Download Pathology Probes

Pathology Probes
Pathology Probe Range
Probe Name
Chromosome Region
Probe Type
Control Probe
No. Tests
Cat. No*
ALK
2p23.2-p23.1
CHOP (DDIT3)
12q13.3
Breakapart
–
5 or 10
LPS 019
Breakapart
–
5 or 10
C-MET (MET)
7q31.2
LPS 015
Amplification
D7Z1
5 or 10
LPS 004
EGFR
EML4
7p11.2
Amplification
D7Z1
5 or 10
LPS 003
2p21
Breakapart
–
5 or 10
LPS 020
EWSR1
22q12.1-q12.2
Breakapart
–
5 or 10
LPS 006
EWSR1/ERG Dual Fusion
21q22.13-q22.2/22q12.1-q12.2
Translocation
FGFR1
8p11.23-p11.22
Breakapart/Amplification
FLI1/EWSR1 Dual Fusion
11q24.3/22q12.1-q12.2
HER2 (ERBB2)
MALT1
–
5 or 10
LPS 008
D8Z2
5 or 10
LPS 018
Translocation
–
5 or 10
LPS 007
17q12
Amplification
D17Z1
5 or 10
LPS 001
18q21.31-q21.32
Breakapart
–
5 or 10
LPS 017
MDM2
12q15
Amplification
D12Z1
5 or 10
LPS 016
N-MYC (MYCN)
2p24.3/2q11.2
Amplification
AFF3 (2q11.2)
5 or 10
LPS 009
PAX3
2q36.1
Breakapart
–
5 or 10
LPS 012
PAX7
1p36.13
Breakapart
–
5 or 10
LPS 013
RB1
13q14.2
Deletion
13qter
5 or 10
LPS 011
ROS1
6q22.1
Breakapart
–
5 or 10
LPS 022
SRD (CHD5)
1p36.31
Deletion
1qter
5 or 10
LPS 010
SYT (SS18)
18q11.2
Breakapart
TMPRSS2/ERG
21q22.2-q22.3/21q22.13-q22.2
Deletion/Breakapart
TOP2A
17q21.2
ZNF217
20q13.2
–
5 or 10
LPS 014
ERG (21q22.2)
5 or 10
LPS 021
Amplification/Deletion
D17Z1
5 or 10
LPS 002
Amplification
20pter
5 or 10
LPS 005
Haematopathology Probe Range
Probe Name
Chromosome Region
Probe Type
Control Probe
No. Tests
Cat. No*
BCL2
18q21.33-q22.1
Breakapart
–
5 or 10
LPS 028
BCL6
3q27.3-q28
Breakapart
–
5 or 10
LPS 029
CCND1
11q13.3
Breakapart
–
5 or 10
LPS 030
IGH
14q32.33
Breakapart
–
5 or 10
LPS 032
IGH/BCL2 Dual Fusion
14q32.33/18q21.33
Translocation
–
5 or 10
LPS 033
IGH/CCND1 Dual Fusion
14q32.33/11q13.3
Translocation
–
5 or 10
LPS 031
IGH/MALT1 Dual Fusion
14q32.33/18q21.31-q21.32
Translocation
–
5 or 10
LPS 034
IGH/MYC Dual Fusion
14q32.33/8q24.21
Translocation
–
5 or 10
LPS 035
IGK
2p11.2
Breakapart
–
5 or 10
LPS 038
IGL
22q11.21-q11.23
Breakapart
–
5 or 10
LPS 039
MYC
8q24.21
Breakapart
–
5 or 10
LPS 027
P16 (CDKN2A)
9p21.3
Deletion
D9Z3
5 or 10
LPS 036
P53 (TP53)
17p13.1
Deletion
D17Z1
5 or 10
LPS 037
* for 5 test kit add ‘-S’ to the catalogue number, e.g: LPS ###-S
Cytocell Ltd, 3-4 Technopark,
Newmarket Road, Cambridge, CB5 8PB
T: +44 (0) 1223 294048
F: +44 (0) 1223 294986
E: [email protected]
www.cytocell.com
www.myprobes.com
BNEWPATH-V005/2014_07
Pathology
Lung Cancer
The assessment of genetic changes in tissue biopsies can provide important information for prediction of tumour
progression. The majority of such changes are either chromosome amplifications, deletions, translocations or other
complex rearrangements that can be detected using FISH.
Lung cancer is the most commonly diagnosed cancer as well as the leading cause of cancer death in males.
Worldwide, lung cancer accounted for 1.6 million new cases and 1.4 million deaths in 20081.
Current methodologies, namely immunohistochemistry or Southern blotting, can provide information at the gene
expression level but, when carried out on tissue sections (either cryostat or paraffin embedded), FISH can provide
information at a gene level, In Situ, at the precise site within the tumour. This can reveal cell-to-cell heterogeneity and
enable the detection of small clones of genetically distinct cells. This analysis can be made even more efficient through
the use of automatic image analysis systems and software.
Prostate Cancer
Recent advances have been made in the diagnosis of lung cancer and the use of genomic technologies for the
detection of the most common form, non-small cell lung cancer (NSCLC).
References:
1. Ahmedin J, et al., CA Cancer J Clin 2011;61:69-90
Cat. No. LPS 019-S
(5 tests)
Cat. No. LPS 019
(10 tests)
ALK Breakapart
Prostate cancer is the second leading cause of cancer death behind lung cancer. Worldwide, an estimated 903,500
men were diagnosed with prostate cancer in 2008, with the highest rates recorded primarily in the developed countries
of Australia/New Zealand, Western, Northern Europe and Northern America1.
Lately, great advances have been made using genomic technologies to develop predictive models that anticipate the
risk of developing prostate cancer, prostate cancer progression, and the response of prostate cancer to therapy2.
Rearrangement of the ALK locus on 2p23 has been implicated in the development
of NSCLC4-6. The ALK gene codes for a transmembrane glycoprotein with tyrosine
kinase activity. In-frame rearrangements with the known fusion partners place the
ALK kinase domain under the control of a different gene promoter. This fusion
results in a chimeric protein with constitutive tyrosine kinase activity that has been
demonstrated to play a key role in controlling cell proliferation7-9.
References:
1. Ahmedin J, et al., CA Cancer J Clin 2011;61:69-90
2. Febbo, P.G. et al., Cancer 2009, 115: 3046-3057
References:
4. Soda M, Choi YL, Enomoto M, et al., Nature. 2007;448:561-566
5. Takeuchi K, Choi YL, Soda M, et al., Clin Cancer Res. 2008;14(20):6618-6624
6. Perner S, Wagner PL, Demichelis F, et al., Neoplasia. 2008; 10(3):298-302
7. Rikova K, Guo A, Zeng Q, et al., Cell. 2007; 131:1190-1203
8. Choi YL, Takeuchi K, Soda M, et al., Cancer Res. 2008; 68(13):4971-4976
9. Soda M, Takada S, Takeuchi K, et al., PNAS. 2008;105(50):19893-19897
2p23.2-p23.1
SPDYA FAM179A
CLIP4
PPP1CB WDR43
Cat. No. LPS 021-S
(5 tests)
Cat. No. LPS 021
(10 tests)
TMPRSS2/ERG (21q22) Deletion/Breakapart
D2S2312
TRMT61B
ALK
D2S2383
D2S2934
D2S405
420kb
486kb
100kb
The transmembrane protease serine 2-gene (TMPRSS2) is involved in gene fusions with ERG,
ETV1 or ETV4. In recent studies, it has been described that expression of the TMPRSS2/ERG
fusion gene is a strong prognostic factor for the risk of prostate cancer recurrence in prostate
cancer patients treated by surgery3.
DSCR8 KCNJ15
DSCR4
KCNJ6
D21S1439
ETS2
ERG
100kb
106kb
(5 tests)
Cat. No. LPS 020
(10 tests)
EML4 Breakapart
SHGC-11427
288kb
Cat. No. LPS 020-S
215kb
21q22.13-q22.2
References:
3. Outi R. Saramaki. et al., Clin. Cancer Res 2008, 14;3395-3400
In NSCLC, the rearrangement of the ALK gene was first identified with the
echinoderm microtubule-associated protein-like 4 gene (EML4)4. In-frame
fusions of EML4-ALK genes identified to date include variants containing multiple
breakpoints of the EML4 gene occurring at exons 2, 6, 13, 14, 15, 18, and 20 and
all variants starting at a portion of the ALK gene encoded by exon 204-5,8,10-12.
21q22.2-q22.3
References:
4. Soda M, Choi YL, Enomoto M, et al., Nature. 2007;448:561-566
5. Takeuchi K, Choi YL, Soda M, et al., Clin Cancer Res. 2008;14(20):6618-6624
8. Choi YL, Takeuchi K, Soda M, et al., Cancer Res. 2008; 68(13):4971-4976
10. Takeuchi K. Choi YL, Togashi Y, et al., Clin Cancer Res. 2009;15(9):3143-3149
11. Wong DW, Leung EL, So KK, et al., Cancer. 2009;115(8);1723-1733
12. Koivunen JP, Mermel C, Zejnullahu K, et al., Clin Cancer Res. 2008;14(13):4275-4283
2p21
FAM3B TMPRSS2
MX2 MX1
BACE2
D21S1906
PRDM15 ZBTB21
C2CD2
RIPK4
UMODL1 ABCG1
C2orf91
D21S1863
D21S1260
SHGC-106023
235kb
149kb
143kb
91kb
191kb
100kb
PKDCC
EML4
KCNG3
MTA3
D21S1838
152kb
RH120737
D2S2306
RH94235
161kb
406kb
353kb
100kb
Pathology
Lung Cancer
The assessment of genetic changes in tissue biopsies can provide important information for prediction of tumour
progression. The majority of such changes are either chromosome amplifications, deletions, translocations or other
complex rearrangements that can be detected using FISH.
Lung cancer is the most commonly diagnosed cancer as well as the leading cause of cancer death in males.
Worldwide, lung cancer accounted for 1.6 million new cases and 1.4 million deaths in 20081.
Current methodologies, namely immunohistochemistry or Southern blotting, can provide information at the gene
expression level but, when carried out on tissue sections (either cryostat or paraffin embedded), FISH can provide
information at a gene level, In Situ, at the precise site within the tumour. This can reveal cell-to-cell heterogeneity and
enable the detection of small clones of genetically distinct cells. This analysis can be made even more efficient through
the use of automatic image analysis systems and software.
Prostate Cancer
Recent advances have been made in the diagnosis of lung cancer and the use of genomic technologies for the
detection of the most common form, non-small cell lung cancer (NSCLC).
References:
1. Ahmedin J, et al., CA Cancer J Clin 2011;61:69-90
Cat. No. LPS 019-S
(5 tests)
Cat. No. LPS 019
(10 tests)
ALK Breakapart
Prostate cancer is the second leading cause of cancer death behind lung cancer. Worldwide, an estimated 903,500
men were diagnosed with prostate cancer in 2008, with the highest rates recorded primarily in the developed countries
of Australia/New Zealand, Western, Northern Europe and Northern America1.
Lately, great advances have been made using genomic technologies to develop predictive models that anticipate the
risk of developing prostate cancer, prostate cancer progression, and the response of prostate cancer to therapy2.
Rearrangement of the ALK locus on 2p23 has been implicated in the development
of NSCLC4-6. The ALK gene codes for a transmembrane glycoprotein with tyrosine
kinase activity. In-frame rearrangements with the known fusion partners place the
ALK kinase domain under the control of a different gene promoter. This fusion
results in a chimeric protein with constitutive tyrosine kinase activity that has been
demonstrated to play a key role in controlling cell proliferation7-9.
References:
1. Ahmedin J, et al., CA Cancer J Clin 2011;61:69-90
2. Febbo, P.G. et al., Cancer 2009, 115: 3046-3057
References:
4. Soda M, Choi YL, Enomoto M, et al., Nature. 2007;448:561-566
5. Takeuchi K, Choi YL, Soda M, et al., Clin Cancer Res. 2008;14(20):6618-6624
6. Perner S, Wagner PL, Demichelis F, et al., Neoplasia. 2008; 10(3):298-302
7. Rikova K, Guo A, Zeng Q, et al., Cell. 2007; 131:1190-1203
8. Choi YL, Takeuchi K, Soda M, et al., Cancer Res. 2008; 68(13):4971-4976
9. Soda M, Takada S, Takeuchi K, et al., PNAS. 2008;105(50):19893-19897
2p23.2-p23.1
SPDYA FAM179A
CLIP4
PPP1CB WDR43
Cat. No. LPS 021-S
(5 tests)
Cat. No. LPS 021
(10 tests)
TMPRSS2/ERG (21q22) Deletion/Breakapart
D2S2312
TRMT61B
ALK
D2S2383
D2S2934
D2S405
420kb
486kb
100kb
The transmembrane protease serine 2-gene (TMPRSS2) is involved in gene fusions with ERG,
ETV1 or ETV4. In recent studies, it has been described that expression of the TMPRSS2/ERG
fusion gene is a strong prognostic factor for the risk of prostate cancer recurrence in prostate
cancer patients treated by surgery3.
DSCR8 KCNJ15
DSCR4
KCNJ6
D21S1439
ETS2
ERG
100kb
106kb
(5 tests)
Cat. No. LPS 020
(10 tests)
EML4 Breakapart
SHGC-11427
288kb
Cat. No. LPS 020-S
215kb
21q22.13-q22.2
References:
3. Outi R. Saramaki. et al., Clin. Cancer Res 2008, 14;3395-3400
In NSCLC, the rearrangement of the ALK gene was first identified with the
echinoderm microtubule-associated protein-like 4 gene (EML4)4. In-frame
fusions of EML4-ALK genes identified to date include variants containing multiple
breakpoints of the EML4 gene occurring at exons 2, 6, 13, 14, 15, 18, and 20 and
all variants starting at a portion of the ALK gene encoded by exon 204-5,8,10-12.
21q22.2-q22.3
References:
4. Soda M, Choi YL, Enomoto M, et al., Nature. 2007;448:561-566
5. Takeuchi K, Choi YL, Soda M, et al., Clin Cancer Res. 2008;14(20):6618-6624
8. Choi YL, Takeuchi K, Soda M, et al., Cancer Res. 2008; 68(13):4971-4976
10. Takeuchi K. Choi YL, Togashi Y, et al., Clin Cancer Res. 2009;15(9):3143-3149
11. Wong DW, Leung EL, So KK, et al., Cancer. 2009;115(8);1723-1733
12. Koivunen JP, Mermel C, Zejnullahu K, et al., Clin Cancer Res. 2008;14(13):4275-4283
2p21
FAM3B TMPRSS2
MX2 MX1
BACE2
D21S1906
PRDM15 ZBTB21
C2CD2
RIPK4
UMODL1 ABCG1
C2orf91
D21S1863
D21S1260
SHGC-106023
235kb
149kb
143kb
91kb
191kb
100kb
PKDCC
EML4
KCNG3
MTA3
D21S1838
152kb
RH120737
D2S2306
RH94235
161kb
406kb
353kb
100kb
Pathology Probes
Pathology Probe Range
Probe Name
Chromosome Region
Probe Type
Control Probe
No. Tests
Cat. No*
ALK
2p23.2-p23.1
CHOP (DDIT3)
12q13.3
Breakapart
–
5 or 10
LPS 019
Breakapart
–
5 or 10
C-MET (MET)
7q31.2
LPS 015
Amplification
D7Z1
5 or 10
LPS 004
EGFR
EML4
7p11.2
Amplification
D7Z1
5 or 10
LPS 003
2p21
Breakapart
–
5 or 10
LPS 020
EWSR1
22q12.1-q12.2
Breakapart
–
5 or 10
LPS 006
EWSR1/ERG Dual Fusion
21q22.13-q22.2/22q12.1-q12.2
Translocation
FGFR1
8p11.23-p11.22
Breakapart/Amplification
FLI1/EWSR1 Dual Fusion
11q24.3/22q12.1-q12.2
HER2 (ERBB2)
MALT1
–
5 or 10
LPS 008
D8Z2
5 or 10
LPS 018
Translocation
–
5 or 10
LPS 007
17q12
Amplification
D17Z1
5 or 10
LPS 001
18q21.31-q21.32
Breakapart
–
5 or 10
LPS 017
MDM2
12q15
Amplification
D12Z1
5 or 10
LPS 016
N-MYC (MYCN)
2p24.3/2q11.2
Amplification
AFF3 (2q11.2)
5 or 10
LPS 009
PAX3
2q36.1
Breakapart
–
5 or 10
LPS 012
PAX7
1p36.13
Breakapart
–
5 or 10
LPS 013
RB1
13q14.2
Deletion
13qter
5 or 10
LPS 011
ROS1
6q22.1
Breakapart
–
5 or 10
LPS 022
SRD (CHD5)
1p36.31
Deletion
1qter
5 or 10
LPS 010
SYT (SS18)
18q11.2
Breakapart
TMPRSS2/ERG
21q22.2-q22.3/21q22.13-q22.2
Deletion/Breakapart
TOP2A
17q21.2
ZNF217
20q13.2
–
5 or 10
LPS 014
ERG (21q22.2)
5 or 10
LPS 021
Amplification/Deletion
D17Z1
5 or 10
LPS 002
Amplification
20pter
5 or 10
LPS 005
Haematopathology Probe Range
Probe Name
Chromosome Region
Probe Type
Control Probe
No. Tests
Cat. No*
BCL2
18q21.33-q22.1
Breakapart
–
5 or 10
LPS 028
BCL6
3q27.3-q28
Breakapart
–
5 or 10
LPS 029
CCND1
11q13.3
Breakapart
–
5 or 10
LPS 030
IGH
14q32.33
Breakapart
–
5 or 10
LPS 032
IGH/BCL2 Dual Fusion
14q32.33/18q21.33
Translocation
–
5 or 10
LPS 033
IGH/CCND1 Dual Fusion
14q32.33/11q13.3
Translocation
–
5 or 10
LPS 031
IGH/MALT1 Dual Fusion
14q32.33/18q21.31-q21.32
Translocation
–
5 or 10
LPS 034
IGH/MYC Dual Fusion
14q32.33/8q24.21
Translocation
–
5 or 10
LPS 035
IGK
2p11.2
Breakapart
–
5 or 10
LPS 038
IGL
22q11.21-q11.23
Breakapart
–
5 or 10
LPS 039
MYC
8q24.21
Breakapart
–
5 or 10
LPS 027
P16 (CDKN2A)
9p21.3
Deletion
D9Z3
5 or 10
LPS 036
P53 (TP53)
17p13.1
Deletion
D17Z1
5 or 10
LPS 037
* for 5 test kit add ‘-S’ to the catalogue number, e.g: LPS ###-S
Cytocell Ltd, 3-4 Technopark,
Newmarket Road, Cambridge, CB5 8PB
T: +44 (0) 1223 294048
F: +44 (0) 1223 294986
E: [email protected]
www.cytocell.com
www.myprobes.com
BNEWPATH-V005/2014_07