Correlation of p16 Expression on Cancer and Stromal Cells With Clinicopathologic and Immunohistochemical Features of Lobular Breast Carcinoma

Harbhajanka, Aparna; Lamzabi, Ihab; Bitterman, Pincas; Reddy, Vijaya B.; Ghai, Ritu; Gattuso, Paolo

doi:10.1097/pai.0000000000000679

Cited by 8 publications

(7 citation statements)

References 15 publications

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“…Additionally, restoration of p16 expression in stromal fibroblasts suppressed cancer cell migration and invasion. Thus, these findings proposed positive stromal p16 expression as a treatment strategy to prevent nodal or distant metastasis [98].…”

Section: Tumor Suppressive Components Of Cell Cyclementioning

confidence: 92%

Oncogenic and Tumor Suppressive Components of the Cell Cycle in Breast Cancer Progression and Prognosis

Garg¹,

Sandberg

Goel

et al. 2021

Pharmaceutics

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Cancer, a disease of inappropriate cell proliferation, is strongly interconnected with the cell cycle. All cancers consist of an abnormal accumulation of neoplastic cells, which are propagated toward uncontrolled cell division and proliferation in response to mitogenic signals. Mitogenic stimuli include genetic and epigenetic changes in cell cycle regulatory genes and other genes which regulate the cell cycle. This suggests that multiple, distinct pathways of genetic alterations lead to cancer development. Products of both oncogenes (including cyclin-dependent kinase (CDKs) and cyclins) and tumor suppressor genes (including cyclin-dependent kinase inhibitors) regulate cell cycle machinery and promote or suppress cell cycle progression, respectively. The identification of cyclins and CDKs help to explain and understand the molecular mechanisms of cell cycle machinery. During breast cancer tumorigenesis, cyclins A, B, C, D1, and E; cyclin-dependent kinase (CDKs); and CDK-inhibitor proteins p16, p21, p27, and p53 are known to play significant roles in cell cycle control and are tightly regulated in normal breast epithelial cells. Following mitogenic stimuli, these components are deregulated, which promotes neoplastic transformation of breast epithelial cells. Multiple studies implicate the roles of both types of components—oncogenic CDKs and cyclins, along with tumor-suppressing cyclin-dependent inhibitors—in breast cancer initiation and progression. Numerous clinical studies have confirmed that there is a prognostic significance for screening for these described components, regarding patient outcomes and their responses to therapy. The aim of this review article is to summarize the roles of oncogenic and tumor-suppressive components of the cell cycle in breast cancer progression and prognosis.

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Section: Tumor Suppressive Components Of Cell Cyclementioning

confidence: 92%

Oncogenic and Tumor Suppressive Components of the Cell Cycle in Breast Cancer Progression and Prognosis

Garg¹,

Sandberg

Goel

et al. 2021

Pharmaceutics

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“…On the contrary, p16 was not or was weakly expressed in cancer cells [ 46 ]. Furthermore, stromal p16 overexpression was observed in atypical polypoid adenomyoma [ 47 ], breast carcinoma [ 48 , 49 ], and adult granulosa cell tumors of the ovary [ 50 ], suggesting the occurrence of stromal cell senescence. In one other study, senescent T-cell infiltration was identified in the stromal compartment of colorectal cancer tissues [ 51 ].…”

Section: The Discovery Of Senescent Stromamentioning

confidence: 99%

Senescent Stromal Cells in the Tumor Microenvironment: Victims or Accomplices?

Huang

et al. 2023

Cancers

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Cellular senescence is a unique cellular state. Senescent cells enter a non-proliferative phase, and the cell cycle is arrested. However, senescence is essentially an active cellular phenotype, with senescent cells affecting themselves and neighboring cells via autocrine and paracrine patterns. A growing body of research suggests that the dysregulation of senescent stromal cells in the microenvironment is tightly associated with the development of a variety of complex cancers. The role of senescent stromal cells in impacting the cancer cell and tumor microenvironment has also attracted the attention of researchers. In this review, we summarize the generation of senescent stromal cells in the tumor microenvironment and their specific biological functions. By concluding the signaling pathways and regulatory mechanisms by which senescent stromal cells promote tumor progression, distant metastasis, immune infiltration, and therapy resistance, this paper suggests that senescent stromal cells may serve as potential targets for drug therapy, thus providing new clues for future related research.

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“…IHC was performed on the collected samples as previously described. 15 Briefly, the slides of LUAD tissues were dewaxed with xylene and rehydrated with graded ethanol. Then, heat mediated antigen retrieval was conducted with citrate buffer for UVE2V2 detection and with ethylene diamine tetraacetic acid buffer for PD-L1 detection.…”

Section: Immunohistochemistry (Ihc) and Ihc Scoringmentioning

confidence: 99%

UBE2V2 Positively Correlates With PD-L1 Expression and Confers Poor Patient Survival in Lung Adenocarcinoma

Hua

Liu

Sheng

et al. 2021

Applied Immunohistochemistry &Amp; Molecular Morphology

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This research aims to explore the diagnostic and prognostic value of ubiquitin-conjugating enzyme E2 variant 2 (UBE2V2) in lung adenocarcinoma (LUAD). The expression of UBE2V2 in clinical specimens was evaluated by bioinformatics analyses and immunohistochemistry. Bioinformatics analyses relying on the The Cancer Genome Atlas (TCGA) database suggested the elevated UBE2V2 mRNA levels in LUAD in comparison to adjacent normal tissues. Gene set enrichment analyses and gene ontology term enrichment analyses further showed the involvement of UBE2V2 in the modulation of cell cycle and immune associated signaling. The correlation analyses in TCGA LUAD data set revealed the positive correlation between UBE2V2 and CCNE1, CCNE2, CCNA2, CCNB1, CCNB2, cyclin-dependent kinase (CDK)2, CDK4, and CDK1 at the mRNA level. Moreover, UBE2V2 mRNA levels were positively correlated with PD-L1 mRNA levels, the T classification, and poor survival of LUAD patients, and were negatively correlated with type II interferon response. Consistent with the results obtained from TCGA data mining, immunohistochemistry demonstrated that UBE2V2 protein levels were upregulated in LUAD in comparison to normal tissues and were positively associated with T classification. Intriguingly, a positive correlation between UBE2V2 protein levels and PD-L1 expression was also elucidated in clinical samples. Besides, UBE2V2 expression indicated a poor prognosis in LUAD patients. Our study found that UBE2V2 was identified as an independent prognostic indicator for LUAD and might serve as an alternative target for LUAD treatment.

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Correlation of p16 Expression on Cancer and Stromal Cells With Clinicopathologic and Immunohistochemical Features of Lobular Breast Carcinoma

Cited by 8 publications

References 15 publications

Oncogenic and Tumor Suppressive Components of the Cell Cycle in Breast Cancer Progression and Prognosis

Oncogenic and Tumor Suppressive Components of the Cell Cycle in Breast Cancer Progression and Prognosis

Senescent Stromal Cells in the Tumor Microenvironment: Victims or Accomplices?

UBE2V2 Positively Correlates With PD-L1 Expression and Confers Poor Patient Survival in Lung Adenocarcinoma

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