MKI67 (Marker of proliferation Ki-67)

Further mechanistic investigations indicate that the scaffold protein ANKHD1 directly interacts with RBM39 to facilitate the splicing and expression of MKI67 pre-mRNA, thereby driving the malignant progression of NNK-exposed CRC cells. In summary, this study provides novel insights, proposing that targeting the p300-mediated H3K27ac modification pathway to suppress ANKHD1 expression may represent a promising therapeutic strategy and prognostic marker for CRC patients with a history of smoking.

Our data suggested that expression of nuclear CCND1 was associated with clinopathological and biological markers that are involved in proliferation and survival in PCa. Cytoplasmic CCND1 shared some of these findings, but they were less statistically significant. These findings provide evidence that increased CCND1 promotes proliferation and facilitate disease progression, especially in the nucleus. Cyclin D1 might become a potential biomarker for the prediction of biochemical recurrence in PCa.

High MKI67 expression identifies highly proliferative tumors that are associated with genomic instability and immune activity and is associated with higher pCR rates following neoadjuvant chemotherapy in ER+/HER2- BC.

This study analyzed the gene expression characteristics of 11 types of epithelial cells during the malignant progression of CRC. KCNMA1+ and MKI67+ epithelial subpopulations are important indicators for the malignant progression of CRC.

Further analysis identified TFDP1 as a key gene associated with SASM and adverse prognosis, which was upregulated in tumor tissues and promoted ESCC cell proliferation in vitro. Overall, our study delineates stemness‑related tumor heterogeneity in ESCC, proposes a prognostic scoring system with immunological relevance, and highlights TFDP1 as a potential therapeutic target.

We did not find any MP effects on the claudins, mucins, proapoptotic factor Bax, or on the proliferation marker Mki67 gene expression in the medial colon, nor on the serum level of TNFα, IL-1β, IL-6, and IL-10 cytokines. Thus, MPs promote the CAC development in mice by exacerbating intestinal local inflammation and damaging the epithelial barrier, and MPs may represent a potential environmental cofactor contributing to CAC risk.

Diverse PD-1, CD163, and FOXP3 profiles were observed in primary and metastatic microenvironments of prostate cancer. These findings may contribute to the development of personalized therapeutic strategies and novel prognostic tools beyond conventional histological and TNM staging.

The combination treatment had an IC₅₀ of 78 µg/mL in A549 LC cells and significantly reduced cell proliferation, migration, and TOP2A gene expression, as assessed by MTT assay, wound healing assay, and RT-PCR. The results corroborate the computational predictions and support the utility of EGCG and hesperetin in targeting LC at the cellular level.

A stem cell-based prognostic model (SCPM) was constructed and validated, enabling accurate prediction of survival and immunotherapy response in LUAD patients. Patients with immunologically "cold" tumors, as identified by the SCPM, may benefit from alternative therapeutic strategies.

Elevated expression of MRPL15 advanced the proliferation of LUAD cells; conversely, downregulation of MRPL15 restrained the proliferation of LUAD cells. In conclusion, MRPL15 promotes the proliferation of LUAD cells, and MRPL15 may serve as a potential marker or a therapeutic target for LUAD.

MKI67 expression was slightly increased in HT-29 and BJ, while decreased in Caco-2 cells. Our study shed new light on the cellular processes occurring under the influence of alkalization, but it is difficult to assess what role alkalization may play in the potential therapy of CRC, therefore, further studies are necessary.

Gene expression analyses showed an increase in MKI-67 expression in SF wild-type patients, but no differences were observed in several immune-related genes including IL7R and PD-L1. Addition of durvalumab to azacitidine did not improve ORR or OS among older patients with newly diagnosed AML and HR-MDS independent of SF mutation status.Trial registration: NCT02775903.