Mucins in cancer: function, prognosis and therapy
- D. Kufe
- BiologyNature Reviews. Cancer
- 1 December 2009
The findings that certain transmembrane mucins induce transformation and promote tumour progression have provided the experimental basis for demonstrating that inhibitors of their function are effective as anti-tumour agents in preclinical models.
Translocation of SAPK/JNK to Mitochondria and Interaction with Bcl-xL in Response to DNA Damage*
Findings indicate that translocation of SAPK to mitochondria is functionally important for interactions with Bcl-xL in the apoptotic response to genotoxic stress.
p73 is regulated by tyrosine kinase c-Abl in the apoptotic response to DNA damage
It is shown that c-Abl binds to p73 in cells, interacting through its SH3 domain with the carboxy-terminal homo-oligomerization domain of p73, and that p73 participates in the apoptotic response to DNA damage.
Blockage of the vascular endothelial growth factor stress response increases the antitumor effects of ionizing radiation.
It is reported that VEGF expression is induced in Lewis lung carcinomas (LLCs) both in vitro and vivo after exposure to ionizing radiation (IR) and in human tumor cell lines (Seg-1 esophageal adenocarcinoma, SQ20B squamous cell carcinoma, T98 and U87 glioblastomas, and U1 melanoma) in vitro.
Induction of antitumor activity by immunization with fusions of dendritic and carcinoma cells
The results show that the fusion cells stimulate naive T cells in the primary mixed lymphocyte reaction (MLR) and induce MC38 tumor-specific CTLs in vivo and induces rejection of established metastases.
The Epidermal Growth Factor Receptor Regulates Interaction of the Human DF3/MUC1 Carcinoma Antigen with c-Src and β-Catenin*
It is demonstrated that MUC1 associates constitutively with the epidermal growth factor receptor (EGF-R) in human ZR-75-1 breast carcinoma cells and a novel role for EGF-R in regulating interactions of M UC1 with c-Src and β-catenin is supported.
Blockade of the Vascular Endothelial Growth Factor Stress Response Increases the Antitumor Effects of Ionizing Radiation
It is reported that VEGF expression is induced in Lewis lung carcinomas (LLCs) both in vitro and in vivo after exposure to ionizing radiation (IR) and in human tumor cell lines (Seg-1 esophageal adenocarcinoma, SQ20B squamous cell carcinoma, T98 and U87 glioblastomas, and U1 melanoma) in vitro.
Increased tumor necrosis factor alpha mRNA after cellular exposure to ionizing radiation.
- D. Hallahan, D. Spriggs, M. Beckett, D. Kufe, R. Weichselbaum
- Biology, MedicineProceedings of the National Academy of Sciences…
- 1 December 1989
It is reported that tumor necrosis factor alpha mRNA is increased after treatment with x-rays in certain human sarcoma cells, and production of TNF-alpha may add to radiation lethality through autocrine and paracrine mechanisms.
Proteolytic Activation of Protein Kinase C δ by an ICE/CED 3-like Protease Induces Characteristics of Apoptosis
The present studies demonstrate that full-length PKCδ is cleaved at DMQD330N to a catalytically active fragment by the cysteine protease CPP32, and suggest that proteolytic activation of PKC δ by a C PP32-like protease contributes to phenotypic changes associated with apoptosis.
Regulation of Rad51 Function by c-Abl in Response to DNA Damage*
- Zhi-Min Yuan, Yinyin Huang, D. Kufe
- Biology, ChemistryJournal of Biological Chemistry
- 13 February 1998
These findings represent the first demonstration that Rad51 is regulated by phosphorylation and support a functional role for c-Abl in regulating Rad51-dependent recombination in the response to DNA damage.