BACKGROUND. Synchronous multiple primary lung tumors (SMPLT) have been estimated to occur in 1% of lung carcinoma patients. Criteria for SMPLT diagnosis include different cancer histologies, location in different lobes of the lung, or genetic discordance. Patients with SMPLT have a poor clinical pro
Very frequent p53 mutations in metastatic prostate carcinoma and in matched primary tumors
β Scribed by Frederick J. Meyers; Paul H. Gumerlock; Sung Gil Chi; Holger Borchers; Arline D. Deitch; Ralph W. deVere White
- Publisher
- John Wiley and Sons
- Year
- 1998
- Tongue
- English
- Weight
- 113 KB
- Volume
- 83
- Category
- Article
- ISSN
- 0008-543X
No coin nor oath required. For personal study only.
β¦ Synopsis
BACKGROUND.
The frequency of mutant p53 in bone marrow metastases of patients with carcinoma of the prostate (CaP) and in matched sets of metastatic and primary lesions from the same patients was investigated. The data were examined in relation to prior treatment with androgen ablation (AA) therapy and were compared with the frequency of mutant p53 reported for primary CaP.
METHODS.
Seventeen patients with M1b (bone metastasis: TNM Stage IV) CaP had either unilateral or bilateral bone marrow biopsies taken for these studies. Specimens were divided and the outer one-third examined histologically to confirm the presence of CaP cells. Immunohistochemical (IHC) staining for accumulated p53 protein was performed by an antibody cocktail technique. RNA was extracted from the remaining portion of the biopsy, and p53 transcripts were amplified by reverse transcriptase-polymerase chain reaction (RT-PCR) and screened for base sequence changes in the exon 4 -11 region using nonisotopic single-strand conformation polymorphism (SSCP) analysis and direct DNA sequencing.
π SIMILAR VOLUMES
Numerous ectopic hormones and markers have been described in small cell carcinoma of the lung as well as in extrapulmonary small cell carcinomas. The authors report a case of a patient with metastatic small cell carcinoma of unknown primary who had very high prostatic acid phosphatase (PAP) and pros
The tumor suppressor gene CDKN2 (p16/MTS1) resides on chromosome 9p21 and encodes a 16 kDa inhibitor of the cyclin-dependent kinases. Inactivation of CDKN2 by homozygous deletion, point mutation, and recently described aberrant methylation in the 5' promoter region may increase progression through t
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