1.The role of fos oncogene protein on the induction of differentiation of F9 teratocarcinoma cells.
Soo Kyung BAE ; Chang Mo KANG ; Byung Chae PARK ; Kyoo Won KIM
Journal of the Korean Cancer Association 1993;25(1):47-53
No abstract available.
Oncogene Proteins*
;
Oncogenes*
;
Teratocarcinoma*
3.Experimental study of the expression of c-myc, c-fos and proto-oncogenes on hypertrophic and scars.
Zhenfu HU ; Lisheng LOU ; Shengkang LUO
Chinese Journal of Plastic Surgery 2002;18(3):165-167
OBJECTIVETo investigate the correlation between the expression of key proto-oncogenes playing major roles in tumorigenic process and abnormal sarring.
METHODSImmunohistochemical technique was performed to detect the expressions of c-myc, c-fos and ras p21 proteins on hypertrophic scars, keloids and normal skin. Image analysis was used to compare their quantitative difference of expression.
RESULTSC-myc and c-fos expressions on the nucleus of fibroblasts of hypertrophic and keloid scars were significantly higher than normal skin controls, and there was no difference between the two lesions. Ras p21 expression was not detected on the fibroblasts of hypertrophic and keloid scars.
CONCLUSION1. c-myc and c-fos oncogenes are activated on hypertrophic and keloid scars, which may contribute to proliferation and differentiation of fibroblasts, synthesis and degradation of collagen and regulation of cytokines and induce abnormal scarring, the mechanisms of their effects remain to be further studied. 2. Ras gene may not mutate or its mutations may not play a major role in the process of abnormal scarring. 3. Only part of proto-oncogenes moderately expressed on abnormal scars. The expression of multiple oncogenes does not coexist in abnormal scars may be the cause of their less chances to induce malignant transformation.
Cicatrix, Hypertrophic ; metabolism ; Humans ; Immunohistochemistry ; Proto-Oncogene Proteins c-fos ; analysis ; Proto-Oncogene Proteins c-myc ; analysis ; Proto-Oncogene Proteins p21(ras) ; analysis ; Proto-Oncogenes
4.Advances in the Diagnosis and Therapy of Double-hit Lymphoma--Review.
Xin-Xin WEI ; Qing ZHAO ; De-Peng LI ; Yi-Hong HUANG
Journal of Experimental Hematology 2019;27(4):1311-1315
Abstract Double-hit lymphoma (DHL) is a high-grade B-cell lymphoma with MYC and BCL-2/BCL-6 rearrangement, which is a invasive disease with a poor prognosis. FISH is the most important diagnostic method. There is no standard protocol for this disease yet. New therapeutic approaches including targeted therapy,checkpoint inhibitors and chimeric antigen receptor T-cell therapy are changing the paradigm of treatment for DHL. This review summarizes new developments in diagnosis and treatment of double-hit lymphoma.
Genetic Predisposition to Disease
;
Humans
;
Immunotherapy, Adoptive
;
Lymphoma, B-Cell
;
Proto-Oncogene Proteins c-bcl-2
;
Proto-Oncogene Proteins c-bcl-6
;
Proto-Oncogene Proteins c-myc
5.Predictive Significance of KRAS and Tau for Chemoresponse in Advanced Non-Small-Cell Lung Cancer.
Jinyoung YOO ; Byoung Yong SHIM ; Chang Young YOO ; Seok Jin KANG ; Kyo Young LEE
Korean Journal of Pathology 2009;43(5):435-440
BACKGROUND: Taxane-platinum combinations are often used as first-line treatments for patients with advanced non-small cell lung cancer (NSCLC). Response to chemotherapy for these patients is still poor. The aim of our study was to investigate, for this disease, whether KRAS and Tau proteins affect responses to taxane-platinum combinations. METHODS: Expression of KRAS and Tau was examined immunohistochemically in 71 tumor samples obtained from patients with stage IIIB or IV NSCLC prior to combination therapy. Expression was correlated with tumor responses. RESULTS: The response rate was 55% (39 of 71). KRAS and Tau were expressed in seven (10%) and 31 (44%) patients, respectively. All seven KRAS-positive patients were non-responders (p=0.014). Among Tau-positive patients, 35% (11 of 31) responded to therapy, whereas a partial response was observed in 70% (28 of 40) of Tau-negatives (p=0.045). Two were positive for both, and they were non-responders. In patients negative for both, the response rate was 71% (25 of 35) (p=0.012). CONCLUSIONS: Expression of KRAS and Tau are significantly correlated with poor responses to this combination therapy in advanced NSCLC patients, and may be a useful marker for chemoresistance.
Carcinoma, Non-Small-Cell Lung
;
Humans
;
Lung
;
Lung Neoplasms
;
Proto-Oncogene Proteins
;
ras Proteins
;
tau Proteins
6.DNA ploidy, S-phase activity and c-erbB-2 oncogene protein expression in breast cancer and its relationship to prognosis.
Dong Young NOH ; Kuk Jin CHOE ; Jin Pok KIM ; In Ae PARK ; Seong Hoe PARK ; Keun Young YOO
Journal of the Korean Cancer Association 1992;24(1):73-81
No abstract available.
Breast Neoplasms*
;
Breast*
;
DNA*
;
Oncogene Proteins*
;
Oncogenes*
;
Ploidies*
;
Prognosis*
7.Research progress of N-Myc roles in hematopoiesis and hematologic malignancies.
Li-Jing SHEN ; Lan-Fang CAO ; Fang-Yuan CHEN
Journal of Experimental Hematology 2013;21(2):503-507
N-Myc oncogene plays an important role in the process of hematopoietic cell proliferation and differentiation in embryos. Once the body suffers from hematologic malignancies, the expression of N-Myc would increase and significantly associate with disease progression. In this article the structure of N-Myc, the regulatory mechanism in the different hematopoietic lineages, the interaction in each signal pathways, the transgenic animal model of overexpression, and intervention by drugs are reviewed.
Hematologic Neoplasms
;
Hematopoiesis
;
Humans
;
Proto-Oncogene Proteins c-myc
;
metabolism
9.BRAF gene in hematological neoplasms.
Jiefei BAI ; Wei ZHANG ; Daobin ZHOU
Chinese Journal of Hematology 2014;35(9):866-868
10.Research progress of proto-oncogene c-myb in megakaryocyte-erythroid hematopoiesis.
Xiao-Qin LIU ; Xiao-Xia WANG ; Li ZHAO
Journal of Experimental Hematology 2012;20(2):518-522
The nuclear proto-oncogene c-myb is an essential regulator of hematopoiesis, it involves in the growth, survival, proliferation and differentiation of hematopoietic cells. More recently, different cell lines and transgenic mouse studies have suggested that c-myb plays a pivotal role in the megakaryocyte-erythroid progenitor cell lineage commitment. The deletion of the proto-oncogene c-myb would lead to profoundly impaired definitive erythropoiesis, but little influence in definitive megakaryopoiesis. Moreover, transient transfection and immunoprecipitation studies have demonstrated that c-myb exerts its physiological function in normal hematopoiesis by influencing a network of regulator molecules. Now therefore, insight into the structure, function and related molecular regulation mechanism of c-myb gene can help to further clarify its function in megakaryocyte-erythroid hematopoiesis and can provide new ideas for molecular target therapy of the platelet diseases and red blood cell diseases. In this article, c-myb structure, function and related effects involved in megakaryocyte-erythroid hematopoiesis as well as related molecular mechanisms are reviewed.
Animals
;
Hematopoiesis
;
Humans
;
Megakaryocytes
;
Mice
;
Proto-Oncogene Proteins c-myb