage III, and 5/26 to stage IV. Immunoreactivity was scored according to the percentage and intensity of positive cytoplasmic bcl‐2 staining. All tumors had low percentage of positively stained bcl‐2 cells, with mean values for lower/higher intensity of 8.3 ± 2.5/34.4 ± 7, 7.5 ± 1.1/31.9 ± 4.3, and 8.4 ± 5.8/31.5 ± 5.8 within stages II, III, and IV, respectively. Low level of bcl‐2 expression in our sample seems to be associated with higher survival rate: 77% for the 5‐year follow‐up period. Comparing clinicopathologic and risk factors data within each and between three groups of analyzed tumors (lip–tongue P= 0.58, tongue–floor of the mouth, P= 0.21, lip–floor of the mouth, P= 0.50) there was no significant difference. However, our results suggest that the level of bcl‐2 expression could be a valuable predictor of tumor behavior and disease outcome.
AbstractList Apoptosis is a genetically regulated process involved in tissue size regulation, morphogenesis, and elimination of genetically damaged cells. A pallet of genes is involved in the control of apoptosis, such as bcl-2 family whose oncogenic potential has been demonstrated in oral tumorigenesis. Different members of bcl-2 family may promote or inhibit apoptosis by synthesizing anti- and proapoptotic proteins. One of antiapoptotic proteins, bcl-2, with a crucial role in apoptosis regulation was the object of our study. By means of immunohistochemistry we estimated the level of overexpression of bcl-2 proteins in a series of the 26 formalin fixed, paraffin-embedded samples of oral squamous cell carcinoma (OSCC). Analyzed tumors originated from different sites of oral cavity; 7/26 belonged to stage II, 14/26 to stage III, and 5/26 to stage IV. Immunoreactivity was scored according to the percentage and intensity of positive cytoplasmic bcl-2 staining. All tumors had low percentage of positively stained bcl-2 cells, with mean values for lower/higher intensity of 8.3 +/- 2.5/34.4 +/- 7, 7.5 +/- 1.1/31.9 +/- 4.3, and 8.4 +/- 5.8/31.5 +/- 5.8 within stages II, III, and IV, respectively. Low level of bcl-2 expression in our sample seems to be associated with higher survival rate: 77% for the 5-year follow-up period. Comparing clinicopathologic and risk factors data within each and between three groups of analyzed tumors (lip-tongue P = 0.58, tongue-floor of the mouth, P = 0.21, lip-floor of the mouth, P = 0.50) there was no significant difference. However, our results suggest that the level of bcl-2 expression could be a valuable predictor of tumor behavior and disease outcome.
Apoptosis is a genetically regulated process involved in tissue size regulation, morphogenesis, and elimination of genetically damaged cells. A pallet of genes is involved in the control of apoptosis, such as bcl-2 family whose oncogenic potential has been demonstrated in oral tumorigenesis. Different members of bcl-2 family may promote or inhibit apoptosis by synthesizing anti- and proapoptotic proteins. One of antiapoptotic proteins, bcl-2, with a crucial role in apoptosis regulation was the object of our study. By means of immunohistochemistry we estimated the level of overexpression of bcl-2 proteins in a series of the 26 formalin fixed, paraffin-embedded samples of oral squamous cell carcinoma (OSCC). Analyzed tumors originated from different sites of oral cavity; 7/26 belonged to stage II, 14/26 to stage III, and 5/26 to stage IV. Immunoreactivity was scored according to the percentage and intensity of positive cytoplasmic bcl-2 staining. All tumors had low percentage of positively stained bcl-2 cells, with mean values for lower/higher intensity of 8.3 +/- 2.5/34.4 +/- 7, 7.5 +/- 1.1/31.9 +/- 4.3, and 8.4 +/- 5.8/31.5 +/- 5.8 within stages II, III, and IV, respectively. Low level of bcl-2 expression in our sample seems to be associated with higher survival rate: 77% for the 5-year follow-up period. Comparing clinicopathologic and risk factors data within each and between three groups of analyzed tumors (lip-tongue P = 0.58, tongue-floor of the mouth, P = 0.21, lip-floor of the mouth, P = 0.50) there was no significant difference. However, our results suggest that the level of bcl-2 expression could be a valuable predictor of tumor behavior and disease outcome.Apoptosis is a genetically regulated process involved in tissue size regulation, morphogenesis, and elimination of genetically damaged cells. A pallet of genes is involved in the control of apoptosis, such as bcl-2 family whose oncogenic potential has been demonstrated in oral tumorigenesis. Different members of bcl-2 family may promote or inhibit apoptosis by synthesizing anti- and proapoptotic proteins. One of antiapoptotic proteins, bcl-2, with a crucial role in apoptosis regulation was the object of our study. By means of immunohistochemistry we estimated the level of overexpression of bcl-2 proteins in a series of the 26 formalin fixed, paraffin-embedded samples of oral squamous cell carcinoma (OSCC). Analyzed tumors originated from different sites of oral cavity; 7/26 belonged to stage II, 14/26 to stage III, and 5/26 to stage IV. Immunoreactivity was scored according to the percentage and intensity of positive cytoplasmic bcl-2 staining. All tumors had low percentage of positively stained bcl-2 cells, with mean values for lower/higher intensity of 8.3 +/- 2.5/34.4 +/- 7, 7.5 +/- 1.1/31.9 +/- 4.3, and 8.4 +/- 5.8/31.5 +/- 5.8 within stages II, III, and IV, respectively. Low level of bcl-2 expression in our sample seems to be associated with higher survival rate: 77% for the 5-year follow-up period. Comparing clinicopathologic and risk factors data within each and between three groups of analyzed tumors (lip-tongue P = 0.58, tongue-floor of the mouth, P = 0.21, lip-floor of the mouth, P = 0.50) there was no significant difference. However, our results suggest that the level of bcl-2 expression could be a valuable predictor of tumor behavior and disease outcome.
Abstract :  Apoptosis is a genetically regulated process involved in tissue size regulation, morphogenesis, and elimination of genetically damaged cells. A pallet of genes is involved in the control of apoptosis, such as bcl‐2 family whose oncogenic potential has been demonstrated in oral tumorigenesis. Different members of bcl‐2 family may promote or inhibit apoptosis by synthesizing anti‐ and proapoptotic proteins. One of antiapoptotic proteins, bcl‐2, with a crucial role in apoptosis regulation was the object of our study. By means of immunohistochemistry we estimated the level of overexpression of bcl‐2 proteins in a series of the 26 formalin fixed, paraffin‐embedded samples of oral squamous cell carcinoma (OSCC). Analyzed tumors originated from different sites of oral cavity; 7/26 belonged to stage II, 14/26 to stage III, and 5/26 to stage IV. Immunoreactivity was scored according to the percentage and intensity of positive cytoplasmic bcl‐2 staining. All tumors had low percentage of positively stained bcl‐2 cells, with mean values for lower/higher intensity of 8.3 ± 2.5/34.4 ± 7, 7.5 ± 1.1/31.9 ± 4.3, and 8.4 ± 5.8/31.5 ± 5.8 within stages II, III, and IV, respectively. Low level of bcl‐2 expression in our sample seems to be associated with higher survival rate: 77% for the 5‐year follow‐up period. Comparing clinicopathologic and risk factors data within each and between three groups of analyzed tumors (lip–tongue P = 0.58, tongue–floor of the mouth, P = 0.21, lip–floor of the mouth, P = 0.50) there was no significant difference. However, our results suggest that the level of bcl‐2 expression could be a valuable predictor of tumor behavior and disease outcome.
:  Apoptosis is a genetically regulated process involved in tissue size regulation, morphogenesis, and elimination of genetically damaged cells. A pallet of genes is involved in the control of apoptosis, such as bcl‐2 family whose oncogenic potential has been demonstrated in oral tumorigenesis. Different members of bcl‐2 family may promote or inhibit apoptosis by synthesizing anti‐ and proapoptotic proteins. One of antiapoptotic proteins, bcl‐2, with a crucial role in apoptosis regulation was the object of our study. By means of immunohistochemistry we estimated the level of overexpression of bcl‐2 proteins in a series of the 26 formalin fixed, paraffin‐embedded samples of oral squamous cell carcinoma (OSCC). Analyzed tumors originated from different sites of oral cavity; 7/26 belonged to stage II, 14/26 to stage III, and 5/26 to stage IV. Immunoreactivity was scored according to the percentage and intensity of positive cytoplasmic bcl‐2 staining. All tumors had low percentage of positively stained bcl‐2 cells, with mean values for lower/higher intensity of 8.3 ± 2.5/34.4 ± 7, 7.5 ± 1.1/31.9 ± 4.3, and 8.4 ± 5.8/31.5 ± 5.8 within stages II, III, and IV, respectively. Low level of bcl‐2 expression in our sample seems to be associated with higher survival rate: 77% for the 5‐year follow‐up period. Comparing clinicopathologic and risk factors data within each and between three groups of analyzed tumors (lip–tongue P= 0.58, tongue–floor of the mouth, P= 0.21, lip–floor of the mouth, P= 0.50) there was no significant difference. However, our results suggest that the level of bcl‐2 expression could be a valuable predictor of tumor behavior and disease outcome.
Author JEKIĆ, B.
JURIŠIĆ, V.
VUKADINOVIĆ, M.
NOVAKOVIĆ, I.
MILAŠIN, J.
TEPAVČEVIĆ, Z.
LUKOVIĆ, L.J.
POPOVIĆ, B.
Author_xml – sequence: 1
  givenname: B.
  surname: POPOVIĆ
  fullname: POPOVIĆ, B.
  organization: Institute of Biology and Human Genetics, School of Dentistry, University of Belgrade, Belgrade 11000, Serbia and Montenegro
– sequence: 2
  givenname: B.
  surname: JEKIĆ
  fullname: JEKIĆ, B.
  organization: Institute of Biology and Human Genetics, School of Medicine, University of Belgrade, Belgrade 11000, Serbia and Montenegro
– sequence: 3
  givenname: I.
  surname: NOVAKOVIĆ
  fullname: NOVAKOVIĆ, I.
  organization: Institute of Biology and Human Genetics, School of Medicine, University of Belgrade, Belgrade 11000, Serbia and Montenegro
– sequence: 4
  givenname: L.J.
  surname: LUKOVIĆ
  fullname: LUKOVIĆ, L.J.
  organization: Institute of Biology and Human Genetics, School of Medicine, University of Belgrade, Belgrade 11000, Serbia and Montenegro
– sequence: 5
  givenname: Z.
  surname: TEPAVČEVIĆ
  fullname: TEPAVČEVIĆ, Z.
  organization: Institute of Pathology, School of Dentistry, University of Belgrade, Belgrade 11000, Serbia and Montenegro
– sequence: 6
  givenname: V.
  surname: JURIŠIĆ
  fullname: JURIŠIĆ, V.
  organization: Institute of Pathophysiology, School of Medicine, University of Kragujevac, 34000 Kragujevac, Serbia and Montenegro
– sequence: 7
  givenname: M.
  surname: VUKADINOVIĆ
  fullname: VUKADINOVIĆ, M.
  organization: Clinic of Maxillofacial Surgery, School of Dentistry, University of Belgrade, Belgrade 11000, Serbia and Montenegro
– sequence: 8
  givenname: J.
  surname: MILAŠIN
  fullname: MILAŠIN, J.
  organization: Institute of Biology and Human Genetics, School of Dentistry, University of Belgrade, Belgrade 11000, Serbia and Montenegro
BackLink https://www.ncbi.nlm.nih.gov/pubmed/17404013$$D View this record in MEDLINE/PubMed
BookMark eNqFkDtPwzAURi0EoqUws6FMbGn9iO1kLAEKAlEhoBUsluM4kiGP1k4F_HscBTogISYP95zr-30HYLduag3AMYJjhBI2kXUtSzdGJOFjCMkOGCIeJSFjBO-CIYSch3GCyQAcOPcKIcJxxPfBwEMwgogMATxTZYiDi4-V1c6Zpg5MHcytLIOH9UZWzcYFqS7LIJVWmbqp5CHYK_yX-uj7HYGny4vH9Cq8nc-u0-ltqAjlJCSqoJnGFOdUZQlVOsozzZBCEc5oIllG_CQpcqaxDxLHnBIaU6w1hBgxzsgInPZ7V7ZZb7RrRWWc8qfIWvurBIeEkCjqwJNvcJNVOhcrayppP8VPRg_QHlC2cc7qQijTytZnba00pUBQdF2KvkvRdSl8l96b_PK2q_80cG-8m1J__oeLu-fpQyeFvWRcqz-2krRvgnHCqVjezcRNen--fFnMxIJ8AbFulRM
CitedBy_id crossref_primary_10_1016_j_jobcr_2015_12_011
crossref_primary_10_1371_journal_pone_0056634
crossref_primary_10_3390_biomedicines8090296
crossref_primary_10_18632_oncotarget_19262
crossref_primary_10_1016_j_oraloncology_2008_05_021
crossref_primary_10_1111_j_1365_2559_2010_03621_x
crossref_primary_10_1186_s40064_016_3310_2
crossref_primary_10_1055_s_0044_1786810
crossref_primary_10_1007_s13105_024_01007_0
crossref_primary_10_1111_jop_12225
crossref_primary_10_1002_ijc_27728
crossref_primary_10_4132_KoreanJPathol_2012_46_2_177
crossref_primary_10_1515_biol_2022_0817
crossref_primary_10_1007_s10616_024_00638_x
crossref_primary_10_1097_CAD_0b013e32835455f1
crossref_primary_10_1155_2019_8040361
crossref_primary_10_12659_MSMBR_884004
crossref_primary_10_1016_j_jcpa_2008_02_001
crossref_primary_10_1007_s13402_017_0336_6
crossref_primary_10_1021_acsomega_3c08376
crossref_primary_10_1016_j_critrevonc_2023_104021
crossref_primary_10_4103_ijohs_ijohs_36_21
crossref_primary_10_1177_154405910808700104
crossref_primary_10_2174_0115733947249560231003111214
crossref_primary_10_3390_ijms23031562
Cites_doi 10.1056/NEJM199309023291003
10.1002/(SICI)1097-0215(19960703)67:1<138::AID-IJC22>3.0.CO;2-9
10.1016/S0964-1955(97)00033-X
10.1007/978-3-642-79437-7_8
10.1002/1097-0142(19940415)73:8<2013::AID-CNCR2820730802>3.0.CO;2-J
10.1056/NEJM199301213280306
10.1053/joms.2002.29804
10.1083/jcb.124.1.1
10.1002/(SICI)1097-0142(19960115)77:2<255::AID-CNCR6>3.0.CO;2-L
10.1016/0092-8674(93)90509-O
10.1016/S1368-8375(02)00002-7
10.1038/bjc.1998.449
10.1007/PL00008207
10.1053/ejso.2002.1287
10.1002/(SICI)1097-0142(19990915)86:6<913::AID-CNCR4>3.0.CO;2-A
10.1007/BF03033719
10.1038/sj.leu.2402090
ContentType Journal Article
DBID BSCLL
AAYXX
CITATION
CGR
CUY
CVF
ECM
EIF
NPM
7X8
DOI 10.1196/annals.1397.003
DatabaseName Istex
CrossRef
Medline
MEDLINE
MEDLINE (Ovid)
MEDLINE
MEDLINE
PubMed
MEDLINE - Academic
DatabaseTitle CrossRef
MEDLINE
Medline Complete
MEDLINE with Full Text
PubMed
MEDLINE (Ovid)
MEDLINE - Academic
DatabaseTitleList MEDLINE
MEDLINE - Academic
CrossRef

Database_xml – sequence: 1
  dbid: NPM
  name: PubMed
  url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
  sourceTypes: Index Database
– sequence: 2
  dbid: EIF
  name: MEDLINE
  url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search
  sourceTypes: Index Database
DeliveryMethod fulltext_linktorsrc
Discipline Sciences (General)
Biology
EISSN 1749-6632
EndPage 25
ExternalDocumentID 17404013
10_1196_annals_1397_003
NYAS3
ark_67375_WNG_KCQDWZVG_V
Genre article
Research Support, Non-U.S. Gov't
Journal Article
GroupedDBID ---
--Z
-~X
.3N
.55
.GA
.GJ
.Y3
05W
0R~
10A
1CY
1OB
1OC
23M
31~
33P
3O-
3SF
4.4
50Y
50Z
51W
51X
52M
52N
52O
52P
52S
52T
52U
52W
52X
53G
5GY
5HH
5LA
5RE
5VS
66C
692
6J9
702
79B
7PT
8-0
8-1
8-3
8-4
8-5
8UM
930
A03
AAESR
AAEVG
AAHQN
AAMMB
AAMNL
AANHP
AANLZ
AAONW
AASGY
AAXRX
AAYCA
AAZKR
ABCQN
ABCUV
ABDBF
ABEML
ABJNI
ABLJU
ABPVW
ACAHQ
ACBWZ
ACCZN
ACGFO
ACGFS
ACIWK
ACPOU
ACPRK
ACRPL
ACSCC
ACUHS
ACXBN
ACXQS
ACYXJ
ADBBV
ADEOM
ADIZJ
ADKYN
ADMGS
ADNMO
ADOZA
ADXAS
ADXHL
ADZMN
AEFGJ
AEGXH
AEIGN
AEIMD
AELAQ
AENEX
AEUYR
AEYWJ
AFBPY
AFFNX
AFFPM
AFGKR
AFRAH
AFSWV
AFWVQ
AFZJQ
AGHNM
AGQPQ
AGXDD
AGYGG
AHBTC
AHDLI
AHEFC
AHMBA
AI.
AIAGR
AIDQK
AIDYY
AIQQE
AITYG
AIURR
AJXKR
ALAGY
ALMA_UNASSIGNED_HOLDINGS
ALUQN
ALVPJ
AMBMR
AMYDB
ATUGU
AUFTA
AZBYB
AZFZN
AZVAB
BAFTC
BDRZF
BFHJK
BHBCM
BIYOS
BMNLL
BMXJE
BNHUX
BROTX
BRXPI
BSCLL
BY8
C45
CAG
CO8
COF
CS3
D-E
D-F
DC6
DCZOG
DPXWK
DR2
DRFUL
DRSTM
EBD
EBS
EJD
EMOBN
ESX
F00
F01
F04
F5P
FEDTE
FZ0
G-S
G.N
GODZA
H.T
H.X
HF~
HGLYW
HVGLF
HZI
HZ~
I-F
IH2
IX1
J0M
K48
L7B
LATKE
LC2
LC3
LEEKS
LH4
LITHE
LOXES
LP6
LP7
LUTES
LW6
LYRES
MEWTI
MK4
MRFUL
MRSTM
MSFUL
MSSTM
MXFUL
MXSTM
N04
N05
N9A
NF~
NHB
O66
O9-
OHT
OIG
OK1
OVD
P2P
P2W
P2X
P4D
PALCI
PQQKQ
Q.N
Q11
QB0
R.K
RAG
RIWAO
RJQFR
ROL
RX1
S10
SAMSI
SJN
SUPJJ
SV3
TEORI
TUS
UB1
UPT
V8K
VH1
W8V
W99
WBKPD
WH7
WHWMO
WIH
WIK
WOHZO
WQJ
WVDHM
WXSBR
X7M
XG1
YBU
YOC
YSK
ZGI
ZKB
ZXP
ZZTAW
~02
~IA
~KM
~WT
AAHHS
AAMDK
ACCFJ
ADZOD
AEEZP
AEQDE
AEUQT
AFPWT
AIWBW
AJBDE
WRC
WUP
AAYXX
CITATION
CGR
CUY
CVF
ECM
EIF
NPM
7X8
ID FETCH-LOGICAL-c3573-3cf5be252d5cb95ce4dbe61c142b59a6b32d59fd6e2119887535852ee00216763
IEDL.DBID DR2
ISSN 0077-8923
IngestDate Thu Jul 10 19:01:47 EDT 2025
Thu Apr 03 07:02:46 EDT 2025
Thu Apr 24 23:08:57 EDT 2025
Wed Oct 01 04:28:05 EDT 2025
Wed Jan 22 16:38:00 EST 2025
Sun Sep 21 06:13:24 EDT 2025
IsPeerReviewed true
IsScholarly true
Issue 1
Language English
License http://onlinelibrary.wiley.com/termsAndConditions#vor
LinkModel DirectLink
MergedId FETCHMERGED-LOGICAL-c3573-3cf5be252d5cb95ce4dbe61c142b59a6b32d59fd6e2119887535852ee00216763
Notes ArticleID:NYAS3
istex:D25295593156726B0CBBF33569080C58437686CB
ark:/67375/WNG-KCQDWZVG-V
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
PMID 17404013
PQID 70333446
PQPubID 23479
PageCount 7
ParticipantIDs proquest_miscellaneous_70333446
pubmed_primary_17404013
crossref_citationtrail_10_1196_annals_1397_003
crossref_primary_10_1196_annals_1397_003
wiley_primary_10_1196_annals_1397_003_NYAS3
istex_primary_ark_67375_WNG_KCQDWZVG_V
ProviderPackageCode CITATION
AAYXX
PublicationCentury 2000
PublicationDate 2007-01
January 2007
2007-01-00
2007-Jan
20070101
PublicationDateYYYYMMDD 2007-01-01
PublicationDate_xml – month: 01
  year: 2007
  text: 2007-01
PublicationDecade 2000
PublicationPlace Malden, USA
PublicationPlace_xml – name: Malden, USA
– name: United States
PublicationTitle Annals of the New York Academy of Sciences
PublicationTitleAlternate Ann N Y Acad Sci
PublicationYear 2007
Publisher Blackwell Publishing Inc
Publisher_xml – name: Blackwell Publishing Inc
References Binder, C. et al . 1997. Differential expression of apoptosis associated genes bax and bcl-2 in ovarian cancer. Anticancer Res. 17: 2233-2240.
Stoll, C. et al . 2000. Prognostic significance of apoptosis and associated factors in oral squamous cell carcinoma. Virchows Arch. 436: 102-108.
Kerr, J.F., C.M. Winterford & B.V. Harmon.1994. Apoptosis: its significance in cancer and cancer therapy. Cancer 73: 2013-2026.
Loro, L.L., A.C. Johannessen & O.K. Vintermyr. 2002. Decreased expression of bcl-2 in moderate and severe oral epithelia dysplasias. Oral Oncol. 38: 691-698.
Lo Muzio, L. et al . 2003. Expression of bcl-2 in oral squamous cell carcinoma: an immunohistochemical study of 90 cases with clinico-pathological correlations. Oncol. Rep. 10: 285-291.
Reed, J.C. et al . 1994. Bcl-2 and the regulation of programmed cell death. J Cell. Biol. 124: 1-6.
Vokes, E.E. et al . 1993. Head and neck cancer. N. Engl. J. Med. 328: 184-194.
Ruvolo, P.P., X. Deng & W.S. May. 2001. Phosphorylation of Bcl2 and regulation of apoptosis. Leukemia 15: 515-522.
Bareton, G.B. et al . 1996. Apoptosis and immunohistochemical bcl-2 expression in colorectal adenomas and carcinomas. Aspects of carcinogenesis and prognostic significance. Cancer 77: 255-264.
Yuen, A.P. et al . 2002. Clinicopathologic significance of bcl-2 expression in surgical treatment of oral tongue carcinoma. Eur. J. Surg. Oncol. 28: 667-672.
Boise, L.H. et al . 1995. Bcl-2 and Bcl-2 related proteins in apoptosis regulation. Curr. Top. Microbial. Immunol. 200: 107-121.
Nikitakis, N.G. et al . 2002. Bimarkers predictive of lymph node metastases in oral squamous cell carcinoma. J. Oral Maxillofac. Surg. 60: 142-147.
Wagner, C. et al . 1996. Induction of death-promoting gene bax-alpha sensitizes cultured breast cancer cells to drug-induced apoptosis. Int J. Cancer 67: 138-141.
Xie, X. et al . 1998. Bax expression has prognostic significance that is enhanced when combined with AgNOR counts in glottic carcinomas. Br. J. Cancer 78: 100-105.
Birchall, M.A. et al . 1997. Apoptosis, mitosis, PCNA and bcl-2 in normal, leukoplakic and malignant epithelia of the human oral cavity. Oral Oncol. 33: 419-425.
Oltvai, Z.N., C.L. Milliman & S.J. Korsmeyer. 1993. Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programmed cell death. Cell 74: 609-619.
Birchall, M.A. et al . 1997. Apoptosi, mitosis, PCNA and bsl-2 in normal, leukoplakic and malignant epithelia of the human oral cavity: prospective, in vivo study. Oral Oncol. 33: 419-425.
Xie, X. et al . 1999. The prognostic value of spontaneous apoptosis, bax, bcl-2, and p53 in oral squamous cell carcinoma of the tongue. Cancer 86: 913-920.
Pezzella, F. et al . 1993. Bcl-2 protein in non-small lung carcinoma. N. Engl. J. Med. 329: 690-694.
Teni, T. et al . 2002. Expression of bcl-2 and bax in chewing tobacco-induced oral cancers and oral lesions from India. Path. Oncol. Res. 8: 109-114.
2002; 38
1994; 124
2002; 28
1993; 329
1993; 328
1997; 33
2000; 436
1993; 74
2002; 8
1997; 17
1999; 86
2001; 15
2002; 60
1995; 200
1998; 78
1994; 73
2003; 10
1996; 67
1996; 77
Lo Muzio L. (e_1_2_6_19_2) 2003; 10
Binder C. (e_1_2_6_7_2) 1997; 17
e_1_2_6_20_2
e_1_2_6_8_2
e_1_2_6_18_2
e_1_2_6_9_2
e_1_2_6_4_2
e_1_2_6_3_2
e_1_2_6_6_2
e_1_2_6_5_2
e_1_2_6_12_2
e_1_2_6_13_2
e_1_2_6_2_2
e_1_2_6_10_2
e_1_2_6_11_2
e_1_2_6_21_2
e_1_2_6_16_2
e_1_2_6_17_2
e_1_2_6_14_2
e_1_2_6_15_2
References_xml – reference: Reed, J.C. et al . 1994. Bcl-2 and the regulation of programmed cell death. J Cell. Biol. 124: 1-6.
– reference: Binder, C. et al . 1997. Differential expression of apoptosis associated genes bax and bcl-2 in ovarian cancer. Anticancer Res. 17: 2233-2240.
– reference: Yuen, A.P. et al . 2002. Clinicopathologic significance of bcl-2 expression in surgical treatment of oral tongue carcinoma. Eur. J. Surg. Oncol. 28: 667-672.
– reference: Birchall, M.A. et al . 1997. Apoptosi, mitosis, PCNA and bsl-2 in normal, leukoplakic and malignant epithelia of the human oral cavity: prospective, in vivo study. Oral Oncol. 33: 419-425.
– reference: Ruvolo, P.P., X. Deng & W.S. May. 2001. Phosphorylation of Bcl2 and regulation of apoptosis. Leukemia 15: 515-522.
– reference: Xie, X. et al . 1999. The prognostic value of spontaneous apoptosis, bax, bcl-2, and p53 in oral squamous cell carcinoma of the tongue. Cancer 86: 913-920.
– reference: Boise, L.H. et al . 1995. Bcl-2 and Bcl-2 related proteins in apoptosis regulation. Curr. Top. Microbial. Immunol. 200: 107-121.
– reference: Kerr, J.F., C.M. Winterford & B.V. Harmon.1994. Apoptosis: its significance in cancer and cancer therapy. Cancer 73: 2013-2026.
– reference: Stoll, C. et al . 2000. Prognostic significance of apoptosis and associated factors in oral squamous cell carcinoma. Virchows Arch. 436: 102-108.
– reference: Vokes, E.E. et al . 1993. Head and neck cancer. N. Engl. J. Med. 328: 184-194.
– reference: Oltvai, Z.N., C.L. Milliman & S.J. Korsmeyer. 1993. Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programmed cell death. Cell 74: 609-619.
– reference: Xie, X. et al . 1998. Bax expression has prognostic significance that is enhanced when combined with AgNOR counts in glottic carcinomas. Br. J. Cancer 78: 100-105.
– reference: Bareton, G.B. et al . 1996. Apoptosis and immunohistochemical bcl-2 expression in colorectal adenomas and carcinomas. Aspects of carcinogenesis and prognostic significance. Cancer 77: 255-264.
– reference: Lo Muzio, L. et al . 2003. Expression of bcl-2 in oral squamous cell carcinoma: an immunohistochemical study of 90 cases with clinico-pathological correlations. Oncol. Rep. 10: 285-291.
– reference: Pezzella, F. et al . 1993. Bcl-2 protein in non-small lung carcinoma. N. Engl. J. Med. 329: 690-694.
– reference: Wagner, C. et al . 1996. Induction of death-promoting gene bax-alpha sensitizes cultured breast cancer cells to drug-induced apoptosis. Int J. Cancer 67: 138-141.
– reference: Nikitakis, N.G. et al . 2002. Bimarkers predictive of lymph node metastases in oral squamous cell carcinoma. J. Oral Maxillofac. Surg. 60: 142-147.
– reference: Loro, L.L., A.C. Johannessen & O.K. Vintermyr. 2002. Decreased expression of bcl-2 in moderate and severe oral epithelia dysplasias. Oral Oncol. 38: 691-698.
– reference: Birchall, M.A. et al . 1997. Apoptosis, mitosis, PCNA and bcl-2 in normal, leukoplakic and malignant epithelia of the human oral cavity. Oral Oncol. 33: 419-425.
– reference: Teni, T. et al . 2002. Expression of bcl-2 and bax in chewing tobacco-induced oral cancers and oral lesions from India. Path. Oncol. Res. 8: 109-114.
– volume: 74
  start-page: 609
  year: 1993
  end-page: 619
  article-title: Bcl‐2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programmed cell death
  publication-title: Cell
– volume: 328
  start-page: 184
  year: 1993
  end-page: 194
  article-title: Head and neck cancer
  publication-title: N. Engl. J. Med.
– volume: 86
  start-page: 913
  year: 1999
  end-page: 920
  article-title: The prognostic value of spontaneous apoptosis, bax, bcl‐2, and p53 in oral squamous cell carcinoma of the tongue
  publication-title: Cancer
– volume: 33
  start-page: 419
  year: 1997
  end-page: 425
  article-title: Apoptosi, mitosis, PCNA and bsl‐2 in normal, leukoplakic and malignant epithelia of the human oral cavity: prospective, study
  publication-title: Oral Oncol.
– volume: 15
  start-page: 515
  year: 2001
  end-page: 522
  article-title: Phosphorylation of Bcl2 and regulation of apoptosis
  publication-title: Leukemia
– volume: 200
  start-page: 107
  year: 1995
  end-page: 121
  article-title: Bcl‐2 and Bcl‐2 related proteins in apoptosis regulation
  publication-title: Curr. Top. Microbial. Immunol.
– volume: 8
  start-page: 109
  year: 2002
  end-page: 114
  article-title: Expression of bcl‐2 and bax in chewing tobacco‐induced oral cancers and oral lesions from India
  publication-title: Path. Oncol. Res.
– volume: 28
  start-page: 667
  year: 2002
  end-page: 672
  article-title: Clinicopathologic significance of bcl‐2 expression in surgical treatment of oral tongue carcinoma
  publication-title: Eur. J. Surg. Oncol.
– volume: 17
  start-page: 2233
  year: 1997
  end-page: 2240
  article-title: Differential expression of apoptosis associated genes bax and bcl‐2 in ovarian cancer
  publication-title: Anticancer Res.
– volume: 67
  start-page: 138
  year: 1996
  end-page: 141
  article-title: Induction of death‐promoting gene bax‐alpha sensitizes cultured breast cancer cells to drug‐induced apoptosis
  publication-title: Int J. Cancer
– volume: 10
  start-page: 285
  year: 2003
  end-page: 291
  article-title: Expression of bcl‐2 in oral squamous cell carcinoma: an immunohistochemical study of 90 cases with clinico‐pathological correlations
  publication-title: Oncol. Rep.
– volume: 73
  start-page: 2013
  year: 1994
  end-page: 2026
  article-title: Apoptosis: its significance in cancer and cancer therapy
  publication-title: Cancer
– volume: 124
  start-page: 1
  year: 1994
  end-page: 6
  article-title: Bcl‐2 and the regulation of programmed cell death
  publication-title: J Cell. Biol.
– volume: 60
  start-page: 142
  year: 2002
  end-page: 147
  article-title: Bimarkers predictive of lymph node metastases in oral squamous cell carcinoma
  publication-title: J. Oral Maxillofac. Surg.
– volume: 436
  start-page: 102
  year: 2000
  end-page: 108
  article-title: Prognostic significance of apoptosis and associated factors in oral squamous cell carcinoma
  publication-title: Virchows Arch.
– volume: 38
  start-page: 691
  year: 2002
  end-page: 698
  article-title: Decreased expression of bcl‐2 in moderate and severe oral epithelia dysplasias
  publication-title: Oral Oncol.
– volume: 329
  start-page: 690
  year: 1993
  end-page: 694
  article-title: Bcl‐2 protein in non‐small lung carcinoma
  publication-title: N. Engl. J. Med.
– volume: 33
  start-page: 419
  year: 1997
  end-page: 425
  article-title: Apoptosis, mitosis, PCNA and bcl‐2 in normal, leukoplakic and malignant epithelia of the human oral cavity
  publication-title: Oral Oncol.
– volume: 77
  start-page: 255
  year: 1996
  end-page: 264
  article-title: Apoptosis and immunohistochemical bcl‐2 expression in colorectal adenomas and carcinomas. Aspects of carcinogenesis and prognostic significance
  publication-title: Cancer
– volume: 78
  start-page: 100
  year: 1998
  end-page: 105
  article-title: Bax expression has prognostic significance that is enhanced when combined with AgNOR counts in glottic carcinomas
  publication-title: Br. J. Cancer
– ident: e_1_2_6_8_2
  doi: 10.1056/NEJM199309023291003
– ident: e_1_2_6_10_2
  doi: 10.1002/(SICI)1097-0215(19960703)67:1<138::AID-IJC22>3.0.CO;2-9
– ident: e_1_2_6_13_2
  doi: 10.1016/S0964-1955(97)00033-X
– ident: e_1_2_6_5_2
  doi: 10.1007/978-3-642-79437-7_8
– ident: e_1_2_6_4_2
  doi: 10.1002/1097-0142(19940415)73:8<2013::AID-CNCR2820730802>3.0.CO;2-J
– ident: e_1_2_6_2_2
  doi: 10.1056/NEJM199301213280306
– ident: e_1_2_6_21_2
  doi: 10.1053/joms.2002.29804
– ident: e_1_2_6_3_2
  doi: 10.1083/jcb.124.1.1
– volume: 10
  start-page: 285
  year: 2003
  ident: e_1_2_6_19_2
  article-title: Expression of bcl‐2 in oral squamous cell carcinoma: an immunohistochemical study of 90 cases with clinico‐pathological correlations
  publication-title: Oncol. Rep.
– ident: e_1_2_6_9_2
  doi: 10.1016/S0964-1955(97)00033-X
– ident: e_1_2_6_12_2
  doi: 10.1002/(SICI)1097-0142(19960115)77:2<255::AID-CNCR6>3.0.CO;2-L
– ident: e_1_2_6_6_2
  doi: 10.1016/0092-8674(93)90509-O
– ident: e_1_2_6_16_2
  doi: 10.1016/S1368-8375(02)00002-7
– ident: e_1_2_6_11_2
  doi: 10.1038/bjc.1998.449
– ident: e_1_2_6_15_2
  doi: 10.1007/PL00008207
– volume: 17
  start-page: 2233
  year: 1997
  ident: e_1_2_6_7_2
  article-title: Differential expression of apoptosis associated genes bax and bcl‐2 in ovarian cancer
  publication-title: Anticancer Res.
– ident: e_1_2_6_20_2
  doi: 10.1053/ejso.2002.1287
– ident: e_1_2_6_14_2
  doi: 10.1002/(SICI)1097-0142(19990915)86:6<913::AID-CNCR4>3.0.CO;2-A
– ident: e_1_2_6_17_2
  doi: 10.1007/BF03033719
– ident: e_1_2_6_18_2
  doi: 10.1038/sj.leu.2402090
SSID ssj0012847
Score 2.0265849
Snippet :  Apoptosis is a genetically regulated process involved in tissue size regulation, morphogenesis, and elimination of genetically damaged cells. A pallet of...
Abstract :  Apoptosis is a genetically regulated process involved in tissue size regulation, morphogenesis, and elimination of genetically damaged cells. A...
Apoptosis is a genetically regulated process involved in tissue size regulation, morphogenesis, and elimination of genetically damaged cells. A pallet of genes...
SourceID proquest
pubmed
crossref
wiley
istex
SourceType Aggregation Database
Index Database
Enrichment Source
Publisher
StartPage 19
SubjectTerms Adult
Aged
apoptosis
Apoptosis - genetics
bcl-2 expression
Carcinoma, Squamous Cell - chemistry
Carcinoma, Squamous Cell - metabolism
Carcinoma, Squamous Cell - pathology
Female
Humans
Lip Neoplasms - chemistry
Lip Neoplasms - metabolism
Lip Neoplasms - pathology
Male
Middle Aged
Mouth Neoplasms - chemistry
Mouth Neoplasms - metabolism
Mouth Neoplasms - pathology
oral cavity
oral squamous cell carcinoma
Prognosis
Proto-Oncogene Proteins c-bcl-2 - biosynthesis
Proto-Oncogene Proteins c-bcl-2 - genetics
Tongue Neoplasms - chemistry
Tongue Neoplasms - metabolism
Tongue Neoplasms - pathology
Title Bcl-2 Expression in Oral Squamous Cell Carcinoma
URI https://api.istex.fr/ark:/67375/WNG-KCQDWZVG-V/fulltext.pdf
https://onlinelibrary.wiley.com/doi/abs/10.1196%2Fannals.1397.003
https://www.ncbi.nlm.nih.gov/pubmed/17404013
https://www.proquest.com/docview/70333446
Volume 1095
hasFullText 1
inHoldings 1
isFullTextHit
isPrint
journalDatabaseRights – providerCode: PRVEBS
  databaseName: EBSCOhost Academic Search Ultimate
  customDbUrl: https://search.ebscohost.com/login.aspx?authtype=ip,shib&custid=s3936755&profile=ehost&defaultdb=asn
  eissn: 1749-6632
  dateEnd: 20241001
  omitProxy: true
  ssIdentifier: ssj0012847
  issn: 0077-8923
  databaseCode: ABDBF
  dateStart: 20060501
  isFulltext: true
  titleUrlDefault: https://search.ebscohost.com/direct.asp?db=asn
  providerName: EBSCOhost
– providerCode: PRVWIB
  databaseName: Wiley Online Library - Core collection (SURFmarket)
  issn: 0077-8923
  databaseCode: DR2
  dateStart: 19970101
  customDbUrl:
  isFulltext: true
  eissn: 1749-6632
  dateEnd: 99991231
  omitProxy: false
  ssIdentifier: ssj0012847
  providerName: Wiley-Blackwell
link http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV1LT9wwEB4hKqReaKEPQlvwoUKgKmETx8nmSJeXqLqId-Fi2Y4jVbuEArsS7ak_ob-xv4QZx7sI1KqqOMdOnBn788x4_A3A-8zYIq1wAebtFg_TohRhO61sSEdeVaxavHLJ45-72fZRuvNFjLIJ6S5Mww8xDrjRynB4TQtcaV-FpPDstqigiCyYqOH7jLlwB7X7YwIpB74Oi3PEYrRlPLkPvmH1Qf97-9ITEvHNn4zO-zas24Q2n4EeDb_JPelFw4GOzI8HzI6P-r_nMO1NVLbWzKkZmLD1LEw1RSu_z8KMh4Nrtuw5q1deQPLR9H___JWwjRufWVuzrzXbxafs4HKoKMDAOrbfZx0qXlRfnKuXcLS5cdjZDn05htBwkfOQm0pom4ikFEYXwti01DaLTZwmWhQq0xyfFFWZWWKNa5MjhL5IYi3ZERni2CuYrC9qOweMIwaXGVd5rDIEEaV0Ycs4rXSCDhXPywCikTKk8VzlVDKjL53PUrh71CgdSdIhetMAlscdvjU0HX9vuuS0O26nrnqU3ZYLedLdkp86e-snZ8db8jiAxZH6Ja45OkhRtUVxSURJztGPDuB1MyvuvpmnLfJYA_jgdPuvwcju6doBn_-v1m_gaRNgpjjQW5gcXA3tO7SMBnrBTf5bIAoGjw
linkProvider Wiley-Blackwell
linkToHtml http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV1Lb9QwEB6hVhVc-gLalNL6gFArlLCJ42RzLNvHlraLoK-lF8t2HAntkj7YlQonfgK_kV_CjJNd2ooKIc52nGTG83lmPP4M8CIxNosLNMC02eB-nOXCb8aF9WnLqwhVgxeuePygk7SP47dd0b1xFqbihxgn3MgyHF6TgVNCurLyrKa3RQ0F5MIEjvBzknbpyDg3P4wppBz8OjROEY3Rm6npfXCI13cGuLUyTZKQr__kdt72Yt0ytD0DZvQDVfVJLxgOdGC-3eF2_L8_nIXp2ktlG9W0moMHtpyHqereyq_zMFcjwhe2VtNWrz-G6I3p__z-I2Jb13Vxbck-lewdtrLDy6GiHANr2X6ftej-ovL8s3oCx9tbR622X9_I4BsuUu5zUwhtIxHlwuhMGBvn2iahCeNIi0wlmmNLVuSJJeK4JsVCGI5E1pIrkSCUPYWJ8ry0i8A4wnCecJWGKkEcUUpnNg_jQkcYU_E09yAYaUOamq6cbs3oSxe2ZO4oNUpHknSI4dSDtfEDFxVTx_1dXzr1jvupqx4VuKVCnnZ25F7r_ebp2cmOPPFgdaR_iWZHeymqtCguiUDJOYbSHixU0-L3O9O4QUGrB6-ccv_2MbLzceOQL_1T71V42D462Jf7u529Z_CoyjdTWmgZJgZXQ_scHaWBXnGW8AuD-wqr
linkToPdf http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV1Lb9QwEB6hViAu0JZXKFAfECpCCZv4kc2xbLstFJZH6fNi2Y4joS7pg12p5cRP4DfyS5hxsotagRDiHMdxZjyfZ8bjzwCPlfOFqNAA826Hx6IoZdwVlY9py6tKTYdXoXj8zUBtbItXe3JSTUhnYRp-iGnCjSwj4DUZ-HFZNUZetOy2qKCEPJgk8H3OCoUxFvlFH6YMUgF9AxjnCMbozLTsPtjF80sdXFiYZknGZ7_zOi86sWEV6t8EOxl_U3xymIxHNnFfL1E7_tcPzsGN1kdlK82kmocrvl6Aq82tlecLMN_iwRe23JJWP70F2Qs3_PHte8bWztrS2pp9qtlbfMq2TsaGMgys54dD1qPbi-qjz-Y2bPfXPvY24vY-hthxmfOYu0pan8mslM4W0nlRWq9Sl4rMysIoy_FJUZXKE21clyIhDEYy78mRUAhkd2CmPqr9PWAcQbhU3OSpUYgixtjCl6mobIYRFc_LCJKJMrRrycrpzoyhDkFLEQ5So3Q0SYf4TSNYnr5w3PB0_Lnpk6DdaTtzekjlbbnUu4N1vdl7v7p7sLOudyJYmqhfo9HRToqpPYpLI0xyjoF0BHebWfHrm7noUMgawbOg278NRg_2V7b4_X9qvQTX3q329euXg81FuN4kmykn9ABmRqdj_xC9pJF9FOzgJ1x9CVo
openUrl ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Bcl%E2%80%902+Expression+in+Oral+Squamous+Cell+Carcinoma&rft.jtitle=Annals+of+the+New+York+Academy+of+Sciences&rft.au=POPOVI%C4%86%2C+B.&rft.au=JEKI%C4%86%2C+B.&rft.au=NOVAKOVI%C4%86%2C+I.&rft.au=LUKOVI%C4%86%2C+L.J.&rft.date=2007-01-01&rft.pub=Blackwell+Publishing+Inc&rft.issn=0077-8923&rft.eissn=1749-6632&rft.volume=1095&rft.issue=1&rft.spage=19&rft.epage=25&rft_id=info:doi/10.1196%2Fannals.1397.003&rft.externalDBID=10.1196%252Fannals.1397.003&rft.externalDocID=NYAS3
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0077-8923&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0077-8923&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0077-8923&client=summon