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{{Infobox_gene}}
{{Infobox_gene}}
'''Melanoma antigen preferentially expressed in tumors''' is a [[protein]] that in humans is encoded by the ''PRAME'' [[gene]].<ref name="pmid9047241">{{cite journal | vauthors = Ikeda H, Lethé B, Lehmann F, van Baren N, Baurain JF, de Smet C, Chambost H, Vitale M, Moretta A, Boon T, Coulie PG | title = Characterization of an antigen that is recognized on a melanoma showing partial HLA loss by CTL expressing an NK inhibitory receptor | journal = Immunity | volume = 6 | issue = 2 | pages = 199–208 | date = Feb 1997 | pmid = 9047241 | pmc = | doi = 10.1016/S1074-7613(00)80426-4 }}</ref><ref name="pmid10591208">{{cite journal | vauthors = Dunham I, Shimizu N, Roe BA, Chissoe S, Hunt AR, Collins JE, Bruskiewich R, Beare DM, Clamp M, Smink LJ, Ainscough R, Almeida JP, Babbage A, Bagguley C, Bailey J, Barlow K, Bates KN, Beasley O, Bird CP, Blakey S, Bridgeman AM, Buck D, Burgess J, Burrill WD, O'Brien KP | title = The DNA sequence of human chromosome 22 | journal = Nature | volume = 402 | issue = 6761 | pages = 489–95 | date = Dec 1999 | pmid = 10591208 | pmc = | doi = 10.1038/990031 }}</ref><ref name="entrez">{{cite web | title = Entrez Gene: PRAME preferentially expressed antigen in melanoma| url = https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=23532| accessdate = }}</ref>
'''Melanoma antigen preferentially expressed in tumors''' is a [[protein]] that in humans is encoded by the ''PRAME'' [[gene]].<ref name="pmid9047241">{{cite journal | vauthors = Ikeda H, Lethé B, Lehmann F, van Baren N, Baurain JF, de Smet C, Chambost H, Vitale M, Moretta A, Boon T, Coulie PG | title = Characterization of an antigen that is recognized on a melanoma showing partial HLA loss by CTL expressing an NK inhibitory receptor | journal = Immunity | volume = 6 | issue = 2 | pages = 199–208 | date = Feb 1997 | pmid = 9047241 | pmc = | doi = 10.1016/S1074-7613(00)80426-4 }}</ref><ref name="pmid10591208">{{cite journal | vauthors = Dunham I, Shimizu N, Roe BA, Chissoe S, Hunt AR, Collins JE, Bruskiewich R, Beare DM, Clamp M, Smink LJ, Ainscough R, Almeida JP, Babbage A, Bagguley C, Bailey J, Barlow K, Bates KN, Beasley O, Bird CP, Blakey S, Bridgeman AM, Buck D, Burgess J, Burrill WD, O'Brien KP | title = The DNA sequence of human chromosome 22 | journal = Nature | volume = 402 | issue = 6761 | pages = 489–95 | date = Dec 1999 | pmid = 10591208 | pmc = | doi = 10.1038/990031 }}</ref><ref name="entrez">{{cite web | title = Entrez Gene: PRAME preferentially expressed antigen in melanoma| url = https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=23532| accessdate = }}</ref> Five alternatively spliced transcript variants encoding the same protein have been observed for this gene.<ref name="entrez"/>


== Function ==
== Function ==


This gene encodes an antigen that is predominantly expressed in human [[melanoma]]s and that is recognized by cytolytic [[T lymphocyte]]s. It is not expressed in normal tissues, except testis. This expression pattern is similar to that of other CT antigens, such as [[Melanoma-associated antigen|MAGE]], [[BAGE (gene)|BAGE]] and [[GAGE (gene)|GAGE]]. However, unlike these other CT antigens, this gene is also expressed in acute [[leukemia]]s. Five alternatively spliced transcript variants encoding the same protein have been observed for this gene.<ref name="entrez"/>
This gene encodes an antigen that is predominantly expressed in human [[melanoma]]s and that is recognized by cytolytic [[T lymphocyte]]s. It is not expressed in normal tissues, except testis. This expression pattern is similar to that of other CT antigens, such as [[Melanoma-associated antigen|MAGE]], [[BAGE (gene)|BAGE]] and [[GAGE (gene)|GAGE]]. However, unlike these other CT antigens, this gene is also expressed in acute [[leukemia]]s. The overexpression of PRAME in tumor tissues and relative low levels in normal somatic tissues make it an attractive target for cancer therapy. In recent years, immunotherapy has spearheaded a new era of cancer therapy resulting in the development of numerous novel antigen-specific immunotherapy approaches. Studies on PRAME-specific immunotherapy primarily involve vaccines and cellular immunotherapies <ref>{{cite journal |last1=Al Khadairi |first1=Ghaneya |last2=Decock |first2=Julie |title=Cancer Testis Antigens and Immunotherapy: Where Do We Stand in the Targeting of PRAME? |journal=Cancers |date=2019 |volume=11 |issue=7 |doi=10.3390/cancers11070984 |pmid=31311081}}</ref>.


PRAME can inhibit [[retinoic acid]] signaling and retinoic acid mediated [[cellular differentiation|differentiation]] and [[apoptosis]].<ref name="PMID 16179254">{{cite journal | vauthors = Epping MT, Wang L, Edel MJ, Carlée L, Hernandez M, Bernards R | title = The human tumor antigen PRAME is a dominant repressor of retinoic acid receptor signaling | journal = Cell | volume = 122 | issue = 6 | pages = 835–47 | date = September 2005 | pmid = 16179254 | doi = 10.1016/j.cell.2005.07.003 }}</ref>
PRAME can inhibit [[retinoic acid]] signaling and retinoic acid mediated [[cellular differentiation|differentiation]] and [[apoptosis]].<ref name="PMID 16179254">{{cite journal | vauthors = Epping MT, Wang L, Edel MJ, Carlée L, Hernandez M, Bernards R | title = The human tumor antigen PRAME is a dominant repressor of retinoic acid receptor signaling | journal = Cell | volume = 122 | issue = 6 | pages = 835–47 | date = September 2005 | pmid = 16179254 | doi = 10.1016/j.cell.2005.07.003 }}</ref> PRAME overexpression in triple negative breast cancer has also been found to promote cancer cell motility through induction of the epithelial-to-mesenchymal transition <ref>{{cite journal |last1=Al Khadairi |first1=Ghaneya |last2=Naik |first2=Adviti |last3=Thomas |first3=Remy |last4=Al Sulaiti |first4=Bushra |last5=Rizly |first5=Shaheen |last6=Decock |first6=Julie |title=PRAME promotes epithelial-to-mesenchymal transition in triple negative breast cancer. |journal=J Transl Med |date=2019 |volume=17 |issue=1 |page=9 |doi=10.1186/s12967-018-1757-3 |pmid=30602372}}</ref>.


== Model organisms ==
== Model organisms ==
Line 86: Line 86:
== Further reading ==
== Further reading ==
{{refbegin | 2}}
{{refbegin | 2}}
* {{cite journal |last1=Al Khadairi |first1=Ghaneya |last2=Decock |first2=Julie |title=Cancer Testis Antigens and Immunotherapy: Where Do We Stand in the Targeting of PRAME? |journal=Cancers |date=2019 |volume=11 |issue=7 |doi=10.3390/cancers11070984 |pmid=31311081}}
* {{cite journal |last1=Al Khadairi |first1=Ghaneya |last2=Naik |first2=Adviti |last3=Thomas |first3=Remy |last4=Al Sulaiti |first4=Bushra |last5=Rizly |first5=Shaheen |last6=Decock |first6=Julie |title=PRAME promotes epithelial-to-mesenchymal transition in triple negative breast cancer. |journal=J Transl Med |date=2019 |volume=17 |issue=1 |page=9 |doi=10.1186/s12967-018-1757-3 |pmid=30602372}}
* {{cite journal | vauthors = Kirkin AF, Dzhandzhugazyan K, Zeuthen J | title = The immunogenic properties of melanoma-associated antigens recognized by cytotoxic T lymphocytes | journal = Experimental and Clinical Immunogenetics | volume = 15 | issue = 1 | pages = 19–32 | year = 1998 | pmid = 9619397 | doi = 10.1159/000019050 }}
* {{cite journal | vauthors = Kirkin AF, Dzhandzhugazyan K, Zeuthen J | title = The immunogenic properties of melanoma-associated antigens recognized by cytotoxic T lymphocytes | journal = Experimental and Clinical Immunogenetics | volume = 15 | issue = 1 | pages = 19–32 | year = 1998 | pmid = 9619397 | doi = 10.1159/000019050 }}
* {{cite journal | vauthors = Matsushita M, Yamazaki R, Ikeda H, Kawakami Y | title = Preferentially expressed antigen of melanoma (PRAME) in the development of diagnostic and therapeutic methods for hematological malignancies | journal = Leukemia & Lymphoma | volume = 44 | issue = 3 | pages = 439–44 | date = Mar 2003 | pmid = 12688312 | doi = 10.1080/1042819021000035725 }}
* {{cite journal | vauthors = Matsushita M, Yamazaki R, Ikeda H, Kawakami Y | title = Preferentially expressed antigen of melanoma (PRAME) in the development of diagnostic and therapeutic methods for hematological malignancies | journal = Leukemia & Lymphoma | volume = 44 | issue = 3 | pages = 439–44 | date = Mar 2003 | pmid = 12688312 | doi = 10.1080/1042819021000035725 }}

Revision as of 09:20, 18 July 2019

PRAME
Identifiers
AliasesPRAME, CT130, MAPE, OIP-4, OIP4, preferentially expressed antigen in melanoma, PRAME nuclear receptor transcriptional regulator
External IDsOMIM: 606021 HomoloGene: 48404 GeneCards: PRAME
Orthologs
SpeciesHumanMouse
Entrez

23532

n/a

Ensembl

ENSG00000185686
ENSG00000275013

n/a

UniProt

P78395

n/a

RefSeq (mRNA)

n/a

RefSeq (protein)

n/a

Location (UCSC)Chr 22: 22.55 – 22.56 Mbn/a
PubMed search[2]n/a
Wikidata
View/Edit Human

Melanoma antigen preferentially expressed in tumors is a protein that in humans is encoded by the PRAME gene.[3][4][5] Five alternatively spliced transcript variants encoding the same protein have been observed for this gene.[5]

Function

This gene encodes an antigen that is predominantly expressed in human melanomas and that is recognized by cytolytic T lymphocytes. It is not expressed in normal tissues, except testis. This expression pattern is similar to that of other CT antigens, such as MAGE, BAGE and GAGE. However, unlike these other CT antigens, this gene is also expressed in acute leukemias. The overexpression of PRAME in tumor tissues and relative low levels in normal somatic tissues make it an attractive target for cancer therapy. In recent years, immunotherapy has spearheaded a new era of cancer therapy resulting in the development of numerous novel antigen-specific immunotherapy approaches. Studies on PRAME-specific immunotherapy primarily involve vaccines and cellular immunotherapies [6].

PRAME can inhibit retinoic acid signaling and retinoic acid mediated differentiation and apoptosis.[7] PRAME overexpression in triple negative breast cancer has also been found to promote cancer cell motility through induction of the epithelial-to-mesenchymal transition [8].

Model organisms

Model organisms have been used in the study of PRAME function. A conditional knockout mouse line called Prametm1a(KOMP)Wtsi was generated at the Wellcome Trust Sanger Institute.[9] Male and female animals underwent a standardized phenotypic screen[10] to determine the effects of deletion.[11][12][13][14] Additional screens performed: - In-depth immunological phenotyping[15]

References

  1. ^ a b c ENSG00000275013 GRCh38: Ensembl release 89: ENSG00000185686, ENSG00000275013 – Ensembl, May 2017
  2. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  3. ^ Ikeda H, Lethé B, Lehmann F, van Baren N, Baurain JF, de Smet C, Chambost H, Vitale M, Moretta A, Boon T, Coulie PG (Feb 1997). "Characterization of an antigen that is recognized on a melanoma showing partial HLA loss by CTL expressing an NK inhibitory receptor". Immunity. 6 (2): 199–208. doi:10.1016/S1074-7613(00)80426-4. PMID 9047241.
  4. ^ Dunham I, Shimizu N, Roe BA, Chissoe S, Hunt AR, Collins JE, Bruskiewich R, Beare DM, Clamp M, Smink LJ, Ainscough R, Almeida JP, Babbage A, Bagguley C, Bailey J, Barlow K, Bates KN, Beasley O, Bird CP, Blakey S, Bridgeman AM, Buck D, Burgess J, Burrill WD, O'Brien KP (Dec 1999). "The DNA sequence of human chromosome 22". Nature. 402 (6761): 489–95. doi:10.1038/990031. PMID 10591208.
  5. ^ a b "Entrez Gene: PRAME preferentially expressed antigen in melanoma".
  6. ^ Al Khadairi, Ghaneya; Decock, Julie (2019). "Cancer Testis Antigens and Immunotherapy: Where Do We Stand in the Targeting of PRAME?". Cancers. 11 (7). doi:10.3390/cancers11070984. PMID 31311081.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  7. ^ Epping MT, Wang L, Edel MJ, Carlée L, Hernandez M, Bernards R (September 2005). "The human tumor antigen PRAME is a dominant repressor of retinoic acid receptor signaling". Cell. 122 (6): 835–47. doi:10.1016/j.cell.2005.07.003. PMID 16179254.
  8. ^ Al Khadairi, Ghaneya; Naik, Adviti; Thomas, Remy; Al Sulaiti, Bushra; Rizly, Shaheen; Decock, Julie (2019). "PRAME promotes epithelial-to-mesenchymal transition in triple negative breast cancer". J Transl Med. 17 (1): 9. doi:10.1186/s12967-018-1757-3. PMID 30602372.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  9. ^ Gerdin AK (2010). "The Sanger Mouse Genetics Programme: high throughput characterisation of knockout mice". Acta Ophthalmologica. 88: 925–7. doi:10.1111/j.1755-3768.2010.4142.x.
  10. ^ a b "International Mouse Phenotyping Consortium".
  11. ^ Skarnes WC, Rosen B, West AP, Koutsourakis M, Bushell W, Iyer V, Mujica AO, Thomas M, Harrow J, Cox T, Jackson D, Severin J, Biggs P, Fu J, Nefedov M, de Jong PJ, Stewart AF, Bradley A (Jun 2011). "A conditional knockout resource for the genome-wide study of mouse gene function". Nature. 474 (7351): 337–42. doi:10.1038/nature10163. PMC 3572410. PMID 21677750.
  12. ^ Dolgin E (Jun 2011). "Mouse library set to be knockout". Nature. 474 (7351): 262–3. doi:10.1038/474262a. PMID 21677718.
  13. ^ Collins FS, Rossant J, Wurst W (Jan 2007). "A mouse for all reasons". Cell. 128 (1): 9–13. doi:10.1016/j.cell.2006.12.018. PMID 17218247.
  14. ^ White JK, Gerdin AK, Karp NA, Ryder E, Buljan M, Bussell JN, Salisbury J, Clare S, Ingham NJ, Podrini C, Houghton R, Estabel J, Bottomley JR, Melvin DG, Sunter D, Adams NC, Tannahill D, Logan DW, Macarthur DG, Flint J, Mahajan VB, Tsang SH, Smyth I, Watt FM, Skarnes WC, Dougan G, Adams DJ, Ramirez-Solis R, Bradley A, Steel KP (Jul 2013). "Genome-wide generation and systematic phenotyping of knockout mice reveals new roles for many genes". Cell. 154 (2): 452–64. doi:10.1016/j.cell.2013.06.022. PMC 3717207. PMID 23870131.
  15. ^ a b "Infection and Immunity Immunophenotyping (3i) Consortium".

Further reading

  • Al Khadairi, Ghaneya; Decock, Julie (2019). "Cancer Testis Antigens and Immunotherapy: Where Do We Stand in the Targeting of PRAME?". Cancers. 11 (7). doi:10.3390/cancers11070984. PMID 31311081.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  • Al Khadairi, Ghaneya; Naik, Adviti; Thomas, Remy; Al Sulaiti, Bushra; Rizly, Shaheen; Decock, Julie (2019). "PRAME promotes epithelial-to-mesenchymal transition in triple negative breast cancer". J Transl Med. 17 (1): 9. doi:10.1186/s12967-018-1757-3. PMID 30602372.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  • Kirkin AF, Dzhandzhugazyan K, Zeuthen J (1998). "The immunogenic properties of melanoma-associated antigens recognized by cytotoxic T lymphocytes". Experimental and Clinical Immunogenetics. 15 (1): 19–32. doi:10.1159/000019050. PMID 9619397.
  • Matsushita M, Yamazaki R, Ikeda H, Kawakami Y (Mar 2003). "Preferentially expressed antigen of melanoma (PRAME) in the development of diagnostic and therapeutic methods for hematological malignancies". Leukemia & Lymphoma. 44 (3): 439–44. doi:10.1080/1042819021000035725. PMID 12688312.
  • Bonaldo MF, Lennon G, Soares MB (Sep 1996). "Normalization and subtraction: two approaches to facilitate gene discovery". Genome Research. 6 (9): 791–806. doi:10.1101/gr.6.9.791. PMID 8889548.
  • Williams JM, Chen GC, Zhu L, Rest RF (Jan 1998). "Using the yeast two-hybrid system to identify human epithelial cell proteins that bind gonococcal Opa proteins: intracellular gonococci bind pyruvate kinase via their Opa proteins and require host pyruvate for growth". Molecular Microbiology. 27 (1): 171–86. doi:10.1046/j.1365-2958.1998.00670.x. PMID 9466265.
  • Neumann E, Engelsberg A, Decker J, Störkel S, Jaeger E, Huber C, Seliger B (Sep 1998). "Heterogeneous expression of the tumor-associated antigens RAGE-1, PRAME, and glycoprotein 75 in human renal cell carcinoma: candidates for T-cell-based immunotherapies?". Cancer Research. 58 (18): 4090–5. PMID 9751617.
  • van Baren N, Chambost H, Ferrant A, Michaux L, Ikeda H, Millard I, Olive D, Boon T, Coulie PG (Sep 1998). "PRAME, a gene encoding an antigen recognized on a human melanoma by cytolytic T cells, is expressed in acute leukaemia cells". British Journal of Haematology. 102 (5): 1376–9. doi:10.1046/j.1365-2141.1998.00982.x. PMID 9753074.
  • Watari K, Tojo A, Nagamura-Inoue T, Nagamura F, Takeshita A, Fukushima T, Motoji T, Tani K, Asano S (Jan 2000). "Identification of a melanoma antigen, PRAME, as a BCR/ABL-inducible gene". FEBS Letters. 466 (2–3): 367–71. doi:10.1016/S0014-5793(00)01112-1. PMID 10682862.
  • Pellat-Deceunynck C, Mellerin MP, Labarrière N, Jego G, Moreau-Aubry A, Harousseau JL, Jotereau F, Bataille R (Mar 2000). "The cancer germ-line genes MAGE-1, MAGE-3 and PRAME are commonly expressed by human myeloma cells". European Journal of Immunology. 30 (3): 803–9. doi:10.1002/1521-4141(200003)30:3<803::AID-IMMU803>3.0.CO;2-P. PMID 10741395.
  • Matsushita M, Ikeda H, Kizaki M, Okamoto S, Ogasawara M, Ikeda Y, Kawakami Y (Mar 2001). "Quantitative monitoring of the PRAME gene for the detection of minimal residual disease in leukaemia". British Journal of Haematology. 112 (4): 916–26. doi:10.1046/j.1365-2141.2001.02670.x. PMID 11298586.
  • Steinbach D, Hermann J, Viehmann S, Zintl F, Gruhn B (Mar 2002). "Clinical implications of PRAME gene expression in childhood acute myeloid leukemia". Cancer Genetics and Cytogenetics. 133 (2): 118–23. doi:10.1016/S0165-4608(01)00570-2. PMID 11943337.
  • Steinbach D, Viehmann S, Zintl F, Gruhn B (Oct 2002). "PRAME gene expression in childhood acute lymphoblastic leukemia". Cancer Genetics and Cytogenetics. 138 (1): 89–91. doi:10.1016/S0165-4608(02)00582-4. PMID 12419593.
  • Lehner B, Semple JI, Brown SE, Counsell D, Campbell RD, Sanderson CM (Jan 2004). "Analysis of a high-throughput yeast two-hybrid system and its use to predict the function of intracellular proteins encoded within the human MHC class III region". Genomics. 83 (1): 153–67. doi:10.1016/S0888-7543(03)00235-0. PMID 14667819.
  • Oberthuer A, Hero B, Spitz R, Berthold F, Fischer M (Jul 2004). "The tumor-associated antigen PRAME is universally expressed in high-stage neuroblastoma and associated with poor outcome". Clinical Cancer Research. 10 (13): 4307–13. doi:10.1158/1078-0432.CCR-03-0813. PMID 15240516.
  • Collins JE, Wright CL, Edwards CA, Davis MP, Grinham JA, Cole CG, Goward ME, Aguado B, Mallya M, Mokrab Y, Huckle EJ, Beare DM, Dunham I (2005). "A genome annotation-driven approach to cloning the human ORFeome". Genome Biology. 5 (10): R84. doi:10.1186/gb-2004-5-10-r84. PMC 545604. PMID 15461802.{{cite journal}}: CS1 maint: unflagged free DOI (link)
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