Differential expression of neuroendocrine markers, TTF-1, p53, and Ki-67 in cervical and pulmonary small cell carcinoma

Liu, Haiping; Zhang, Yan; Chang, Jianfang; Liu, Zhitao; Tang, Ning

doi:10.1097/md.0000000000011604

Cited by 13 publications

(13 citation statements)

References 21 publications

(22 reference statements)

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“…Some studies have shown that 33%–84% of small-cell cervical carcinomas exhibit diffuse nuclear positivity for thyroid transcription factor-1 (TTF-1) 21 25–27. Liu et al 28 compared different expression of neuroendocrine markers, TTF-1, p53, and Ki-67 in 23 cases of cervical small-cell and 56 cases of pulmonary small-cell carcinomas using immunohistochemistry. The TTF-1 expression of small-cell carcinoma of the lung showed significantly higher diffuse and strong positivity in tumor cell nuclei than the cervical counterpart (p=0.003).…”

Section: Immunohistochemistrymentioning

confidence: 99%

Updates and management algorithm for neuroendocrine tumors of the uterine cervix

Salvo

Martín

Gonzales

et al. 2019

Int J Gynecol Cancer

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Neuroendocrine carcinomas of the cervix account for less than 2% of all invasive cervical cancers and are classified as low-grade (carcinoid, atypical carcinoid tumor) or high-grade (known as small- and large-cell) neuroendocrine carcinomas. There are increasing data showing that cervical neuroendocrine carcinomas may be associated with the human papillomavirus (HPV), especially HPV18, and most will stain positive for p16. Immunohistochemistry markers such as synaptophysin and CD56 are the most sensitive markers. Although there are no commonly associated mutations, PIK3CA, KRAS, and TP53 are the most frequently found mutations in neuroendocrine tumors. Neuroendocrine cervical carcinomas are exceedingly aggressive tumors with a high tendency for nodal involvement and distant metastases. Age, lymph node metastases, smoking, pure small-cell histology, and tumor size are independent prognostic factors. Overall, the 5-year survival rate is 36% and the median overall survival ranges between 22 and 25 months. Treatment options are often extrapolated from small-cell lung cancer and limited retrospective studies. The preferred treatment is a multimodal approach of surgery, chemoradiation, and systemic chemotherapy. The most common chemotherapy regimen used as initial therapy is a combination of cisplatin and etoposide. In the setting of recurrent disease, a combination of topotecan, paclitaxel, and bevacizumab has demonstrated favorable outcomes. Multicenter tumor registries, such as the Neuroendocrine Cervical Tumor Registry (NeCTuR), are an opportunity to evaluate patterns of disease treatment and oncologic outcomes.

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Section: Immunohistochemistrymentioning

confidence: 99%

Updates and management algorithm for neuroendocrine tumors of the uterine cervix

Salvo

Martín

Gonzales

et al. 2019

Int J Gynecol Cancer

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“…The literature search identified 39 articles on IHC staining of NE markers fulfilling the criteria (see Materials and Methods). [3][4][5][6][8][9][10][11][12][13][14][15][17][18][19] In Table 4, the accumulated data from these and the current investigation are presented, also specifying data for any/at least 1% (any positivity and 1% stained tumor cells were here considered equal) and at least 10% stained tumor cells as the cutoff for a positive staining, respectively (data not provided in all studies). More details on the identified articles are found in Supplemental (Figure 4, A and B).…”

Section: Review Of the Literaturementioning

confidence: 99%

“…1 A positive NE marker is not strictly required for SCLC, though most cases do express at least 1 such marker. 1,[3][4][5][6][7][8][9] Carcinoid tumors are typically positive for all, or at least several, NE markers. 1,[3][4][5][9][10][11] Neuroendocrine markers may also be expressed in NSCLC, [3][4][5][12][13][14][15] which may cause diagnostic problems, and staining with NE markers is only recommended if NE morphology is evident.…”

mentioning

confidence: 99%

Diagnostic Value of Insulinoma-Associated Protein 1 (INSM1) and Comparison With Established Neuroendocrine Markers in Pulmonary Cancers

Staaf

Tran²,

Söderlund³

et al. 2020

Archives of Pathology &Amp; Laboratory Medicine

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Context.— The diagnostic distinction of pulmonary neuroendocrine (NE) tumors from non–small cell lung carcinomas (NSCLCs) is clinically relevant for prognostication and treatment. Diagnosis is based on morphology and immunohistochemical staining. Objective.— To determine the diagnostic value of insulinoma-associated protein 1 (INSM1), in comparison with established NE markers, in pulmonary tumors. Design.— Fifty-four pulmonary NE tumors and 632 NSCLCs were stained for INSM1, CD56, chromogranin A, and synaptophysin. In a subset, gene expression data were available for analysis. Also, 419 metastases to the lungs were stained for INSM1. A literature search identified 39 additional studies with data on NE markers in lung cancers from the last 15 years. Seven of these included data on INSM1. Results.— A positive INSM1 staining was seen in 39 of 54 NE tumors (72%) and 6 of 623 NSCLCs (1%). The corresponding numbers were 47 of 54 (87%) and 14 of 626 (2%) for CD56, 30 of 54 (56%) and 6 of 629 (1%) for chromogranin A, and 46 of 54 (85%) and 49 of 630 (8%) for synaptophysin, respectively. Analysis of literature data revealed that CD56 and INSM1 were the best markers for identification of high-grade NE pulmonary tumors when considering both sensitivity and specificity, while synaptophysin also showed good sensitivity. INSM1 gene expression was clearly associated with NE histology. Conclusions.— The solid data of both our and previous studies confirm the diagnostic value of INSM1 as a NE marker in pulmonary pathology. The combination of CD56 with INSM1 and/or synaptophysin should be the first-hand choice to confirm pulmonary high-grade NE tumors. INSM1 gene expression could be used to predict NE tumor histology.

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“…Current studies have shown that E6 proteins of HPV16 and HPV18 can bind to wild-type p53 proteins, and with the participation of E6-related proteins, promote the degradation of p53 proteins, eventually lead to the reduction of p53-induced G1 phase arrest in cell cycle, thus completing DNA synthesis and promoting cell proliferation [31,32] . HPV infection also destroys normal sex hormone function, which weakens the antiestrogen effect of progesterone in endometrial lesions and increases the malignant transformation of cells [33] . HPV can induce the cell cycle activity of Ki67 positive cells.…”

Section: Table 4: the Expression Of Er Pr P53 And Ki67 In Patients mentioning

confidence: 99%

Correlation between ER, PR, P53, Ki67 Expression and High-Risk HPV Infection in Patients with Different Levels of Cervical Intraepithelial Neoplasia

Wang¹,

Jin²,

Ni³

et al. 2020

pharmaceutical-sciences

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Wang et al.: Correlation between ER, PR, P53, Ki67 Expression and High-risk HPV Infection To investigate the correlation between high-risk human papillomavirus infection and the expression of ER, PR, P53 and Ki67 in patients with different grades of cervical intraepithelial neoplasia. A retrospective study was conducted in which from June 2016 to June 2018, 140 specimens of cervical intraepithelial neoplasia were collected from the pathology department of the Beijing Tongren Hospital that included 40 specimens of cervical intraepithelial neoplasia1, 50 specimens of cervical intraepithelial neoplasia2 and 50 specimens of cervical intraepithelial neoplasia1. The expression of ER, PR, p53 and Ki67 were determined by immunohistochemistry. High-risk human papillomavirus infections were detected by polymerase chain reaction fluorescence quantification and were given the correlation analysis. Results of the 140 specimens indicated the rates of human papillomavirus16 and human papillomavirus18 in cervical intraepithelial neoplasia1 specimens were 27.5 and 25.0 % respectively, in cervical intraepithelial neoplasia2 specimens were 64.0 and 60.0 %, respectively and in cervical intraepithelial neoplasia3 specimens were 90.0 and 92.0 % respectively, the difference were statistically significant (p<0.05). There was no significant correlation between human papillomavirus 16 and human papillomavirus 18 positive rate and patient age, tissue differentiation, and tumour size. With the increasing cervical intraepithelial neoplasia grade, the rate of ER, PR, p53 and Ki67 expression in specimens was also increased significantly (p<0.05). Pearson correlation analysis showed there were positive correlation between the rates of human papillomavirus 16 and human papillomavirus 18 and the rates of ER, PR, p53 and Ki67 expression (p<0.05). In conclusion with increasing cervical intraepithelial neoplasia level, rate of high-risk human papillomavirus infection increased along with increased rate of expression of ER, PR, p53 and Ki67.

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Differential expression of neuroendocrine markers, TTF-1, p53, and Ki-67 in cervical and pulmonary small cell carcinoma

Cited by 13 publications

References 21 publications

Updates and management algorithm for neuroendocrine tumors of the uterine cervix

Updates and management algorithm for neuroendocrine tumors of the uterine cervix

Diagnostic Value of Insulinoma-Associated Protein 1 (INSM1) and Comparison With Established Neuroendocrine Markers in Pulmonary Cancers

Correlation between ER, PR, P53, Ki67 Expression and High-Risk HPV Infection in Patients with Different Levels of Cervical Intraepithelial Neoplasia

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