Tumor apoptosis in cervical cancer: <i>Its role as a prognostic factor in 42 radiotherapy patients</i>

Kim, Joo-Young; Cho, Hyun-Yee; Lee, Kyu-Chan; Hwang, You-Jin; Lee, Myung-Hak; Roberts, Stephen A; Kim, Chul‐Hwan

doi:10.1002/ijc.1033

Cited by 16 publications

(8 citation statements)

References 26 publications

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“…Cervix cancer provides a setting where radiation is the prime modality and several studies have addressed the issue of pretreatment apoptotic indices and clinical outcome. [18][19][20][21][22][23][24][25][26][27][28] The results of these studies are summarized in Table 1.…”

Section: Assessment Of Apoptotic Cells ("Apoptotic Index")mentioning

confidence: 99%

Apoptosis Genes and Resistance to Cancer Therapy: What Does the Experimental and Clinical Data Tell Us?

Brown

Wilson²

2003

Cancer Biology & Therapy

109

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The dominant paradigm in cancer treatment is that cancer cells die from the common pathway of apoptosis subsequent to DNA damage by anticancer agents and that cells resistant to apoptosis are resistant to therapy. In this review we trace the logic that brought about this view and discuss whether the clinical and experimental data that have now accumulated over the past decade support the position. We show that there is support for the apoptosis model only for certain malignancies of hematopoietic origin. For the majority of cancers (which are of epithelial origin), even though some may exhibit apoptosis after treatment, there is little or no support for the concept that apoptosis, and the genes that govern it, determine the response to therapy. In general, whether apoptosis matters for overall tumor response depends on how soon after treatment apoptosis occurs. If it occurs early (within 4 to 6 hours after treatment), it is likely to be important for determining the overall response of the cell or tumor. This is the case for some tumors of myeloid and lymphoid origin. On the other hand, if apoptosis occurs long after exposure, 24-48 hrs, and usually after mitosis, then it is unlikely to be the determinant of cytotoxicity, and modifying it is unlikely to affect overall cell killing. This is the situation for most, if not all, tumors of epithelial or mesenchymal origin. What then causes cancer cells to die following treatment with anticancer agents? The evidence from ionizing radiation is clear: DNA damage leading to chromosome breaks. We argue that the situation is similar for most anticancer drugs. Indeed inability to repair the DNA damage produced by these agents, and the levels of the proteins involved in these repair processes, may explain the treatment sensitivity of some cancers. Further clinical studies in this area are needed.

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Section: Assessment Of Apoptotic Cells ("Apoptotic Index")mentioning

confidence: 99%

Apoptosis Genes and Resistance to Cancer Therapy: What Does the Experimental and Clinical Data Tell Us?

Brown

Wilson²

2003

Cancer Biology & Therapy

109

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“…Ferrandina et al demonstrated that positive expression of COX2 is associated with a worse prognosis, bad response to conventional treatment and that the ratio of COX2 in adjacent histogically normal epithelium with tumor was important prognostic factor for response and survival: more minor ratio than better prognostic [24][25][26]. Several studies largely confirmed these data [27][28][29][30][31]. Combination therapy of RT with use of a COX-2 inhibitor may yield improved outcomes for patients with COX-2 expressing cervical cancer.…”

Section: Introductionmentioning

confidence: 80%

Molecular profiling of uterine cervix carcinoma: an overview with a special focus on rationally designed target-based anticancer agents

Magné

Chargari

Deutsch

et al. 2008

Cancer Metastasis Rev

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Although conventional multimodality approaches allowed improvement in the prognosis of patients with cervix cancer, several tumors do not respond similarly to standard approaches. Recent advances in basic research and genomics have improved our understanding of the biologic basis of the tumor development and progression. Tumor profiling allows for more selective therapeutic strategies leading to the identification of biomarkers or indicators of treatment response and to increased clinical efficacy through development of targeted therapies. Several markers have been identified, that are involved in cellular proliferation, interaction with angiogenesis, extracellular matrice adhesion/invasion, apoptosis, cell cycle pathways and DNA repair mechanisms. In this report, molecular profiling of uterine cervix carcinoma were reviewed with a special focus on rationally designed target-based anticancer agents, in order to clarify and to summary the present state of art in these particular promising area in cervix cancer management.

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“…Dysregulation of the apoptotic pathway has been implicated in the pathogenesis of cancer [30] and various aspects of apoptosis with regard to oncogene expression, tumor growth, and prognosis in cervical cancer have been analyzed [31][32][33]. The p53 tumor-suppressor protein is a critical mediator of apoptosis and tumorigenesis [34] and its functional inactivation by the HPV E6 protein is crucial for HPV-induced malignant progression.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of Expression of Apoptosis-Related Proteins and Their Correlation with HPV, Telomerase Activity, and Apoptotic Index in Cervical Cancer

et al. 2004

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Objective: The aim of this study was to examine the expression of apoptosis-related proteins in cervical cancer, and investigate their correlation with the apoptotic index (AI), telomerase activity, human papilloma virus (HPV) infection and clinicopathological characteristics. Methods: Fifty cervical cancer samples and 20 normal cervical tissues were assessed for the protein expression of survivin, Bcl-2, Cox-2, p53 and p73 by immunohistochemistry. HPV DNA was detected by PCR, telomerase activity by PCR-ELISA, and AI by TUNEL assay. Results: 46/50 cervical tumors (92%) showed an increased telomerase activity as compared to 3/20 (15%) controls. 45/50 (90%) cervical tumors were positive for HPV, of which 30 were HPV-16 positive and 5 were HPV-18 positive. 24/50 (48%) tumors were positive for survivin, 14 (28%) for Bcl-2, 13 (26%) for Cox-2, 19/45 (42%) for p73, 10/45 (24%) for p53. Telomerase activity was highest in tumors with the poorest grade. A positive correlation was seen between survivin and Bcl-2, survivin and tumor stage, Bcl-2 and Cox-2, p73 and p53 and p73 and the AI. Despite the overexpression of various antiapoptotic proteins, no significant difference was observed in the AI between tumors and controls. Conclusions: Since deregulation of the apoptotic pathway appears to occur in cervical cancer, some apoptosis-related proteins could be assessed as potential markers for progression/prognosis in cervical cancer. Additionally, newer proteins such as p73 may play a compensatory role for the nonfunctional proteins such as p53.

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Tumor apoptosis in cervical cancer: Its role as a prognostic factor in 42 radiotherapy patients

Cited by 16 publications

References 26 publications

Apoptosis Genes and Resistance to Cancer Therapy: What Does the Experimental and Clinical Data Tell Us?

Apoptosis Genes and Resistance to Cancer Therapy: What Does the Experimental and Clinical Data Tell Us?

Molecular profiling of uterine cervix carcinoma: an overview with a special focus on rationally designed target-based anticancer agents

Evaluation of Expression of Apoptosis-Related Proteins and Their Correlation with HPV, Telomerase Activity, and Apoptotic Index in Cervical Cancer

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