scholarly journals Expression of xeroderma pigmentosum complementation group C protein predicts cisplatin resistance in lung adenocarcinoma patients

2011 ◽  
Vol 25 (5) ◽  
Author(s):  
Chow
Keyword(s):  
Lung Adenocarcinoma ◽  
Xeroderma Pigmentosum ◽  
Cisplatin Resistance ◽  
Complementation Group ◽  
C Protein

scholarly journals Xeroderma pigmentosum complementation group C protein (XPC) serves as a general sensor of damaged DNA

DNA Repair ◽  
2013 ◽  
Vol 12 (11) ◽  
pp. 947-953 ◽  
Author(s):  
Steven M. Shell ◽  
Edward K. Hawkins ◽  
Miaw-Sheue Tsai ◽  
Aye Su Hlaing ◽  
Carmelo J. Rizzo ◽  
...  
Keyword(s):  
Xeroderma Pigmentosum ◽  
Complementation Group ◽  
C Protein ◽  
Damaged Dna

scholarly journals Biochemical and Structural Domain Analysis of Xeroderma Pigmentosum Complementation Group C Protein†

Biochemistry ◽  
2006 ◽  
Vol 45 (50) ◽  
pp. 14965-14979 ◽  
Author(s):  
Christopher G. Bunick ◽  
Michael R. Miller ◽  
Brian E. Fuller ◽  
Ellen Fanning ◽  
Walter J. Chazin
Keyword(s):  
Xeroderma Pigmentosum ◽  
Domain Analysis ◽  
Complementation Group ◽  
Structural Domain ◽  
C Protein

The Carboxy-Terminal Domain of Xeroderma Pigmentosum Complementation Group C Protein, Involved in TFIIH and Centrin Binding, Is Highly Disordered†

Biochemistry ◽  
2008 ◽  
Vol 47 (5) ◽  
pp. 1403-1413 ◽  
Author(s):  
Simona Miron ◽  
Patricia Duchambon ◽  
Yves Blouquit ◽  
Dominique Durand ◽  
Constantin T. Craescu
Keyword(s):  
Xeroderma Pigmentosum ◽  
Complementation Group ◽  
C Protein ◽  
Terminal Domain ◽  
Carboxy Terminal Domain ◽  
Carboxy Terminal

Sid patients bearing basaliomas in xeroderma pigmentosum complementation group F.

1990 ◽  
Vol 52 (2) ◽  
pp. 279-284 ◽  
Author(s):  
Seiji KONDO ◽  
Chizu MIYAMOTO ◽  
Chin-Huai KEONG ◽  
Yoshiaki SATOH ◽  
Yoshisada FUJIWARA ◽  
...  
Keyword(s):  
Xeroderma Pigmentosum ◽  
Complementation Group

scholarly journals Lung adenocarcinoma concomitant with xeroderma pigmentosum: a case report

2021 ◽  
Vol 15 (1) ◽  
Author(s):  
Masataka Matsumoto ◽  
Kazumi Kaneshiro ◽  
Kiyonobu Takatsuki
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Side Effects ◽  
Epidermal Growth Factor ◽  
Lung Adenocarcinoma ◽  
Xeroderma Pigmentosum ◽  
Growth Factor Receptor ◽  
Consanguineous Marriage ◽  
History Of ◽  
Epidermal Growth

Abstract Background Xeroderma pigmentosum is a rare, autosomal-recessive photosensitive dermatosis. Patients with xeroderma pigmentosum have an impaired ability to repair deoxyribonucleic acid damage caused by ultraviolet rays, resulting in skin cancer. Patients with xeroderma pigmentosum are more susceptible to some cancers. We herein report a case of xeroderma pigmentosum accompanied by lung cancer. Case presentation The patient was a Japanese woman in her 70s with a family history of consanguineous marriage. Her medical history included squamous cell carcinoma and basal cell carcinoma, in addition to xeroderma pigmentosum. She presented with dry skin with small, pigmented spots, which were particularly focused around the areas exposed to sunlight. Chest computed tomography was conducted to assess for any evidence of metastatic skin carcinoma, and revealed a tumor in the left upper subpleural lobe of the lung. Consequently, she was referred to our department. Finally, we diagnosed lung adenocarcinoma (pT2aN0M1b: stage IVA). She had an epidermal growth factor receptor (EGFR) mutation (p.L858R). Treatment with an epidermal growth factor receptor tyrosine kinase inhibitor (gefitinib) was initiated, and the tumor gradually regressed. No side effects were observed. However, she later died from aspiration pneumonia. Conclusions Although xeroderma pigmentosum is rare, a history of consanguineous marriage should be verified. Because of the severe side effects of cisplatin and radiotherapy in xeroderma pigmentosum patients, the risks and benefits of treatment should be considered thoroughly.

XERODERMA PIGMENTOSUM COMPLEMENTATION GROUP F: MORE ASSIGNMENTS AND REPAIR CHARACTERISTICS

1985 ◽  
Vol 41 (5) ◽  
pp. 629-634 ◽  
Author(s):  
Y. Fujiwara ◽  
Y. Uehara ◽  
M. Ichihashi ◽  
K. Nishioka
Keyword(s):  
Xeroderma Pigmentosum ◽  
Complementation Group

Xeroderma pigmentosum complementation group C cells remove pyrimidine dimers selectively from the transcribed strand of active genes

1991 ◽  
Vol 11 (8) ◽  
pp. 4128-4134
Author(s):  
J Venema ◽  
A van Hoffen ◽  
V Karcagi ◽  
A T Natarajan ◽  
A A van Zeeland ◽  
...  
Keyword(s):  
Xeroderma Pigmentosum ◽  
Mammalian Cells ◽  
Excision Repair ◽  
Complementation Group ◽  
C Cells ◽  
Dhfr Gene ◽  
Normal Cells ◽  
Pyrimidine Dimers ◽  
Normal Human ◽  
Active Genes

We have measured the removal of UV-induced pyrimidine dimers from DNA fragments of the adenosine deaminase (ADA) and dihydrofolate reductase (DHFR) genes in primary normal human and xeroderma pigmentosum complementation group C (XP-C) cells. Using strand-specific probes, we show that in normal cells, preferential repair of the 5' part of the ADA gene is due to the rapid and efficient repair of the transcribed strand. Within 8 h after irradiation with UV at 10 J m-2, 70% of the pyrimidine dimers in this strand are removed. The nontranscribed strand is repaired at a much slower rate, with 30% dimers removed after 8 h. Repair of the transcribed strand in XP-C cells occurs at a rate indistinguishable from that in normal cells, but the nontranscribed strand is not repaired significantly in these cells. Similar results were obtained for the DHFR gene. In the 3' part of the ADA gene, however, both normal and XP-C cells perform fast and efficient repair of either strand, which is likely to be caused by the presence of transcription units on both strands. The factor defective in XP-C cells is apparently involved in the processing of DNA damage in inactive parts of the genome, including nontranscribed strands of active genes. These findings have important implications for the understanding of the mechanism of UV-induced excision repair and mutagenesis in mammalian cells.

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