1. |
p53Fifteen Years After Discovery |
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Advances in Anatomic Pathology,
Volume 2,
Issue 2,
1995,
Page 71-88
John Batsakis,
Adel EL-Naggar,
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摘要:
AbstractSince its discovery 15 years ago, the p53 gene and its protein products have been the subjects of an almost unprecedented investigation. Justification for this lies in the critical role p53 plays as one of the cell cycle check points that control proliferation and differentiation. P53 is a tumor-suppressor gene found on chromosome 17p, and alterations (mussense mutation or deletion) within the coding sequences of gene are among the most frequent genetic changes detected in human neoplasnis. Mutation usually teads to the loss of DNA binding and transcriptional regulatory regulatory activities of the p53 nuclear phosphoprotein, with a corresponding loss of its growth suppressive activity. The tumor suppressor function of the normal gene and its wild-type (wt) p53 protein is replaced by the mutant form's oncognic properties. The mutated product of p53 is a protein with abnormal conformation, impaired DNA-binding, and a prolonged (stabilized) half-life, the latter of which results in Immunohistochemically detectable levels within nuclei in nearly all neoplasms showing p53 gene mutatin. Mutations of p53 or a complete loss of the gene is one of the important causes of failure to prevent cells from entering the S-phase of the cell cycle and malignancy. As more basic imformation of the molecular functions and cellular interactions of p53 accrues, it becomes evident that the genetic complexity of the gene and its protein products render simplisticclinicalinterpretations untenable. This ia especially true for prognostic or predictive screenings. Nonetheless, analysis of p53 in neoplastic or predictive states is a powerful molecular tool for dissecting the oncogenic process. In this review, we offer a contemporary assessment of the basic science and clinical status of p53.
ISSN:1072-4109
出版商:OVID
年代:1995
数据来源: OVID
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2. |
Usual Interstitial Pneumonia, Idiopathic Pulmonary Fibrosis, and All That JazzWhat Is, What Isn't, and How to Tell Them Apart |
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Advances in Anatomic Pathology,
Volume 2,
Issue 2,
1995,
Page 89-93
Jeffrey Myers,
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ISSN:1072-4109
出版商:OVID
年代:1995
数据来源: OVID
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3. |
Salivary Gland Anlage TumorA Newly Recognized Clinicopathologic Entity of Uncertain Histogenesis |
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Advances in Anatomic Pathology,
Volume 2,
Issue 2,
1995,
Page 94-98
John Buchino,
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ISSN:1072-4109
出版商:OVID
年代:1995
数据来源: OVID
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4. |
CD30+ (Ki‐1) Lymphomat(2;5) Translocation, the Implicated Genes, and More |
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Advances in Anatomic Pathology,
Volume 2,
Issue 2,
1995,
Page 99-104
John Chan,
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ISSN:1072-4109
出版商:OVID
年代:1995
数据来源: OVID
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5. |
Neuroendocrine Differentitatin in Prostatic Adenocarcinoma |
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Advances in Anatomic Pathology,
Volume 2,
Issue 2,
1995,
Page 105-107
Michael Cohen,
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ISSN:1072-4109
出版商:OVID
年代:1995
数据来源: OVID
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6. |
Florid Hyperplasia of Mesonephric RemnantsYet Another Differential Diagnostic Consideration Under “Smaa; Acinar Proliferation of the Prostate” |
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Advances in Anatomic Pathology,
Volume 2,
Issue 2,
1995,
Page 108-113
Mahul Amin,
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ISSN:1072-4109
出版商:OVID
年代:1995
数据来源: OVID
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7. |
Will p53 Immunoreactivity Be a Reliable Prognostic Indicator in Thyroid Carcinomas? |
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Advances in Anatomic Pathology,
Volume 2,
Issue 2,
1995,
Page 114-116
Ronald Nishiyama,
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ISSN:1072-4109
出版商:OVID
年代:1995
数据来源: OVID
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8. |
Recurrent pituitary adenomas can change their immunophenotype |
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Advances in Anatomic Pathology,
Volume 2,
Issue 2,
1995,
Page 117-117
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ISSN:1072-4109
出版商:OVID
年代:1995
数据来源: OVID
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9. |
The guardian of the genome also guards Rb |
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Advances in Anatomic Pathology,
Volume 2,
Issue 2,
1995,
Page 118-118
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ISSN:1072-4109
出版商:OVID
年代:1995
数据来源: OVID
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10. |
EWSan important gene implicated in several soft‐tissue tumors |
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Advances in Anatomic Pathology,
Volume 2,
Issue 2,
1995,
Page 119-119
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ISSN:1072-4109
出版商:OVID
年代:1995
数据来源: OVID
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