Abstract A29: Detection of ultra-rare mutations during breast stem cell tumor progression by Duplex Sequencing

2016 ◽  
Author(s):  
Eun Hyun Ahn ◽  
Kensen Hirohata ◽  
Seung Hyuk Lee ◽  
Joon Yup Kim ◽  
Brendan F. Kohrn ◽  
...  
Keyword(s):  
Stem Cell ◽  
Tumor Progression ◽  
Cell Tumor ◽  
Rare Mutations ◽  
Breast Stem Cell ◽  
Duplex Sequencing

Tu1631 A TGF-β-Ctcf Regulated Pathway Suppresses Stem Cell Associated Tumor Progression

2016 ◽  
Vol 150 (4) ◽  
pp. S1153-S1154
Author(s):  
Jian Chen ◽  
Zhixing Yao ◽  
Jiun-Sheng Chen ◽  
YoungJin Gi ◽  
Yun Seong Jeong ◽  
...  
Keyword(s):  
Stem Cell ◽  
Tumor Progression

Spheres isolated from human glioblastoma possess cancer stem cell-like phenotype and promote tumor progression

2010 ◽  
Vol 68 ◽  
pp. e429
Author(s):  
Hisaaki Takahashi ◽  
Kana Kobayashi ◽  
Akihiro Inoue ◽  
Hironobu Harada ◽  
Hajime Yano ◽  
...  
Keyword(s):  
Stem Cell ◽  
Cancer Stem Cell ◽  
Tumor Progression ◽  
Human Glioblastoma

scholarly journals Is Ewing's Sarcoma a Stem Cell Tumor?

2007 ◽  
Vol 1 (1) ◽  
pp. 13-15 ◽  
Author(s):  
Paul S. Meltzer
Keyword(s):  
Stem Cell ◽  
Ewing’S Sarcoma ◽  
Ewing's Sarcoma ◽  
Cell Tumor

Salvage Treatment With Paclitaxel, Ifosfamide, and Cisplatin Plus High-Dose Carboplatin, Etoposide, and Thiotepa Followed by Autologous Stem-Cell Rescue in Patients With Relapsed or Refractory Germ Cell Cancer

2001 ◽  
Vol 19 (1) ◽  
pp. 81-88 ◽  
Author(s):  
O. Rick ◽  
C. Bokemeyer ◽  
J. Beyer ◽  
J. T. Hartmann ◽  
N. Schwella ◽  
...  
Keyword(s):  
Stem Cell ◽  
Germ Cell ◽  
Tumor Progression ◽  
Stable Disease ◽  
Multiorgan Failure ◽  
Cell Cancer ◽  
Germ Cell Tumors ◽  
Salvage Treatment ◽  
High Dose ◽  
Salvage Regimen

PURPOSE: To study feasibility and efficacy of a new salvage regimen in patients with relapsed and/or refractory germ cell tumors. PATIENTS AND METHODS: Between May 1995 and February 1997, 80 patients were entered onto a phase II study. Conventional-dose salvage treatment with three cycles of paclitaxel 175 mg/m2, ifosfamide 5 × 1.2 g/m2, and cisplatin 5 × 20 mg/m2 (TIP) was followed by one cycle of high-dose chemotherapy (HDCT) with carboplatin 500 mg/m2 × 3, etoposide 600 mg/m2 × 4, and thiotepa 150 to 250 mg/m2 × 3 (CET). In 23 patients, one additional cycle of paclitaxel 175 mg/m2 and ifosfamide 5 g/m2 (TI) was given immediately before TIP to improve stem-cell mobilization. RESULTS: Fifty-five (69%) of 80 patients responded to TIP, 24 (30%) of 80 patients had stable disease (n = 5) or tumor progression (n = 19), and one patient died. Only 62 (78%) of 80 patients received subsequent HDCT. Among those, 41 (66%) of 62 patients responded and 20 (32%) of 62 patients had stable disease (n = 3) or tumor progression (n = 17). One patient died after HDCT from multiorgan failure. Survival probabilities at 3 years were 30% for overall and 25% for event-free survival. Peripheral neurotoxicity with sensorimotor impairment grade 2 through 4 in 29%, paresthesias grade 2 through 4 in 24%, and skin toxicity grade 2 through 3 in 15% of patients were the most relevant side effects. CONCLUSION: Treatment with TIP followed by high-dose CET is feasible and can induce long-term remissions in 25% of patients with relapsed or refractory germ cell tumors. Peripheral nervous toxicity in approximately one third of patients is a disadvantage of this salvage strategy.

scholarly journals Oncogenic Metabolism Acts as a Prerequisite Step for Induction of Cancer Metastasis and Cancer Stem Cell Phenotype

2018 ◽  
Vol 2018 ◽  
pp. 1-28 ◽  
Author(s):  
Su Yeon Lee ◽  
Min Kyung Ju ◽  
Hyun Min Jeon ◽  
Yig Ji Lee ◽  
Cho Hee Kim ◽  
...  
Keyword(s):  
Stem Cell ◽  
Transcription Factors ◽  
Cancer Stem Cell ◽  
Tumor Progression ◽  
Cancer Cells ◽  
Cancer Metastasis ◽  
Metabolic Reprogramming ◽  
Glutamine Metabolism ◽  
Cell Phenotype ◽  
Mesenchymal Transition

Metastasis is a major obstacle to the efficient and successful treatment of cancer. Initiation of metastasis requires epithelial-mesenchymal transition (EMT) that is regulated by several transcription factors, including Snail and ZEB1/2. EMT is closely linked to the acquisition of cancer stem cell (CSC) properties and chemoresistance, which contribute to tumor malignancy. Tumor suppressor p53 inhibits EMT and metastasis by negatively regulating several EMT-inducing transcription factors and regulatory molecules; thus, its inhibition is crucial in EMT, invasion, metastasis, and stemness. Metabolic alterations are another hallmark of cancer. Most cancer cells are more dependent on glycolysis than on mitochondrial oxidative phosphorylation for their energy production, even in the presence of oxygen. Cancer cells enhance other oncogenic metabolic pathways, such as glutamine metabolism, pentose phosphate pathway, and the synthesis of fatty acids and cholesterol. Metabolic reprogramming in cancer is regulated by the activation of oncogenes or loss of tumor suppressors that contribute to tumor progression. Oncogenic metabolism has been recently linked closely with the induction of EMT or CSC phenotypes by the induction of several metabolic enzyme genes. In addition, several transcription factors and molecules involved in EMT or CSCs, including Snail, Dlx-2, HIF-1α, STAT3, TGF-β, Wnt, and Akt, regulate oncogenic metabolism. Moreover, p53 induces metabolic change by directly regulating several metabolic enzymes. The collective data indicate the importance of oncogenic metabolism in the regulation of EMT, cell invasion and metastasis, and adoption of the CSC phenotype, which all contribute to malignant transformation and tumor development. In this review, we highlight the oncogenic metabolism as a key regulator of EMT and CSC, which is related with tumor progression involving metastasis and chemoresistance. Targeting oncometabolism might be a promising strategy for the development of effective anticancer therapy.

Sign in / Sign up

Export Citation Format

Share Document