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Abnormal AP-1 protein expression in primary cutaneous B-cell lymphomas
1Skin Tumour Unit, St John's Institute of Dermatology, St Thomas' Hospital, King's College London, UK. mxmayo@yahoo.co.uk
Insights
This study reveals abnormal activator protein 1 (AP-1) expression in primary cutaneous B-cell lymphoma (PCBCL), with increased JUND, CCND1, and alphaPAK and decreased JUNB. These findings offer insights into PCBCL pathogenesis.
Area of Science:
- Dermatology
- Oncology
- Molecular Biology
Background:
- Primary cutaneous B-cell lymphoma (PCBCL) encompasses several subtypes, including PCMZL, PCFCL, and PCLBCL-LT.
- The activator protein 1 (AP-1) transcription factor family, including JUN and FOS proteins, plays a role in cellular processes.
Purpose of the Study:
- To investigate the expression patterns of AP-1 transcription factors in various subtypes of PCBCL.
- To identify potential correlations between AP-1 family members and PCBCL development.
Main Methods:
- Immunohistochemistry was employed to analyze paraffin-embedded tissue sections from 24 PCBCL cases.
- Antibodies targeting c-JUN, JUNB, JUND, c-FOS, RAF1, alphaPAK, CD30, and CCND1 were used.
Main Results:
- JUND protein expression was notably high in PCFCL (86%), PCLBCL-LT (83%), and PCMZL (56%).
- CCND1 expression was observed in PCLBCL-LT (67%), PCFCL (57%), and PCMZL (44%).
- AlphaPAK expression was detected in PCLBCL-LT (50%), PCMZL (22%), and PCFCL (14%), while c-JUN, c-FOS, RAF1, JUNB, and CD30 showed minimal to no expression.
Conclusions:
- Abnormal AP-1 protein expression, specifically upregulation of JUND, CCND1, and alphaPAK, and downregulation of JUNB, is associated with PCBCL.
- These findings suggest a role for altered AP-1 signaling in the pathogenesis of primary cutaneous B-cell lymphomas.
Background:
Primary cutaneous B-cell lymphoma (PCBCL) consists mainly of primary cutaneous marginal zone B-cell lymphoma (PCMZL), primary cutaneous follicle centre lymphoma (PCFCL) and primary cutaneous large B-cell lymphoma, leg type (PCLBCL-LT). The activator protein 1 (AP-1) transcription factor includes JUN, FOS and other family members.
Objectives:
To assess the expression pattern of AP-1 transcription factors in PCBCL.
Methods:
We analysed paraffin tissue sections from nine cases of PCMZL, seven PCFCL, six PCLBCL-LT and two unspecified PCBCL cases by using immunohistochemistry with antibodies against c-JUN, JUNB, JUND, c-FOS, RAF1, alphaPAK, CD30 and CCND1.
Results:
A positive staining for JUND (++) was observed in six cases of PCFCL (86%), five PCLBCL-LT (83%) and five PCMZL (56%). Positive CCND1 protein expression was present in four cases of PCLBCL-LT (67%), four PCFCL (57%) and four PCMZL (44%), and the two unspecified PCBCL cases. Expression of alphaPAK protein was seen in three cases of PCLBCL-LT (50%), two PCMZL (22%) and one PCFCL. However, c-JUN, c-FOS and RAF1 protein were rarely expressed in the PCBCL cases analysed; JUNB and CD30 protein expression was absent in these cases.
Conclusions:
These findings suggest that the presence of abnormal AP-1 protein expression is associated with upregulation of JUND, CCND1 and alphaPAK and downregulation of JUNB in PCBCL.
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