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1
Replacement of Fhit in cancer cells suppresses tumorigenicity.
Proc Natl Acad Sci U S A. 1997 Dec 9;94(25):13771-6. doi: 10.1073/pnas.94.25.13771.
2
Fhit, a putative tumor suppressor in humans, is a dinucleoside 5',5"'-P1,P3-triphosphate hydrolase.
Biochemistry. 1996 Sep 10;35(36):11529-35. doi: 10.1021/bi961415t.
5
Control of 5',5'-dinucleoside triphosphate catabolism by APH1, a Saccharomyces cerevisiae analog of human FHIT.
J Bacteriol. 1998 May;180(9):2345-9. doi: 10.1128/JB.180.9.2345-2349.1998.
7
FHITness and cancer.
Oncol Res. 1998;10(7):341-5.
9
Translocation breakpoints in FHIT and FRA3B in both homologs of chromosome 3 in an esophageal adenocarcinoma.
Genes Chromosomes Cancer. 2001 Mar;30(3):292-8. doi: 10.1002/1098-2264(2000)9999:9999<::aid-gcc1095>3.0.co;2-f.
10
The role of deletions at the FRA3B/FHIT locus in carcinogenesis.
Recent Results Cancer Res. 1998;154:200-15. doi: 10.1007/978-3-642-46870-4_12.

引用本文的文献

1
Inhibition of GSK3β is synthetic lethal with FHIT loss in lung cancer by blocking homologous recombination repair.
Exp Mol Med. 2025 Feb;57(1):167-183. doi: 10.1038/s12276-024-01374-0. Epub 2025 Jan 6.
3
Integrated analysis of gene alterations in cancer.
Cell Cycle. 2024 Jan;23(1):92-113. doi: 10.1080/15384101.2024.2304509. Epub 2024 Jan 18.
4
Expression of Tumor Suppressor Is Regulated by the -SNAIL Axis in Human Lung Adenocarcinoma.
Int J Mol Sci. 2023 Nov 30;24(23):17011. doi: 10.3390/ijms242317011.
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Molecular Biology of the Gene That Spans Chromosomal Fragile Site .
Cells. 2021 Jun 29;10(7):1637. doi: 10.3390/cells10071637.
10
Effects of FHIT gene on proliferation and apoptosis of osteosarcoma cells.
Oncol Lett. 2019 Jan;17(1):877-882. doi: 10.3892/ol.2018.9696. Epub 2018 Nov 14.

本文引用的文献

1
The FHIT gene, a multiple tumor suppressor gene encompassing the carcinogen sensitive chromosome fragile site, FRA3B.
Biochim Biophys Acta. 1997 Jun 7;1332(3):M65-70. doi: 10.1016/s0304-419x(97)00009-7.
7
Chromosome 3p14 homozygous deletions and sequence analysis of FRA3B.
Hum Mol Genet. 1997 Feb;6(2):193-203. doi: 10.1093/hmg/6.2.193.

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