MKI67 (Marker of proliferation Ki-67)

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.

We report the first known case of a pancreatic NET with response to venetoclax. BCL2 expression correlated with high MKI67 expression, worse survival, and a highly immune-enriched microenvironment.

The expression is also significantly associated with key clinical variables. Our results suggest that MKI67 and RACGAP1 could serve as promising biomarkers for detecting and predicting HCC caused by HBV/HCV via lactylation, opening a new direction for immune-targeted therapies.

Moxibustion inhibited the proliferation of colon tumors in CAC mice, inhibited the activation of the tumor-promoting signaling pathway KDM4D/β-Catenin, and improved lipid metabolism disorders in the colon, thus providing a promising strategy for the clinical adjuvant treatment of colorectal cancer.

Extrachromosomal amplification of MYC-paralogs shapes suppressive TIME, identifying potential subgroup of immunotherapy resistant patients.

It, however, showed no direct relationship between age and Ki67 proliferative index. Determination of the Ki67 proliferative index is recommended for routine assessment of prostate cancer patients to help in risk stratification and instituting treatment plans.

Our comprehensive analysis may supply useful guidance on MKI67 applicability across various cancer types. These observed results contribute to the promise of MKI67 in a realistic clinical setting and improve the outcomes of cancer patients.