Immunohistochemical detection of p53 protein in mammary carcinoma: An important new independent indicator of prognosis?

Barnes, Diana M.; Dublin, Edwin A.; Fisher, C.J.; Levison, David A.; Millis, Rosemary R.

doi:10.1016/0046-8177(93)90158-d

Cited by 208 publications

(96 citation statements)

References 22 publications

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“…The proportion of cancers with p53 mutation (20%), p53 allele loss (41%), p53 mRNA expression (54%) and overexpression (28%) or p53 protein expression (32%) are similar to the reported series (Cattoretti et al, 1988;Davidoff, 1991;Iwaya, 1991;Kovach et al, 1991;Osborne et al, 1991;Runnebaum et al, 1991;Varley et al, 1991;Vojtesek et al, 1992;Andersen et al, 1993;Barnes, 1993;Friedrichs, 1993;Martinazzi, 1993;Thorlacius et al, 1993;Tsuda et al, 1993;Marks et al, 1994;Bergh et al, 1995;Borressen et al, 1995;Stenmark-Askmalm et al, 1995).…”

Section: Discussionsupporting

confidence: 74%

“…Furthermore, the precise location of the mutation may add further information of prognostic value (Bergh et al, 1995;Borressen et al, 1995) and predict response to chemotherapy (Elledge et al, 1995;Aas et al, 1996). p53 protein expression has been identified as a predictor of disease recurrence (Iwaya et al, 1991;Barnes et al, 1993;Friedrichs et al, 1993;Marks et al, 1994), even for patients without nodal involvement at the time of diagnosis (Allred et al, 1993;Barnes et al, 1993;Silvestrini et al, 1993;MacGrogan et al, 1995) and for poor survival (Isola et al, 1992;Allred et al, 1993;Silvestrini et al, 1993;Received 12 March 1997 Revised 25 July 1997 Accepted 21 August 1997 Correspondence to: AM Thompson Elledge and Borg et al, 1995;MacGrogan et al, 1995;Silvestrini et al, 1996). Although molecular lesions at p53 and at YNZ22 loci occur independently (Coles et al, 1990), it is not clear to what extent allelic imbalance on chromosome 17p telomeric to the p53 locus may reflect direct or indirect involvement of p53 itself.…”

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confidence: 99%

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Allelic imbalance at chromosome 17p13.3 (YNZ22) in breast cancer is independent of p53 mutation or p53 overexpression and is associated with poor prognosis at medium-term follow-up

Thompson

Crichton²,

Elton³

et al. 1998

Br J Cancer

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Summary Molecular and immunohistochemical studies of genetic events on chromosome 17p were prospectively compared with conventional clinical and pathological parameters and disease behaviour at a minimum of 72 months follow-up. In a series of 91 patients with primary operable breast cancer, 37 out of 91 (41 %) patients had disease relapse and 23 out of 91 (25%) had died during the follow-up period. Allelic imbalance at the YNZ22 locus (1 7p1 3.3), demonstrated in 33 out of 63 (52%) informative patients, was significantly associated with disease recurrence (P < 0.01, 2 d.f. Cox analysis) and showed a trend towards impaired survival (P = 0.08, 2 d.f. Cox analysis) after a mean follow-up of 84 months for survivors. By contrast, p53 mutation (in 10 out of 60, 17% of cancers), p53 allelic imbalance (in 23 out of 56, 41% informative patients), p53 mRNA expression (in 47 out of 87, 54% patients), p53 mRNA overexpression (in 24 out of 87, 28%) or p53 protein expression (detected in 25/76, 32%) were not associated with disease behaviour. There was no significant association between allelic imbalance at YNZ22 and any abnormality of p53 DNA, RNA or protein. Allelic imbalance at 17p13.3 (YNZ22) serves as a marker of poor prognosis in breast cancer. As yet unidentified genes on 17p13.3, distinct from and telomeric to p53, are therefore likely to be of clinical importance in breast cancer.

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Section: Discussionsupporting

confidence: 74%

mentioning

confidence: 99%

Allelic imbalance at chromosome 17p13.3 (YNZ22) in breast cancer is independent of p53 mutation or p53 overexpression and is associated with poor prognosis at medium-term follow-up

Thompson

Crichton²,

Elton³

et al. 1998

Br J Cancer

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“…In contrast, diffuse (homogeneous) expression, the positive staining in the majority of cells, is frequently associated with mutation (Baas et al, 1994;Shiao et al, 2000). This view is supported by the clinical data, in which the differences in expression patterns are significantly correlated with the patient's prognosis (Barnes et al, 1993;Shiao et al, 2000). In addition, the intensity of staining should not be considered for the judgment of staining results, according to the principle of immunohistochemical evaluation using multiple clinical samples (Kamoshida et al, 2004).…”

Section: Discussionmentioning

confidence: 86%

Immunostaining of thymidylate synthase and p53 for predicting chemoresistance to S-1/cisplatin in gastric cancer

et al. 2007

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High expression of thymidylate synthase (TS) and inactivation of p53 are allegedly associated with chemoresistance. The authors evaluated TS and p53 expression in gastric cancer treated with neoadjuvant S-1/cisplatin chemotherapy. Paraffin sections of pretreatment biopsy and surgical specimens from 41 gastric cancers were immunostained for TS and p53 protein after appropriate antigen retrieval. Fifty-one cases without neoadjuvant chemotherapy were also studied. In the pretreatment biopsies, high expression of TS was seen in 8% of the histologic responders, in 28% of the nonresponders and in 31% of the controls. High expression of p53 was observed in 56% of the nonresponders, but in 8% of the responders and in 29% of the controls (Po0.01 and Po0.05, respectively). The TS-and/or p53-high phenotype was seen in 76% of the nonresponders and in 54% of the controls, but in 8% of the responders (Po0.0001 and Po0.005, respectively). The data of the surgical specimens were consistent with those of the pretreatment biopsies. These results suggest that immunostaining for TS and p53 protein is useful for pretreatment selection of gastric cancer patients unresponsive to S-1/cisplatin chemotherapy.

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“…Both in situ and invasive low-grade lesions express oestrogen and progesterone receptors, but are usually negative for oncoproteins (HER/neu and p53). High-grade lesions exhibit the reverse (Hitchcock et al, 1989;Gullick et al, 1991;Barnes et al, 1993;Millis et al, 1996;Ellis et al, 1999). Molecular genetic studies find that low-grade lesions often demonstrate 16q deletions, while high-grade lesions have allelic losses of more chromosomal areas frequently including 1p, 1q, 6q, 9p, 11p, 13q and 17q.…”

Section: Discussionmentioning

confidence: 99%

Grade of recurrent in situ and invasive carcinoma following treatment of pure ductal carcinoma in situ of the breast

et al. 2004

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The grade of recurrent in situ and invasive carcinoma occurring after treatment of pure ductal carcinoma in situ (DCIS) has been compared with the grade of the original DCIS in 122 patients from four different centres (The Royal Marsden Hospitals, London and Sutton, 57 patients; Guy's Hospital, London, 19 patients; Nottingham City Hospital, 31 patients and The Royal Liverpool Hospital, 15 patients). The recurrent carcinoma was pure DCIS in 70 women (57%) and in 52 women (43%) invasive carcinoma was present, which was associated with an in situ element in 43. In all, 19 patients developed a second recurrence (pure DCIS in 11 and invasive with or without an in situ element in eight). The majority of invasive carcinomas followed high-grade DCIS. There was strong agreement between the grade of the original DCIS and that of the recurrent DCIS (k ¼ 0.679), which was the same in 95 of 113 patients (84%). The grade of the original DCIS showed only fair agreement with the grade of recurrent invasive carcinoma (k ¼ 0.241), although agreement was stronger with the pleomorphism score of the recurrent carcinoma (k ¼ 0.396). There was moderate agreement, in recurrent invasive lesions, between the grade of the DCIS and that of the associated invasive element (k ¼ 0.515). Other features that showed moderate or strong agreement between the original and recurrent DCIS were necrosis and periductal inflammation. The similarity between the histological findings of the original and subsequent DCIS is consistent with the concept that recurrent lesions represent regrowth of residual carcinoma. In addition, although agreement between the grade of the original DCIS and that of any subsequent invasive carcinoma was only fair, there is no suggestion that low-grade DCIS lesions progress to higher grade lesions or to the development of higher grade invasive carcinoma. This is in agreement with immunohistochemical and molecular data indicating that low-grade and high-grade mammary carcinomas are quite different lesions.

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Immunohistochemical detection of p53 protein in mammary carcinoma: An important new independent indicator of prognosis?

Cited by 208 publications

References 22 publications

Allelic imbalance at chromosome 17p13.3 (YNZ22) in breast cancer is independent of p53 mutation or p53 overexpression and is associated with poor prognosis at medium-term follow-up

Allelic imbalance at chromosome 17p13.3 (YNZ22) in breast cancer is independent of p53 mutation or p53 overexpression and is associated with poor prognosis at medium-term follow-up

Immunostaining of thymidylate synthase and p53 for predicting chemoresistance to S-1/cisplatin in gastric cancer

Grade of recurrent in situ and invasive carcinoma following treatment of pure ductal carcinoma in situ of the breast

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