Ginsenoside Rb1에 의한 발암유전자 ras의 활성 억제

이선주,전병학 대한암예방학회 2003 Journal of cancer prevention Vol.8 No.2

Oncogene-Driven Metabolic Alterations in Cancer

Min, Hye-Young,Lee, Ho-Young The Korean Society of Applied Pharmacology 2018 Biomolecules & Therapeutics(구 응용약물학회지) Vol.26 No.1

Cancer is the leading cause of human deaths worldwide. Understanding the biology underlying the evolution of cancer is important for reducing the economic and social burden of cancer. In addition to genetic aberrations, recent studies demonstrate metabolic rewiring, such as aerobic glycolysis, glutamine dependency, accumulation of intermediates of glycolysis, and upregulation of lipid and amino acid synthesis, in several types of cancer to support their high demands on nutrients for building blocks and energy production. Moreover, oncogenic mutations are known to be associated with metabolic reprogramming in cancer, and these overall changes collectively influence tumor-microenvironment interactions and cancer progression. Accordingly, several agents targeting metabolic alterations in cancer have been extensively evaluated in preclinical and clinical settings. Additionally, metabolic reprogramming is considered a novel target to control cancers harboring un-targetable oncogenic alterations such as KRAS. Focusing on lung cancer, here, we highlight recent findings regarding metabolic rewiring in cancer, its association with oncogenic alterations, and therapeutic strategies to control deregulated metabolism in cancer.

Oncogene-Driven Metabolic Alterations in Cancer

( Hye-young Min ),( Ho-young Lee ) 한국응용약물학회 2018 Biomolecules & Therapeutics(구 응용약물학회지) Vol.26 No.1

Cancer is the leading cause of human deaths worldwide. Understanding the biology underlying the evolution of cancer is important for reducing the economic and social burden of cancer. In addition to genetic aberrations, recent studies demonstrate metabolic rewiring, such as aerobic glycolysis, glutamine dependency, accumulation of intermediates of glycolysis, and upregulation of lipid and amino acid synthesis, in several types of cancer to support their high demands on nutrients for building blocks and energy production. Moreover, oncogenic mutations are known to be associated with metabolic reprogramming in cancer, and these overall changes collectively influence tumor-microenvironment interactions and cancer progression. Accordingly, several agents targeting metabolic alterations in cancer have been extensively evaluated in preclinical and clinical settings. Additionally, meta-bolic reprogramming is considered a novel target to control cancers harboring un-targetable oncogenic alterations such as KRAS. Focusing on lung cancer, here, we highlight recent findings regarding metabolic rewiring in cancer, its association with oncogenic alterations, and therapeutic strategies to control deregulated metabolism in cancer.

Using $^{18}F$-FDG PET/CT to Detect an Occult Mesenchymal Tumor Causing Oncogenic Osteomalacia

Seo, Hyo-Jung,Choi, Yun-Jung,Kim, Hyun-Jeong,Jeong, Yong-Hyu,Cho, Arthur,Lee, Jae-Hoon,Yun, Mi-Jin,Lee, Jong-Doo,Kang, Won-Jun The Korea Society of Nuclear Medicine 2011 핵의학 분자영상 Vol.45 No.3

Oncogenic osteomalacia is a rare paraneoplastic syndrome characterized by renal phosphate excretion, hypophosphatemia, and osteomalacia. This syndrome is often caused by tumors of mesenchymal origin. Patients with oncogenic osteomalacia have abnormal bone mineralization, resulting in a high frequency of fractures. Tumor resection is the treatment of choice, as it will often correct the metabolic imbalance. Although oncogenic osteomalacia is a potentially curable disease, diagnosis is difficult and often delayed because of the small size and sporadic location of the tumor. Bone scintigraphy and radiography best characterize osteomalacia; magnetic resonance imaging findings are nonspecific. Here, we report a case of oncogenic osteomalacia secondary to a phosphaturic mesenchymal tumor that was successfully detected by $^{18}F$-fluorodeoxyglucose positron emission tomography/computed tomography ($^{18}F$-FDG PET/CT). This case illustrates the advantages of $^{18}F$-FDG PET/CT in detecting the occult mesenchymal tumor that causes oncogenic osteomalacia.

한국식품 중 잔류농약의 종양유발성 평가

이미경,이서래 이화여자대학교 생명과학연구소 1995 생명과학연구논문집 Vol.6 No.-

국내에서 소비되고 있는 농약 중 종양유발지수가 알려진 12개 성분의 식품군별 식이섭취량과 그들의 위해성을 평가하였다. 한국인에 대한 종양유발성(70년 평생을 통한 부가적 종양발생율)은 농약잔류 허용기준에 의한 경우 2.17x10^-3, 실제 잔류량 최대치에 의한 경우 4.33x10^-5, 실제 잔류량 평균치에 의한 경우 5.10x10^-6으로서 미국EPA의 무시될 수 있는 위험기준인 1x10^-6을 초과하였다. 발암성 농약의 남용에 대한 국민들의 불안을 해소하기 위해서는 종양유발성 농약에 대한 체계적인 후속연구가 추진되어야 할 것이다. Dietary intake and oncogenic risk of 12 pesticides used in Korea whose oncogenic risk od 12 pesticides used in Korea whose oncogenic potency was known were assessed from published data. Dietary oncogenic risk (excess tumor incidence for a 70year human life span) for Korean population was estimated to be 2.17×10^-3 on the basis of legal maximum residue liomit, 4.33×10^-5 on the basis of maximum practical residue level and 5.10×10^-6 on the basis of mean practical residue level of examined pesticides, all of which exceeded the negligible risk standard 1×10^-6 of US EPA. A systematic follow-up study on those oncogenic pesticides should be undertaken in order to mitigate the people's worry about the cancer risk by the abuse of pesticides in food production.

Changes in oncogenic protein levels in peri-implant oral malignancy: a case report

Seo, Mi Hyun,Myoung, Hoon,Lee, Jong Ho,Kim, Soung Min,Lee, Suk Keun Korean Association of Maxillofacial Plastic and Re 2019 Maxillofacial Plastic Reconstructive Surgery Vol.41 No.-

Background: Oral squamous cell carcinoma (OSCC) constitutes a group of tumors that exhibit heterogeneous biology, histopathology, and clinical behaviors. Case presentation: A 73-year-old male had a whitish leukoplakia-like lesion around inflamed peri-implant area (#42, #43, and #44), and this lesion had transformed to OSCC within 3 years. He underwent mass resection, selective neck dissection, and reconstructive surgery. To detect any carcinogenesis progression, we examined the removed tumor tissue as well as the patient's preoperative and postoperative sera to identify causative oncogenic proteins using immunoprecipitation high-performance liquid chromatography (IP-HPLC). Conclusions: The protein expression levels of p53, E-cadherin, β-catenin, MMP-10, HER2, NRAS, Met, HER2, and ERb were significantly lower in the serum collected on postoperative day 10 than in the preoperative serum, and if these proteins are consistently not elevated in the serum 3 months after surgery compared with the preoperative serum, these proteins can be potential oncogenic proteins. However, we also found that the serum extracted 3 months after the operation had elevated levels of oncogenic proteins compared with that of the preoperative and 10-day postoperative serum indicating the possibility of tumor recurrence. At postoperative follow-up period, ipsilateral neck metastasis and second primary lesion were found and additional surgery was performed to the patient. IP-HPLC using the patient's serum shows the possibility of oncogenic protein detection. However, follow-up IP-HPLC data is needed to find out patient-specific prognostic factors.

Kimchi and an Active Component, β-Sitosterol, Reduce Oncogenic H-Ras(V12)-Induced DNA Synthesis

( Kun Young Park ),( Eun Ju Cho ),( Sook Hee Rhee ),( Keun Ok Jung ),( Sun Ju Yi ),( Byung H. Jhun ) 부산대학교 김치연구소 2003 김치의 과학과 기술 Vol.9 No.-

Oncogenic Challenges in Stem Cells and the Link to Cancer Initiation

이지선,차혁진,배갑용,이미옥 대한약학회 2012 Archives of Pharmacal Research Vol.35 No.2

Adult stem cells, which are characterized by self-renewal and multi-potency, are classified as specialized cell types, responsible for the regeneration of damaged tissues. There is growing evidence that senescence of stem cells (or stem cell aging) is closely associated with a variety of aging-related diseases such as tissue atrophy, degenerative diseases and onset of cancers. Alterations in the systemic environment during aging may trigger stress signaling in stem cells and reduce stem cell characteristics, resulting in loss of differentiation potential and defective self-renewal (referred to as mal-differentiation). Thus, it has been suggested that aging-related disorders such as retarded regeneration of damaged tissue and onset of cancer may result from the mal-differentiation of stem cells. In particular, many types of cancers such as leukemia, intestinal cancer, skin cancer and sarcoma have been shown to originate from adult stem cells after a variety of oncogenic challenges. This review summarizes recent studies on cancers originating from stem cells, demonstrating possible molecular mechanisms that govern the susceptibility of stem cells to oncogenic challenges.

다발성 부전골절을 동반한 종양성 골연화증 - 증례 보고 -

박영창 ( Young-chang Park ),서준오 ( Joon-oh Seo ),양규현 ( Kyu-hyun Yang ) 대한골절학회 2017 대한골절학회지 Vol.30 No.3

종양성 골연화증은 종양에서 분비하는 FGF-23으로 인하여 발생되는 저인산혈증, 신장 인산염 소모, 골연화증 및 다발성 부전골절을 특징으로 하는 드문 부종양성 증후군이다. 치료는 원인이 되는 종양을 찾아내어 완전절제 하는 것이 원칙이며, 수술 후 극적인 회복을 기대할 수 있다. 저자들은 후 경골근 주위에 발생한 종양성 골연화증의 원인이 되는 종양을 제거하여 증상 및 골밀도가 극적으로 회복된 사례를 보고하는 바이다. Oncogenic osteomalacia is a rare paraneoplastic syndrome, characterized by hypophosphatemia, renal phosphate wasting, osteomalacia, and multiple insufficiency fractures, as a result of the tumor. A wide excision of the causative tumor is considered as the treatment of choice, following which, a dramatic recovery is expected. Authors report a case in which the symptoms and bone mineral density were dramatically recovered after an excision of the causative tumor around the tibialis posterior muscle in oncogenic osteomalacia.

SURF4 has oncogenic potential in NIH3T3 cells

Kim, Jayoung,Hong, Chae Mi,Park, Su Min,Shin, Dong Hoon,Kim, Jee Yeon,Kwon, Sang-Mo,Kim, Jae Ho,Kim, Chi Dae,Lim, Dae-Sik,Lee, Dongjun Elsevier 2018 Biochemical and biophysical research communication Vol.502 No.1

<P><B>Abstract</B></P> <P>SURF4, which is located in the Surfeit gene cluster, encodes for a conserved integral membrane protein containing multiple putative transmembrane regions. However, the physiological role of SURF4 has not been determined. We found that <I>SURF4</I> demonstrated aberrant amplification and increased expression in the tumor tissues of several human cancer patients. Overexpression of SURF4 led to increased cell proliferation, migration, and maintenance of anchorage-independent growth. In addition, NIH3T3 cells overexpressing SURF4 induced tumor growth in the mice. Collectively, our findings demonstrate that SURF4 has the potential for inducing cellular transformation and cell migration <I>in vitro</I> and has oncogenic transformation ability <I>in vivo</I>.</P> <P><B>Highlights</B></P> <P> <UL> <LI> <I>SURF4</I> was found to be amplified and highly expressed in the tumor tissues of several human cancer patients. </LI> <LI> Patients with tumors exhibiting high <I>SURF4</I> expression had significantly shorter overall survival than low <I>SURF4</I> expression. </LI> <LI> <I>SURF4</I> can induce cellular transformation and cell migration <I>in vitro</I> and promotes oncogenic transformation <I>in vivo.</I> </LI> </UL> </P>