|
Abnormal renal function
|
0.100 |
Biomarker
|
phenotype |
HPO |
|
|
|
|
Abnormality of the lymphatic system
|
0.100 |
Biomarker
|
disease |
HPO |
|
|
|
|
Actinic keratosis
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
We searched for p16, Cdk4 and p53 gene mutations in 20 squamous cell carcinomas (SSCs), 1 actinic keratosis (AK), and 28 basal cell carcinomas (BCCs), using PCR-SSCP.
|
10498902 |
1999 |
|
Acute leukemia
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
This study showed that the expression of miR‑34a negatively correlates with the expression of CDK4 and MYB in pediatric patients with acute leukemia. miRNA‑34a downregulates the expression of the CDK4, MYB and SIRT1 genes in vitro; it may thus represent a novel therapeutic target for acute leukemia.
|
24504520 |
2014 |
|
Acute lymphocytic leukemia
|
0.050 |
AlteredExpression
|
disease |
BEFREE |
The sorted populations and B-lineage ALL cell lines (BLIN-1, 2, 3, 4) were examined for expression of cyclins, CDK, and CKI by reverse transcriptase polymerase chain reaction (RT-PCR) and Western blotting.RT-PCR analysis showed that cyclin D2, cyclin D3, CDK4, and CDK6 were ubiquitously expressed in normal B-cell development and in the BLIN ALL cell lines.
|
11301189 |
2001 |
|
Acute lymphocytic leukemia
|
0.050 |
Biomarker
|
disease |
BEFREE |
This investigation demonstrated that cyclin D1 and cdk4 were the most important prognostic factors for children with ALL, and that the combination of them showed the strongest prognostic relevance.
|
9355972 |
1997 |
|
Acute lymphocytic leukemia
|
0.050 |
AlteredExpression
|
disease |
BEFREE |
Since most hematological malignancies-except ALL-are infrequently associated with p16INK4A and retinoblastoma (Rb) gene alteration it seems worthwhile to explore cdk4 and cdk6 expression to determine whether or not the disruption of the p16INK4A/Rb/cdk4/cdk6 regulatory loop might play a role in their pathogenesis.
|
7630199 |
1995 |
|
Acute lymphocytic leukemia
|
0.050 |
Biomarker
|
disease |
BEFREE |
These findings provide novel insight into interphase microtubule function and, from a therapy standpoint, strongly caution against combining microtubule targeting agents and CDK4/6 inhibitors for ALL.
|
29995568 |
2018 |
|
Acute lymphocytic leukemia
|
0.050 |
Biomarker
|
disease |
BEFREE |
Mutation of p16, p21 or cyclin dependent kinase 4 is rare in acute lymphoblastic leukaemia.
|
9827921 |
1998 |
|
Acute respiratory failure
|
0.030 |
Biomarker
|
disease |
BEFREE |
The INK4a-ARF (CDKN2A) locus on chromosome 9p21 encodes two tumour suppressor proteins, p16(INK4a) and p14(ARF), which act as upstream regulators of the Rb-CDK4 and p53 pathways.
|
12375265 |
2002 |
|
Acute respiratory failure
|
0.030 |
GeneticVariation
|
disease |
BEFREE |
Thus, whereas germ-line mutations of PTEN, p53, p16(INK4A)/p14(ARF), and CDK4 are not common events in familial glioma, outside of familial cancer syndromes, point mutations of p53 and hemizygous deletions and other rearrangements of the p16(INK4A)/p14(ARF) tumor suppressor region may account for a subset of familial glioma cases.
|
10797439 |
2000 |
|
Acute respiratory failure
|
0.030 |
Biomarker
|
disease |
BEFREE |
The INK4a-ARF (CDKN2A)- locus on chromosome 9p21 encodes for two tumour suppressor proteins, p16(INK4a) and p14(ARF), that act as upstream regulators of the Rb-CDK4 and p53 pathways.
|
11704835 |
2001 |
|
Adenocarcinoma
|
0.020 |
Biomarker
|
group |
BEFREE |
Furthermore, retention of CDK4 in these TA-like pituitary cells synergizes with loss of p27(Kip1) to induce pituitary adenocarcinomas.
|
18172308 |
2008 |
|
Adenocarcinoma
|
0.020 |
AlteredExpression
|
group |
BEFREE |
Strong CDK4 expression in islets of Langerhans predicted poor relapse-free survival (RFS) (HR 2.874; 95% CI 1.261-6.550; p = .012) and within T3-4 tumors CDK4 expression in adenocarcinoma cells also predicted poor disease-free survival (DFS) (RR 2.148; 95% CI 1.081-4.272; p = .029).
|
29735403 |
2018 |
|
Adenocarcinoma Of Esophagus
|
0.020 |
AlteredExpression
|
disease |
BEFREE |
CDK4/6 dual inhibitor abemaciclib demonstrates compelling preclinical activity against esophageal adenocarcinoma: a novel therapeutic option for a deadly disease.
|
29245989 |
2017 |
|
Adenocarcinoma Of Esophagus
|
0.020 |
Biomarker
|
disease |
BEFREE |
CDK4 gene amplification does not seem to play a role in the development of oesophageal adenocarcinoma.
|
11299766 |
2001 |
|
Adenocarcinoma of lung (disorder)
|
0.170 |
Biomarker
|
disease |
BEFREE |
These data suggest CDK4 is a promising target for development of anti-cancer drugs and CINK4 combined with paclitaxel may be an effective therapeutic strategy for enhancing anti-tumor efficacy in KRAS mutation-positive lung adenocarcinoma.
|
23792647 |
2013 |
|
Adenocarcinoma of lung (disorder)
|
0.170 |
AlteredExpression
|
disease |
BEFREE |
Nevertheless, when compared with the combined human ACs, 39 genes with similar expression changes in murine lung tumors and human ACs/LCCs were identified, such as the oncogene-related BCL7B, the cell cycle regulator CDK4, and the proapoptotic Endophilin B1.
|
14647414 |
2004 |
|
Adenocarcinoma of lung (disorder)
|
0.170 |
GeneticVariation
|
disease |
BEFREE |
We transduced two primary CAF cultures (CAFs-608 and CAFs-621) from lung adenocarcinoma with human telomerase reverse transcriptase (hTERT), mutant forms of cyclin dependent kinase 4 (CDK4R24C) independently and in combination (hTERT/CDK4R24C).
|
28364361 |
2017 |
|
Adenocarcinoma of lung (disorder)
|
0.170 |
AlteredExpression
|
disease |
BEFREE |
In agreement with higher SOX9 expression level in lung adenocarcinoma, the p21 mRNA level was significantly lower in tumors than that in normal tissues, whereas the opposite was true for CDK4, supporting the notion that SOX9 negatively and positively regulated p21 and CDK4, respectively.
|
20651055 |
2010 |
|
Adenocarcinoma of lung (disorder)
|
0.170 |
GeneticVariation
|
disease |
BEFREE |
However, these profiles did not segregate by histology (lung adenocarcinoma-appendiceal cancer (KRAS G12D and GNAS R201C), and lung adenocarcinoma-liposarcoma (CDK4 and MDM2 amplification pairs)).
|
26418953 |
2015 |
|
Adenocarcinoma of lung (disorder)
|
0.170 |
GeneticVariation
|
disease |
CLINVAR |
Identifying recurrent mutations in cancer reveals widespread lineage diversity and mutational specificity.
|
26619011 |
2016 |
|
Adenocarcinoma of lung (disorder)
|
0.170 |
GeneticVariation
|
disease |
BEFREE |
In the remaining cohort of lung AD without these known drivers, 273 cancer-related genes were altered in at least 0.1% of cases, including STK11 (21%), NF1 (13%), MYC (9.8%), RICTOR (6.4%), PIK3CA (5.4%), CDK4 (4.3%), CCND1 (4.0%), BRCA2 (2.5%), NRAS (2.3%), BRCA1 (1.7%), MAP2K1 (1.2%), HRAS (0.7%), NTRK1 (0.7%), and NTRK3 (0.2%).
|
27151654 |
2016 |
|
Adenocarcinoma of lung (disorder)
|
0.170 |
Biomarker
|
disease |
BEFREE |
Mega-analysis revealed that three LA-associated genes, such as solute carrier family 2 member 1 (SLC2A1), endothelial PAS domain protein 1 (EPAS1) and cyclin-dependent kinase 4 (CDK4), were significantly associated with LSCC (P<1.60×10<sup>-8</sup>), with multiple potential pathways identified by functional pathway analysis, which were further validated by co-expression analysis.
|
31516564 |
2019 |
|
Adenoma
|
0.030 |
Biomarker
|
group |
BEFREE |
The authors hypothesize that inhibition of the CDK4/6 pathway by palbociclib contributed to adenoma regression in this patient, and that palbociclib may represent a possible adjuvant therapy for the treatment of nonfunctioning pituitary adenomas.
|
29852762 |
2018 |