c-myc

WordNet

1. the 3rd letter of the Roman alphabet (同)c
2. (music) the keynote of the scale of C major
3. a general-purpose programing language closely associated with the UNIX operating system

PrepTutorEJDIC

1. carbonの化学記号
2. 『私の』 / 《親しみをこめた呼び掛けに用いて》 / 《驚きを表して》おや,まあ
3. case[s]

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2012/11/02 00:45:43」(JST)

wiki en

[Wiki en表示]

V-myc myelocytomatosis viral oncogene homolog (avian)
Structure of the c-Myc (red) in complex with Max (blue) and DNA (PDB 1nkp). Both proteins are binding the major groove of the DNA by forming a fork-like structure.
Available structures PDB Ortholog search: PDBe, RCSB List of PDB id codes 1A93, 1EE4, 1MV0, 1NKP, 2A93
Identifiers
Symbols	MYC; MRTL; bHLHe39; c-Myc
External IDs	OMIM: 190080 MGI: 97250 HomoloGene: 31092 ChEMBL: 1250348 GeneCards: MYC Gene
Gene Ontology Molecular function • DNA binding • double-stranded DNA binding • sequence-specific DNA binding transcription factor activity • protein binding • transcription factor binding • protein complex binding • sequence-specific DNA binding • protein heterodimerization activity • repressing transcription factor binding • E-box binding Cellular component • nucleus • nucleoplasm • nucleolus • cytoplasm • spindle • nuclear body • axon • protein complex Biological process • negative regulation of transcription from RNA polymerase II promoter • MAPK cascade • branching involved in ureteric bud morphogenesis • B cell apoptotic process • release of cytochrome c from mitochondria • positive regulation of mesenchymal cell proliferation • positive regulation of B cell apoptotic process • glucose metabolic process • energy reserve metabolic process • apoptotic DNA fragmentation • chromatin remodeling • transcription, DNA-dependent • transcription initiation from RNA polymerase II promoter • cellular iron ion homeostasis • activation of cysteine-type endopeptidase activity involved in apoptotic process • response to DNA damage stimulus • cell cycle arrest • transforming growth factor beta receptor signaling pathway • Notch signaling pathway • positive regulation of cell proliferation • activation of pro-apoptotic gene products • negative regulation of survival gene product expression • response to gamma radiation • gene expression • oxygen transport • protein processing • negative regulation of protein binding • regulation of telomere maintenance • negative regulation of stress-activated MAPK cascade • cellular response to UV • cellular response to drug • middle ear morphogenesis • response to drug • negative regulation of apoptotic process • response to alkaloid • positive regulation of cysteine-type endopeptidase activity involved in apoptotic process • pigmentation • fibroblast apoptotic process • negative regulation of monocyte differentiation • positive regulation of transcription, DNA-dependent • positive regulation of transcription from RNA polymerase II promoter • positive regulation of fibroblast proliferation • negative regulation of fibroblast proliferation • skeletal system morphogenesis • positive regulation of epithelial cell proliferation • detection of mechanical stimulus involved in sensory perception of sound • chromosome organization • negative regulation of cell division • canonical Wnt receptor signaling pathway • response to growth factor stimulus • positive regulation of metanephric cap mesenchymal cell proliferation • positive regulation of DNA biosynthetic process • positive regulation of response to DNA damage stimulus • negative regulation of G2 phase of mitotic cell cycle Sources: Amigo / QuickGO
Orthologs
Species	Human	Mouse
Entrez	4609	17869
Ensembl	ENSG00000136997	ENSMUSG00000022346
UniProt	P01106	P01108
RefSeq (mRNA)	NM_002467.4	NM_001177352.1
RefSeq (protein)	NP_002458.2	NP_001170823.1
Location (UCSC)	Chr 8: 128.75 – 128.75 Mb	Chr 15: 61.99 – 61.99 Mb
PubMed search	[1]	[2]

Myc (c-Myc) is a regulator gene that codes for a transcription factor.

A mutated version of Myc is found in many cancers, which causes Myc to be constitutively (persistently) expressed. This leads to the unregulated expression of many genes, some of which are involved in cell proliferation and results in the formation of cancer. A common human translocation involving Myc is t(8;14) which is critical to the development of most cases of Burkitt's Lymphoma. A recent study demonstrated that temporary inhibition of Myc selectively kills mouse lung cancer cells, making it a potential cancer drug target.

It has been associated with carcinoma of the cervix, colon, breast, lung and stomach.

In the human genome, Myc is located on chromosome 8 and is believed to regulate expression of 15% of all genes through binding on Enhancer Box sequences (E-boxes) and recruiting histone acetyltransferases (HATs). This means that in addition to its role as a classical transcription factor, Myc also functions to regulate global chromatin structure by regulating histone acetylation both in gene-rich regions and at sites far from any known gene.

Discovery

Myc gene was first discovered in Burkitt's lymphoma patients. In Burkitt's lymphoma, cancer cells show chromosomal translocations, in which Chromosome 8 is frequently involved. Cloning the break-point of the fusion chromosomes revealed a gene that was similar to myelocytomatosis viral oncogene (v-Myc). Thus, the newfound cellular gene was named c-Myc.

Structure

Myc protein belongs to Myc family of transcription factors, which also includes N-Myc and L-Myc genes. Myc family of transcription factors contain bHLH/LZ (basic Helix-Loop-Helix Leucine Zipper) domain. Myc protein, through its bHLH domain can bind to DNA, while the leucine zipper domain allows the dimerization with its partner Max, another bHLH transcription factor.

Myc mRNA contains an IRES (internal ribosome entry site) that allows the RNA to be translated into protein when 5' cap-dependent translation is inhibited, such as during viral infection.

Molecular Function

Myc protein is a transcription factor that activates expression of a great number of genes through binding on consensus sequences (Enhancer Box sequences (E-boxes)) and recruiting histone acetyltransferases (HATs). It can also act as a transcriptional repressor. By binding Miz-1 transcription factor and displacing the p300 co-activator, it inhibits expression of Miz-1 target genes. In addition, myc has a direct role in the control of DNA replication.

Myc is activated upon various mitogenic signals such as Wnt, Shh and EGF (via the MAPK/ERK pathway). By modifying the expression of its target genes, Myc activation results in numerous biological effects. The first to be discovered was its capability to drive cell proliferation (upregulates cyclins, downregulates p21), but it also plays a very important role in regulating cell growth (upregulates ribosomal RNA and proteins), apoptosis (downregulates Bcl-2), differentiation and stem cell self-renewal. Myc is a very strong proto-oncogene and it is very often found to be upregulated in many types of cancers. Myc overexpression stimulates gene amplification, presumably through DNA over-replication.

Myc-Nick

Myc-nick is a cytoplasmic form of Myc produced by a partial proteolytic cleavage of full-length c-Myc and N-Myc. (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2923036/pdf/nihms219804.pdf). Myc cleavage is mediated by the calpain family of calcium-dependent cytosolic proteases (http://en.wikipedia.org/wiki/Calpain).

The cleavage of Myc by calpains is a constitutive process, but is enhanced under conditions that require rapid downregulation of Myc levels, such as during terminal differentiation. Upon cleavage, the C-terminus of Myc (containing the DNA binding domain) is degraded, while Myc-nick, the N-terminal segment 298-residue segment remains in the cytoplasm. Myc-nick contains binding domains for histone acetyltransferases and for ubiquitin ligases.

The functions of Myc-nick are currently under investigation, but this new Myc family member was found to regulate cell morphology, at least in part, by interacting with acetyl transferases to promote the acetylation of α-tubulin. Ectopic expression of Myc-nick accelerates the differentiation of committed myoblasts into muscle cells.

Animal Models

During the discovery of Myc gene, it was realized that chromosomes that translocate to Chromosome 8 contained immunoglobulin genes at the break-point. Enhancers that normally drive expression of immunoglobin genes now lead to overexpression of Myc proto-oncogene in lymphoma cells. To study the mechanism of tumorigenesis in Burkitt's lymphoma by mimicking expression pattern of Myc in these cancer cells, transgenic mouse models were developed. Myc gene placed under the control of IgM heavy chain enhancer in transgenic mice gives rise to mainly lymphomas. Later on, in order to study effects of Myc in other types of cancer, transgenic mice that overexpress Myc in different tissues (liver, breast) were also made. In all these mouse models overexpression of Myc causes tumorigenesis, illustrating the potency of Myc oncogene.

Interactions

Myc has been shown to interact with NMI, NFYC, NFYB, Cyclin T1, RuvB-like 1, GTF2I, BRCA1, T-cell lymphoma invasion and metastasis-inducing protein 1, ACTL6A, PCAF, MYCBP2, MAPK8, Bcl-2, Transcription initiation protein SPT3 homolog, SAP130, DNMT3A, Mothers against decapentaplegic homolog 3, MAX, Mothers against decapentaplegic homolog 2, MYCBP, HTATIP, ZBTB17, Transformation/transcription domain-associated protein, TADA2L, PFDN5, MAPK1, TFAP2A, P73, TAF9, YY1, SMARCB1, SMARCA4, MLH1, EP400 and let-7.

Overview of signal transduction pathways involved in apoptosis.

Effects

A major effect of Myc is B cell proliferation.

c-Myc induces AEG-1 or MTDH gene expression and in turn itself requires AEG-1 oncogene for its expression.

It is associated with carcinoma of the cervix,colon,breast,lung and stomach.

Cancer research

In an online article posted on Thursday, December 8, 2011, from FOCUS, a Harvard University website offering news on important health-related discoveries made there, it was stated that,: "Researchers have found a way to kill human cells hijacked by a genetic accelerator that puts cancer cells into overdrive: the Myc oncogene. The discovery reveals new drug targets for Myc-driven cancers, which tend to be particularly aggressive. The results are to be published online December 8 in Science. In its non-cancerous, healthy form, Myc oversees how genetic information is translated into proteins, typically those involved in growing new cells. But mutations can cause Myc to become hyper-activated, or oncogenic, and when that happens, cells divide uncontrollably and form tumors. Myc-dependent cancer cells are addicted to the oncogene, to the extent that they’ll die if it’s disabled. Scientists have long tried to exploit this vulnerability in drug development. However, in its protein form, Myc is a notoriously difficult target, mainly because it lacks efficient binding sites for drug compounds. So Stephen Elledge, a professor in the Department of Genetics at Harvard Medical School, and a senior author on the paper, and his collaborator and co-senior author Thomas Westbrook, an assistant professor at the Baylor College of Medicine, opted for a different approach. They aimed to suppress Myc by disabling its helper genes rather than the oncogene itself. Taking advantage of “synthetic lethality,” or the cell-killing effect of having two incompatible mutations in a shared pathway, they hoped to mimic the success seen in studies of genes associated with inherited breast cancer. To find the genes, Elledge and Westbrook used a method that relies on tiny RNA molecules (dubbed short-hairpin RNA or shRNAs) that block the activity of specified genes. The scientists used those shRNAs in experiments with human breast epithelial cells in which Myc could be selectively hyper-activated. Each cell in the experiment contained just one silenced gene. If the cell died when Myc’s cancer activity was triggered, then that silenced gene was clearly one Myc needed to form tumors. Altogether they tested nearly 75,000 shRNAs, and ultimately found 403 potential candidates; some familiar to the field of Myc biology and some not. “These genes aren’t oncogenes in and of themselves, but they do code for proteins that Myc relies on to cause cancer,” said Elledge, who is also a professor of medicine at Brigham and Women’s Hospital. “We see them as potential targets for drug therapy—even if you can’t target Myc, you can target these other genes and inactivate its effects. ..."

See also

Myc-tag

References

Further reading

• Ruf IK, Rhyne PW, Yang H, et al. (2002). "EBV regulates c-MYC, apoptosis, and tumorigenicity in Burkitt's lymphoma". Curr. Top. Microbiol. Immunol. 258: 153–60. PMID 11443860. 
• Lüscher B (2001). "Function and regulation of the transcription factors of the Myc/Max/Mad network". Gene 277 (1–2): 1–14. doi:10.1016/S0378-1119(01)00697-7. PMID 11602341. 
• Hoffman B, Amanullah A, Shafarenko M, Liebermann DA (2002). "The proto-oncogene c-myc in hematopoietic development and leukemogenesis". Oncogene 21 (21): 3414–21. doi:10.1038/sj.onc.1205400. PMID 12032779. 
• Pelengaris S, Khan M, Evan G (2002). "c-MYC: more than just a matter of life and death". Nat. Rev. Cancer 2 (10): 764–76. doi:10.1038/nrc904. PMID 12360279. 
• Nilsson JA, Cleveland JL (2004). "Myc pathways provoking cell suicide and cancer". Oncogene 22 (56): 9007–21. doi:10.1038/sj.onc.1207261. PMID 14663479. 
• Dang CV, O'donnell KA, Juopperi T (2005). "The great MYC escape in tumorigenesis". Cancer Cell 8 (3): 177–8. doi:10.1016/j.ccr.2005.08.005. PMID 16169462. 
• Dang CV, Li F, Lee LA (2007). "Could MYC induction of mitochondrial biogenesis be linked to ROS production and genomic instability?". Cell Cycle 4 (11): 1465–6. doi:10.4161/cc.4.11.2121. PMID 16205115. 
• Coller HA, Forman JJ, Legesse-Miller A (2007). ""Myc'ed Messages": Myc Induces Transcription of E2F1 while Inhibiting Its Translation via a microRNA Polycistron". PLoS Genet. 3 (8): e146. doi:10.1371/journal.pgen.0030146. PMC 1959363. PMID 17784791. //www.ncbi.nlm.nih.gov/pmc/articles/PMC1959363/. 
• Astrin SM, Laurence J (1992). "Human immunodeficiency virus activates c-myc and Epstein-Barr virus in human B lymphocytes". Ann. N. Y. Acad. Sci. 651: 422–32. doi:10.1111/j.1749-6632.1992.tb24642.x. PMID 1318011. 
• Bernstein PL, Herrick DJ, Prokipcak RD, Ross J (1992). "Control of c-myc mRNA half-life in vitro by a protein capable of binding to a coding region stability determinant". Genes Dev. 6 (4): 642–54. doi:10.1101/gad.6.4.642. PMID 1559612. 
• Iijima S, Teraoka H, Date T, Tsukada K (1992). "DNA-activated protein kinase in Raji Burkitt's lymphoma cells. Phosphorylation of c-Myc oncoprotein". Eur. J. Biochem. 206 (2): 595–603. doi:10.1111/j.1432-1033.1992.tb16964.x. PMID 1597196. 
• Seth A, Alvarez E, Gupta S, Davis RJ (1992). "A phosphorylation site located in the NH2-terminal domain of c-Myc increases transactivation of gene expression". J. Biol. Chem. 266 (35): 23521–4. PMID 1748630. 
• Takahashi E, Hori T, O'Connell P, et al. (1991). "Mapping of the MYC gene to band 8q24.12----q24.13 by R-banding and distal to fra(8)(q24.11), FRA8E, by fluorescence in situ hybridization". Cytogenet. Cell Genet. 57 (2–3): 109–11. doi:10.1159/000133124. PMID 1914517. 
• Blackwood EM, Eisenman RN (1991). "Max: a helix-loop-helix zipper protein that forms a sequence-specific DNA-binding complex with Myc". Science 251 (4998): 1211–7. doi:10.1126/science.2006410. PMID 2006410. 
• Gazin C, Rigolet M, Briand JP, et al. (1986). "Immunochemical detection of proteins related to the human c-myc exon 1". EMBO J. 5 (9): 2241–50. PMC 1167107. PMID 2430795. //www.ncbi.nlm.nih.gov/pmc/articles/PMC1167107/. 
• Lüscher B, Kuenzel EA, Krebs EG, Eisenman RN (1989). "Myc oncoproteins are phosphorylated by casein kinase II". EMBO J. 8 (4): 1111–9. PMC 400922. PMID 2663470. //www.ncbi.nlm.nih.gov/pmc/articles/PMC400922/. 
• Finver SN, Nishikura K, Finger LR, et al. (1988). "Sequence analysis of the MYC oncogene involved in the t(8;14)(q24;q11) chromosome translocation in a human leukemia T-cell line indicates that putative regulatory regions are not altered". Proc. Natl. Acad. Sci. U.S.A. 85 (9): 3052–6. doi:10.1073/pnas.85.9.3052. PMC 280141. PMID 2834731. //www.ncbi.nlm.nih.gov/pmc/articles/PMC280141/. 
• Showe LC, Moore RC, Erikson J, Croce CM (1987). "MYC oncogene involved in a t(8;22) chromosome translocation is not altered in its putative regulatory regions". Proc. Natl. Acad. Sci. U.S.A. 84 (9): 2824–8. doi:10.1073/pnas.84.9.2824. PMC 304752. PMID 3033665. //www.ncbi.nlm.nih.gov/pmc/articles/PMC304752/. 
• Guilhot S, Petridou B, Syed-Hussain S, Galibert F (1989). "Nucleotide sequence 3' to the human c-myc oncogene; presence of a long inverted repeat". Gene 72 (1–2): 105–8. doi:10.1016/0378-1119(88)90131-X. PMID 3243428. 
• Hann SR, King MW, Bentley DL, et al. (1988). "A non-AUG translational initiation in c-myc exon 1 generates an N-terminally distinct protein whose synthesis is disrupted in Burkitt's lymphomas". Cell 52 (2): 185–95. doi:10.1016/0092-8674(88)90507-7. PMID 3277717. 

External links

• The Myc Protein
• NCBI Human Myc protein
• Myc cancer gene
• myc+Proto-Oncogene+Proteins at the US National Library of Medicine Medical Subject Headings (MeSH)
• Generating iPS Cells from MEFS through Forced Expression of Sox-2, Oct-4, c-Myc, and Klf4
• Drosophila Myc - The Interactive Fly
• FactorBook C-Myc

UpToDate Contents

全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.

• 1. びまん性大細胞型B細胞性リンパ腫の予後 prognosis of diffuse large b cell lymphoma
• 2. バーキットリンパ腫の病理学 pathobiology of burkitt lymphoma
• 3. バーキットリンパ腫の疫学、臨床症状、病理学的特徴、および診断 epidemiology clinical manifestations pathologic features and diagnosis of burkitt lymphoma
• 4. 進行期びまん性大細胞型B細胞性リンパ腫の初期治療 initial treatment of advanced stage diffuse large b cell lymphoma
• 5. 髄芽腫の組織病理および分子学的病因 histopathology and molecular pathogenesis of medulloblastoma

English Journal

• Mitochondrial alteration in malignantly transformed human small airway epithelial cells induced by α-particles.

• Zhang S, Wen G, Huang SX, Wang J, Tong J, Hei TK.SourceCenter for Radiological Research, College of Physicians and Surgeons, Columbia University Medical Center, New York, USA; Cyrus Tang Hematology Center, Jiangsu Institute of Hematology, The First Affiliated Hospital, Soochow University, Suzhou, People's Republic of China; School of Public Health, Medical College, Soochow University, Suzhou, People's Republic of China.
• International journal of cancer. Journal international du cancer.Int J Cancer.2013 Jan 1;132(1):19-28. doi: 10.1002/ijc.27656. Epub 2012 Jul 3.
• Human small airway epithelial cells (SAECs) immortalized with human telomerase reverse transcriptase were exposed to either a single or multiple doses of α-particles. Irradiated cells showed a dose-dependent cytotoxicity and progressive neoplastic transformation phenotype. These included an increas
• PMID 22644783

• Mechanism and Method for Generating Tumor-Free iPS Cells Using Intronic MicroRNA miR-302 Induction.

• Lin SL, Ying SY.SourceDivision of Regenerative Medicine, WJWU and LYNN Institute for Stem Cell Research, Santa Fe Springs, CA, USA, shilungl@mirps.org.
• Methods in molecular biology (Clifton, N.J.).Methods Mol Biol.2013;936:295-312.
• Today's researchers generating induced pluripotent stem cells (iPS cells or iPSCs) usually consider the pluripotency first, then, the potential tumorigenicity. Oncogenic factors such as c-Myc and Klf4 were frequently used to boost the survival and proliferative rates of iPSCs, creating the inevitabl
• PMID 23007517

Japanese Journal

• iPS細胞を用いた脳再生療法の実現に向けて : 腫瘍化をいかに防ぐか(<特集>明日の脳神経外科を拓く神経科学)

• 山下 徹,河相 裕美,阿部 康二
• 脳神経外科ジャーナル 20(8), 585-588, 2011-08-20
• Induced pluripotent stem cells(iPS細胞)は,皮膚線維芽細胞などの体細胞に複数の転写因子を導入することで作製される多能性幹細胞である.さまざまな種類の細胞や組織を分化誘導できる可能性がある反面,細胞移植治療に用いるためには腫瘍形成等の安全性の問題を解決する必要がある.最近,われわれはマウス一過性虚血モデルに複数のiPS細胞株を移植し腫瘍形成などを評価したところ,レト …
• NAID 110008713065

• Induced pluripotent stem cells: opportunities and challenges.

• Okita Keisuke,Yamanaka Shinya
• Philosophical transactions of the Royal Society of London. Series B, Biological sciences 366, 2183-2197, 2011-08-12
• … Somatic cells have been reprogrammed into pluripotent stem cells by introducing a combination of several transcription factors, such as Oct3/4, Sox2, Klf4 and c-Myc. …
• NAID 120003255724

Related Links

• c-Myc ‐ 通信用語の基礎知識

c-Mycは、この一時停止を解除する機能を持っており、自己複製と増殖に必要である。 特徴 ES細胞やiPS細胞は自己複製をする必要がありと似た ...

• c-Myc等のガン遺伝子について質問があります ...- Yahoo!知恵袋

【ベストアンサー】c－MYCは転写因子であり、細胞の分化、成熟等に必要な遺伝子です。iPS細胞でも、c－MYCを加えた場合と加えなかった場合の比較で、c－MYC（－）だと ...

Related Pictures

---

★リンクテーブル★

国試過去問	「105G032」「098G062」「100G060」
リンク元	「EBウイルス」「癌遺伝子」
拡張検索	「c-myc gene」「c-myc癌原遺伝子」「c-myc遺伝子」
関連記事	「C」「my」「c」

「105G032」

　　[★]

• 機能の不活性化がヒトでの発癌につながる遺伝子はどれか。 2つ選べ。

• a　c-myc(MYC)
• b　erbB2(ERBB2)
• c　K-ras(KRAS)
• d　p53(TP53)
• e　Rb(RB)

[正答]

DE

※国試ナビ4※　［105G031］←［国試_105］→［105G033］

「098G062」

　　[★]

• がん抑制遺伝子はどれか。

• a. c-myc
• b. K-ras
• c. bcl-2
• d. erbB-2
• e. Rb

[正答]

E

※国試ナビ4※　［098G061］←［国試_098］→［098G063］

「100G060」

　　[★]

• がん抑制遺伝子はどれか。

• a. bcl-2
• b. c-myc
• c. erbB-2
• d. K-ras
• e. Rb

[正答]

E

※国試ナビ4※　［100G059］←［国試_100］→［100G061］

「EBウイルス」

　　[★]

英

Epstein-Barr virus, EB virus, EBV

同

エプスタイン-バーウイルス エプスタイン-バー・ウイルス、エプスタイン・バーウイルス

関

EBウイルス感染症、ウイルス

ウイルス学

• ヘルペスウイルス科ガンマヘルペスウイルス亜科リンフェクリプトウイルス属
• 二本鎖DNAウイルス。エンベロープあり。
• ウイルスのレセプターはCD21
• Bリンパ球に潜伏感染

EBV関連抗原

• EA, early antigen
• VCA, virus capsid antigen
• EBNA, EB virus determined nuclear antigen
• LMA, late membrane antigen
• LYDMA, lymphocyte-detected membrane antigen

EBV特異抗体

• VCA抗体
• EA抗体
• EBNA抗体

感染症

• 伝染性単核球症：(小児期の初感染ではかぜ、あるいは不顕性感染(乳幼児では不顕性が多い))
• バーキットリンパ腫：悪性リンパ腫。chr8, chr14の相互転座による染色体異常(BL細胞)c-mycの発現が活性化
• B細胞リンパ腫(HIV感染者など)
• NK細胞リンパ腫(097H066)
• Duncan症候群(XLP)
• 慢性活動性EBV感染症(chronic active EBV infection)
• エイズでの日和見感染。日和見Bリンパ腫
• 上咽頭癌：中国で多い
• 胃癌
• 口腔内白斑

感染経路

• 唾液感染

疫学

• 日本では3歳までに80%が感染する (SMB.530)

検査

• 急性期・回復期に、VCA-IGM, VCA-IgG, EA(早期抗原, early antigen)の高値、EBNA(核内抗原)の陰性を証明

EBNAは感染後3ヶ月以上経たないと立ち上がらない。

• Paul-Bunnel反応(1週間40%, 4週間80-90%)

• ウイルス抗体価：急性期（発病2～7日）と回復期（2～3週）の検体を同時測定し、回復期の抗体価が急性期の結果の4倍（2管差）以上に上昇したとき、血清学的に有意とみなす。

抗体のパターン

	VCA IgG	VCA IgM	EBNA	EA IgG
感染前	ー	ー	ー	ー
急性期	＋	＋	ー	＋／ー
回復期	＋	＋／ー	＋／ー	＋／ー
感染既往	＋	ー	＋	＋／ー
再活性化	＋	＋／ー	＋	＋

目的別検査組み合わせ

	VCA IgG	VCA IgM	EBNA	EA IgG	VCA IgA
伝染性単核症	○	○	○	○
EBV再活性化の疑い	○		○	○
既往確認	○		○
バーキットリンパ腫	○		○	○
上咽頭癌	○		○	○	○
慢性活動性EBV感染症	○			○	○
上記以外でのEBV感染疑い	○	○	○	○

「癌遺伝子」

　　[★]

英

oncogene

同

オンコジーン、腫瘍遺伝子、発癌遺伝子、がん遺伝子、発がん遺伝子

関

癌抑制遺伝子

• 原癌遺伝子に変異が導入されて原癌遺伝子の働きが異常になった場合、この状態の遺伝子を癌遺伝子という。
• K-ras、c-erbB2、N-myc、c-myc、c-abl/bcr、Bcl-2

「c-myc gene」

　　[★]

c-myc遺伝子

関

c-myc proto-oncogene、myc gene、myc oncogene、N-myc gene

「c-myc癌原遺伝子」

　　[★]

英

c-myc proto-oncogene

関

c-myc遺伝子、myc遺伝子、N-myc遺伝子

「c-myc遺伝子」

　　[★]

英

c-myc gene

関

myc遺伝子、c-myc癌原遺伝子、N-myc遺伝子

「C」

　　[★]

• 炭素 carbon
• シトシン cytosine
• システイン cysteine
• シチジン
• セルシウス度 摂氏 degrees Celsius degree C
• 産婦人科領域で「子宮外頚 子宮外頚部 exocervix」を表現するための略語

　 　 　 　

「my」

　　[★]

• comb form.

• 筋肉(muscle)

関

muscle, muscular, muscularis, musculus

　

「c」

　　[★]

• 光速, speed of light