• Title/Summary/Keyword: Brain cancer

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GPR78 promotes lung cancer cell migration and metastasis by activation of Gαq-Rho GTPase pathway

  • Dong, Dan-Dan;Zhou, Hui;Li, Gao
    • BMB Reports
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    • v.49 no.11
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    • pp.623-628
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    • 2016
  • GPR78 is an orphan G-protein coupled receptor (GPCR) that is predominantly expressed in human brain tissues. Currently, the function of GPR78 is unknown. This study revealed that GPR78 was expressed in lung cancer cells and functioned as a novel regulator of lung cancer cell migration and metastasis. We found that knockdown of GPR78 in lung cancer cells suppressed cell migration. Moreover, GPR78 modulated the formation of actin stress fibers in A549 cells, in a RhoA- and Rac1-dependent manner. At the molecular level, GPR78 regulated cell motility through the activation of $G{\alpha}q$-RhoA/Rac1 pathway. We further demonstrated that in vivo, the knockdown of GPR78 inhibited lung cancer cell metastasis. These findings suggest that GPR78 is a novel regulator for lung cancer metastasis and may serve as a potential drug target against metastatic human lung cancer.

Hereditary cancer and genetic counseling (유전성 암과 유전상담)

  • Jeong, Seung-Yong
    • Journal of Genetic Medicine
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    • v.4 no.1
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    • pp.15-21
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    • 2007
  • Hereditary syndromes cause approximately 5 to 10% of overall cancer cases. Cancer related with genetic syndromes are found elsewhere, including stomach, breast, colorectum, ovary, brain and so on. Because hereditary cancers are due to germline mutations, these patients have unique clinical features distinct from sporadic cancer. Generally these features include (i) early age-of onset of cancer, (ii) frequent association with synchronous or metachronous tumors, (iii) frequent bilateral involvement in paired organs (iv) frequent association with other site tumors or characteristic clinical manifestation specific to each genetic syndrome. Due to these differences, the management strategy for patients with hereditary cancer is quite different from that for sporadic cancer. Additionally, there are important screening and surveillance implications for family members. Genetic counselling is prerequisite to these families for risk assessment by pedigree analysis, and guidance to clinical or genetic testing. The genes responsible for these syndromes has recently identified, as a result, genetic testing has become important determining factor in clinical decisions.

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Trends and Analysis of Cancer Incidence for Common Male and Female Cancers in the Population of Punjab Province of Pakistan during 1984 to 2014

  • Masood, Khalid;Masood, Andleeb;Zafar, Junaid;Shahid, Abubaker;Kamran, Mujahid;Murad, Sohail;Masood, Misbah;Alluddin, Zafar;Riaz, Masooma;Akhter, Naseem;Ahmad, Munir;Ahmad, Fayyaz;Akhtar, Javaid;Naeem, Muhammad
    • Asian Pacific Journal of Cancer Prevention
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    • v.16 no.13
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    • pp.5297-5304
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    • 2015
  • Background: The Pakistan Atomic Energy Commission Cancer Registry (PAECCR) program has made availability of a common cancer incidence database possible in Pakistan. The cancer incidence data from nuclear medicine and oncology institutes were gathered and presented. Materials and Methods: The cancer incidence data for the last 30 years (1984-2014) are included to describe a data set of male and female patients. The data analysis concerning occurrence, trends of common cancers in male and female patients, stage-wise distribution, and mortality/follow-up cases is also incorporated for the last 10 years (2004-2014). Results: The total population of provincial capital Lahore is 9,800,000. The total number of cancer cases was 80,390 (males 32,156, females 48,134). The crude incidence rates in PAECCR areas were 580.8/$10^5$ during 2010 to 885.4/$10^5$ in 2014 (males 354.1/$10^5$, females 530.1/$10^5$). The cancer incidence rates for head and neck (15.70%), brain tumors (10.5%), and non-Hodgkin lymphoma (NHL, 9.53%) were found to be the highest in male patients, whereas breast cancer (46.7%), ovary tumors (6.80%), and cervix (6.31%) cancer incidence rates were observed to be the most common in female patients. The age range distribution of diagnosed and treated patients in conjunction with the percentage contribution of cancer patients from 15 different cities of Punjab province treated at the Institute of Nuclear Medicine and Oncology, Lahore are also included. Leukemia was found to be the most common cancer for the age group of 1-12 years. It has been identified that the maximum number of diagnosed cases were found in the age range of 51-60 years for males and 41-50 years for female cancer patients. Conclusions: Overall cancer incidence of the thirty years demonstrated that head and neck and breast cancers in males and in females respectively are the most common cancers in Punjab province in Pakistan, at rates almost the highest in Asia, requiring especial attention. The incidence of brain, NHL, and prostate cancers among males and ovarian and cervix cancers among females have increased rapidly. These data from a major population of Punjab province should be helpful for implementation of appropriate planning, prevention and cancer control measures and for determination of risk factors within the country.

USEFULNESS OF $^{18}F$-FDG PET/CT IN THE EVALUATION OF CERVICAL LYMPH NODE METASTASIS IN PATIENTS WITH ORAL CANCER (구강암 환자에서 $^{18}F$ FDG-PET/CT의 경부 림프절 전이 평가 유용성)

  • Yu, Min-Gi;Ryu, Sun-Youl
    • Journal of the Korean Association of Oral and Maxillofacial Surgeons
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    • v.35 no.4
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    • pp.213-220
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    • 2009
  • Purpose: The present study was aimed to examine the usefulness of 18F-FDG PET/CT in the evaluation of cervical lymph node metastasis in patients with oral cancer. Materials and methods: Twenty-two patients who underwent neck dissection to treat oral cancer were subjected for examination. The cervical node metastasis was evaluated by means of clinical examination, CT scan, PET, and histologic examination. By comparing the results of each examination modality with those of histologic examination, it's sensitivity, specificity, positive predictive value, and negative predictive value were determined. Results: The oral cancer was more frequent in males with a ratio of 2.14:1. The sixth decade showed the highest incidence in age distribution with mean of $56{\pm}16$. Histologic findings showed that squamous cell carcinoma was the most common (15 patients), and mucoepidermoid carcinoma (3), malignant melanoma (2), and adenoid cystic carcinoma and ghost cell odontogenic carcinoma (1 each), in order. In most cases, wide surgical excision of the primary cancer and neck dissection was performed, followed by reconstruction with free flaps when necessary. When comparing the results of each examination modality with those of the histologic examination, clinical examination showed sensitivity, specificity, positive predictive value, and negative predictive value at 11%, 85%, 33%, and 58%, respectively. CT scans showed at 67%, 77%, 67%, and 77%, while $^{18}F$-FDG PET/CT at 78%, 77%, 70%, and 83%, respectively. Conclusions: These results suggest that PET is more useful, compared with clinical examination and CT scans, in the evaluation of cervical lymph node metastasis in patients with oral cancer.

Preliminary Results of a Phase I/II Study of Simultaneous Boost Irradiation Radiotherapy for Locally Advanced Nasopharyngeal Carcinoma

  • Xiang, Li;Wang, Yan;Xu, Bing-Qing;Wu, Jing-Bo;Xia, Yun-Fei
    • Asian Pacific Journal of Cancer Prevention
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    • v.14 no.12
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    • pp.7569-7576
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    • 2013
  • Background: The purpose of this article is to present preliminary results of simultaneous boost irradiation radiotherapy for locally advanced nasopharyngeal carcinoma (NPC). Methods: Fifty-eight patients who underwent simultaneous boost irradiation radiotherapy for NPC in Cancer Center of Sun Yat-sen University between September 2004 and December 2009 were eligible. Acute and late toxicities were scored weekly according to the Radiation Therapy Oncology Group (RTOG) acute and late radiation morbidity scoring schemes. An especial focus was on evidence of post-radiation brain injury. Also quality of life was analysed according to the EORTC (European Organisation for Research and Treatment of Cancer) recommendations. Discrete variables were compared by ${\chi}^2$ test. The Kaplan-Meier method was used to calculate the survival rates and generate survival curves. Results: A total of 58 patients with a mean follow-up time of 36 months completed clinical trials.Fifty-seven patients (98.3) achieved complete remission in the primary sites and cervical lymph nodes, with only one patient (1.7%) showing partial remission.The most frequently observed acute toxicities during the concurrent chemoradiotherapy were mucositis and leucopenia. Four patients (6.9%) had RTOG grade 3 mucositis, whereas four patients (6.9%) had grade 3 leucopenia. No patient had grade 4 acute toxicity. Three (5.17%) of the patients exhibited injury to the brain on routine MRI examination, with a median observation of 32 months (range, 25-42months). All of them were RTOG grade 0. The 3-year overall, regional-free and distant metastasis-free survival rates were 85%, 94% and 91%, respectively. Conclusion: Simultaneous boost irradiation radiotherapy is feasible in patients with locally advanced nasopharyngeal carcinoma. The results showed excellent local control and overall survival, with no significant increase the incidence of radiation brain injury or the extent of damage. A larger population of patients and a longer follow-up period are needed to evaluate ultimate tumor control and late toxicity.

CHEMOPREVENTIVE EFFECTS OF XANTHORRHIZOL

  • Park, Kwang-Kyun;Chung, Won-Yoon;Kim, Hee-Ok;Kim, Hee-Kyong;Park, Min-Ah;Kim, Mi-Jeong;Sohn, Joon-Hyung
    • Proceedings of the Korean Society of Toxicology Conference
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    • 2001.05a
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    • pp.145-145
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    • 2001
  • Xanthorrhizol is a sesquiterpenoid isolated from Curcuma xanthorrhiza Roxb. (Zingiberaceae) that has been traditionally used in Indonesia for dietary and medicinal purposes. In our studies to evaluate the cancer chemopreventive potential, xanthorrhizol inhibited the mutagenesis induced by reactive oxygen species in Sa;monella typhimurium TA 102 in a dose-related manner and decreased significantly the incidence and the multiplicity of skin tumors initiated by 7, 12-dimethylbenz[$\alpha$]anthracene and promoted by 12-Ο-tetradecanoylphorbol-13-acetate at 19 weeks.(omitted)

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The CCND1 G870A Gene Polymorphism and Brain Tumor Risk: a Meta-analysis

  • Qin, Ling-Yan;Zhao, Li-Gang;Chen, Xu;Li, Ping;Yang, Zheng;Mo, Wu-Ning
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.8
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    • pp.3607-3612
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    • 2014
  • Background: In recent years, numerous studies have been performed to investigate the CCND1 G870A gene polymorphism impact on brain tumors susceptibility. Unfortunately, the results of previous studies were inconsistent. Therefore, we performed a meta-analysis to derive a more precise estimation of any association. Materials and Methods: We conducted a search in PubMed, Embase and CNKI covering all published papers up to November, 2013. Odds ratios (ORs) and their 95% confidence intervals (95%CIs) were applied to assess associations. Results: A total of 6 publications including 9 case-control studies met the inclusion criteria. The pooled ORs for the total included studies showed significant association among comparison A vs G (OR= 1.246, 95%CI= 1.092-1.423, p= 0.001), homozygote comparison AA vs GG (OR= 1.566, 95%CI= 1.194-2.054, p= 0.001), heterozygote comparison AG vs GG (OR= 1.290, 95%CI= 0.934-1.782, p= 0.122), dominant model AA/GA vs GG (OR= 1.381, 95%CI= 1.048-1.821, p= 0.022) and recessive model AA vs GA/GG (OR= 1.323, 95%CI= 1.057-1.657, p= 0.015) especially in glioma. Conclusions: CCND1 G870A polymorphism may increase brain tumor risk, especially for gliomas. However, more primary large scale and well-designed studies are still required to evaluate the interaction of CCND1 G870A polymorphism with brain tumor risk.

Etoposide Induces Mitochondrial Dysfunction and Cellular Senescence in Primary Cultured Rat Astrocytes

  • Bang, Minji;Kim, Do Gyeong;Gonzales, Edson Luck;Kwon, Kyoung Ja;Shin, Chan Young
    • Biomolecules & Therapeutics
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    • v.27 no.6
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    • pp.530-539
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    • 2019
  • Brain aging is an inevitable process characterized by structural and functional changes and is a major risk factor for neurodegenerative diseases. Most brain aging studies are focused on neurons and less on astrocytes which are the most abundant cells in the brain known to be in charge of various functions including the maintenance of brain physical formation, ion homeostasis, and secretion of various extracellular matrix proteins. Altered mitochondrial dynamics, defective mitophagy or mitochondrial damages are causative factors of mitochondrial dysfunction, which is linked to age-related disorders. Etoposide is an anti-cancer reagent which can induce DNA stress and cellular senescence of cancer cell lines. In this study, we investigated whether etoposide induces senescence and functional alterations in cultured rat astrocytes. Senescence-associated ${\beta}$-galactosidase (SA-${\beta}$-gal) activity was used as a cellular senescence marker. The results indicated that etoposide-treated astrocytes showed cellular senescence phenotypes including increased SA-${\beta}$-gal-positive cells number, increased nuclear size and increased senescence-associated secretory phenotypes (SASP) such as IL-6. We also observed a decreased expression of cell cycle markers, including PhosphoHistone H3/Histone H3 and CDK2, and dysregulation of cellular functions based on wound-healing, neuronal protection, and phagocytosis assays. Finally, mitochondrial dysfunction was noted through the determination of mitochondrial membrane potential using tetramethylrhodamine methyl ester (TMRM) and the measurement of mitochondrial oxygen consumption rate (OCR). These data suggest that etoposide can induce cellular senescence and mitochondrial dysfunction in astrocytes which may have implications in brain aging and neurodegenerative conditions.

Study of Mylabris Phalerata on Anti-cancer Effects in Some Kinds of Cancer Cells (반모가 수종의 인체 암세포에 미치는 영향)

  • Kim, Jin-Sung;Yoon, Sang-Hyub;Ryu, Bong-Ha;Ryu, Ki-Won;Jung, Myung-Chai
    • The Journal of Internal Korean Medicine
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    • v.25 no.2
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    • pp.202-213
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    • 2004
  • Object : Objective: This study was conducted to investigate the anti-cancer effects of Mylabris phalerata (반모) in some kinds of cancer cells. Materials and Methods: Some kinds of cancer cells lines were treated. We used nine kinds of cancer cell lines, such as stomach cancer cells (Kato), lung cancer cells (Calu-1, NCI-H 1395), urinary bladder cancer cells (HS789T), bone cancer cells (Saos-2), brain cancer cells (SK-N-MC), liver cancer cells (Hep-G2), skin cancer cells (Mo-1) and prostate cancer cells (PC-3) with the water decoction of Mylabris phalerata. The histological changes of all cell lines in the media (RPMI-1640) containing the decoction of Mylabris phalerata were observed and we examined cell death assay by trypan blue exclusion testing was examined. Finally, the change of mitochondrial membrane potential was measurd and the inhibitory effect of Mylabris phalerata on cell increase was examined by analyzing the cell cycle. Results: In histologic change all cancer cell lines showed withdrawn and floating appearance that is typical in cellular impairment. Most of the cell lines showed over 50% death rate after 24 hours in trypan blue exclusion tests. Especially the stomach, urinary bladder. brain and liver cell lines showed over 30% death rate after 12 hours. All cell lines treated with Mylabris phalerata were less stained than the control group and the mitochondrial membrane potential in the Mylabris phalerata treated cell lines was markedly lower than that in the control group. The measurement of DNA quantity in all cell lines showed the disappearance of the peak and the thickened left axis, which suggests that all cellular DNA degraded. Conclusion: Mylabris phalerata had cytotoxicity on various kinds of cancer cell lines and the mechanism of that was the impairment of mitochondria by the breakdown of the mitochondrial cell membrane. We propose that this is in part attributable to the destruction of DNA in cancer cells.

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