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Gene Review

RB1  -  retinoblastoma 1

Homo sapiens

Synonyms: OSRC, PPP1R130, RB, Rb, Retinoblastoma-associated protein, ...
 Deloukas,  Clegg,  Ashwell,  Earthrowl,  Bird,  Wilming,  Searle,  Wray,  Burrill,  Kirita,  Faulkner,  Keenan,  Tester,  Burton,  Xiong,  Okabe,  Wright,  Gilbert,  Ashcroft,  Steward,  Young,  Tracey,  Brown,  Mashreghi-Mohammadi,  Oliver,  Leongamornlert,  Howden,  Thomas,  Lloyd,  Whitehead,  Wall,  Dhami,  Ghori,  Lloyd,  Tubby,  Clee,  Heath,  Scott,  Teramoto,  Laird,  Carter,  Schulz,  Erdos,  Grafham,  Gilson,  Bannerjee,  Garnett,  Ikuta,  Nakamura,  Lovell,  Bailey,  Ellington,  Chapman,  Pestell,  Kimberley,  Hunt,  Martin,  Phillimore,  Dunham,  Ross,  Cobley,  Rosen,  Clark,  Burford,  Yuan ,  Corby,  Griffiths,  Babbage,  Garner,  Ambrose,  Hall,  French,  Kontani,  Griffiths-Jones,  Huckle,  Sehra,  Coville,  Carder,  Frankish,  Hunt,  Dunn,  Zhao,  Kishi,  Nickerson,  Smith,  Langford,  Beasley,  Shownkeen,  McLaren,  Beare,  Johnson,  Clarke,  Bentley,  Willey,  Gribble,  Bray-Allen,  Beck,  Hammond,  Fan,  Hart,  Chano,  Sulston,  Porter,  Pelan,  Bates,  Rogers,  Milne,  Frankland,  Ainscough,  Johnson,  West,  Almeida,  Lawlor,  Bagguley,  Hunt,  Ashurst,  Ma,  Barlow,  Ikegawa,  Moore,  Durbin,  Hubbard,  King,  Collins,  Harley,  Dunham,  Rice,  Andrews,  Sycamore,  Wallis,  Peck,  Loveland,  Clamp,  Jones,  Skuce,  Pearce,  Coulson,  Nishimine,  Tromans,  Matthews,  Brown,  Palmer,  Konishi,  Goldberg,  Howe,  Kay,  McMurray,  Meng,  
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Disease relevance of RB1

  • Although it is generally believed that the product of the retinoblastoma susceptibility gene (RB1) is an important regulator of cell proliferation, the biochemical mechanism for its action is unclear [1].
  • Studies of known TSG at these loci, including the menin gene and RB1, would suggest a limited role, if any, in pituitary tumors [2].
  • We have previously reported that approximately two-thirds of glioblastomas (GBs) had abnormalities of G1-S transition control either by mutation/homozygous deletion of RB1 or CDKN2A p16INK4A), or amplification of CDK4 (K [3].
  • A series of 195 human gliomas were studied as to the status of their CDKN2A, CDK4 and RB1 genes [4].
  • Of 13 anaplastic astrocytomas with an altered RB1 pathway, 9 (69%) also showed a dysregulated TP53 pathway [5].
  • In the absence of predisposition, TP53 was biallelically inactivated in one-third of the sarcomas, whereas at least one allele of RB1 was wild type [6].

Psychiatry related information on RB1


High impact information on RB1

  • Wildtype RB1CC1 and RB1 were absent or significantly less abundant than normal in the seven cancers with mutations in RB1CC1, but were abundant in cancers without such mutations [9].
  • Thus, identification of factors that interfere with and/or control the function of the RB protein is critical for understanding both cell-cycle control and oncogenesis [10].
  • Whereas loss of RB function is associated with the loss of cellular proliferative control, introduction of a wild-type RB can suppress cell growth and tumorigenicity [10].
  • Inactivation of the RB gene is common in parathyroid carcinoma and is likely to be an important contributor to its molecular pathogenesis [11].
  • None of the 19 adenomas, including the tumor with loss of an RB allele, had unequivocally abnormal staining for RB protein [11].

Chemical compound and disease context of RB1


Biological context of RB1

  • However, loss of pRB is evident in a proportion of somatotropinomas but is not associated with allelic loss of an RB1 intragenic marker [2].
  • Approaches used to localize and identify the paradigm of tumor suppressors, RB1, have also been applied to localize tumor suppressor genes on 3p, the short arm of chromosome 3 [17].
  • Twelve cell lines had a mutation in exons 5-11 of TP53 and, with only one exception, a concomitant loss of RB1 protein expression [18].
  • The RB1/p16INK4a gene pair displayed aberrant methylayed alleles in 15% of cases, whereas methylation was relatively rare in the other genes (<5%) [19].
  • In contrast, invasive UC are characterized by severe disturbances in proximate cell cycle regulators, e.g. RB1 and CDKN2A/p16(INK4A), which decrease dependency on mitogenic signaling [20].

Anatomical context of RB1


Associations of RB1 with chemical compounds

  • We report that induction of a protein-serine/threonine phosphatase activity by DNA damage signals is at least one of the mechanisms responsible for p53-independent, RB-mediated G1 arrest and consequent apoptosis [26].
  • Furthermore, the induced phosphatase activity coimmunoprecipitated with the hyperphosphorylated RB and was active in a cell-free system that reproduced the growth arrest- and apoptosis-specific RB dephosphorylation, which was inhibitable by calyculin A but not zinc [26].
  • RB contains at least three distinct protein binding functions: (i) the A/B pocket, which binds proteins with the LXCXE motif; (ii) the C pocket, which binds the c-Abl tyrosine kinase; and (iii) the large A/B pocket, which binds the E2F family of transcription factors [27].
  • Additionally, phosphorylation of two serine sites in the insert domain can inhibit E2F binding, but this inhibition requires the presence of the RB N-terminal region [27].
  • By monitoring protein-DNA interactions in living cells using formaldehyde cross-linking and chromatin immunoprecipitation, we show that endogenous RB and AP-2 both bind to the same bcl-2 promoter sequence [28].

Physical interactions of RB1

  • Recent experiments have shown that the E2F transcription factor is in a complex with the RB1 gene product [29].
  • RB binding sites on BRCA1 were identified in the C-terminal BRCT domain (Yarden and Brody, 1999) and in the N-terminus (aa 304-394) (Aprelikova et al., 1999) [30].
  • In this report, we would like to stress particularly that the p53/RB pathway and its complex, interplay with the bcl2 gene family, where paramount elements of apoptosis regulation are operating [31].
  • RB formed stable complexes with all three C/EBP family members [32].
  • In contrast, the TBP-containing complex TFIIIB restores adenovirus VAI but not human U6 transcription in RB-treated extracts, suggesting that TFIIIB is important for RB regulation of tRNA-like genes [33].

Enzymatic interactions of RB1

  • In addition, treatment of G1/S Daudi cells with IFN-alpha also inhibited the ability of CDK2 enzyme to phosphorylate the RB protein in vitro [34].
  • CDK2 and CDK4 known promoter of cell cycling catalyze phosphorylation of RB protein [35].
  • FMS overexpression also progressively increased the relative amount of dephosphorylated RB protein induced, while reducing the total amount of RB protein [36].
  • No UCN-01-induced G1 accumulation in SBC-3 cells was observed in SBC-3/UCN cells and decreased expression of phosphorylated RB protein was found in SBC-3 cells [37].
  • RB is phosphorylated by cyclin-dependent protein kinase during cell cycle progression [38].

Regulatory relationships of RB1

  • Taken together, these results suggest that the interaction of RB with E2F is an important event in the control of cellular proliferation and that the dissociation of the complex is part of the mechanism by which E1A inactivates RB function [1].
  • Conversely, E2F-1 overrode an RB-induced G1 block more efficiently than E2F-4 [39].
  • Consistent with this, APC transfection inhibits RB phosphorylation and reduces levels of cyclin D1 [40].
  • In this study we show that p16INK4a is expressed in cervical cancer cell lines in which the RB gene, Rb, is not functional, either as a consequence of Rb mutation or expression of the human papillomavirus E7 protein [41].
  • This study provides evidence that RB activates bcl-2 and E-cadherin by binding directly to the respective promoter sequences and not indirectly by repressing an inhibitor [28].

Other interactions of RB1

  • The E2F transcription factor is a cellular target for the RB protein [1].
  • Both p53 and retinoblastoma genes are frequently mutated in human cancers, and the simultaneous inactivation of RB and p53 is frequently observed in a variety of naturally occurring human tumours [42].
  • Immortal HUCs and bladder cancer cell lines show either alteration of p16 or pRb, the product of the retinoblastoma (RB) TSG [43].
  • The data suggest the possibility that the premature and prolonged enhancement of CDK activity in thiol-deprived NK cells is associated with, and therefore may contribute to, the reduced expression and phosphorylation of RB, and the associated cell cycle arrest [44].
  • The growth suppressor activities of the RB and p107 products are believed to be mediated by the reversible binding of a heterogeneous family of cellular proteins to a conserved T/E1A pocket domain that is present within both proteins [45].

Analytical, diagnostic and therapeutic context of RB1


  1. The E2F transcription factor is a cellular target for the RB protein. Chellappan, S.P., Hiebert, S., Mudryj, M., Horowitz, J.M., Nevins, J.R. Cell (1991) [Pubmed]
  2. Molecular pathogenesis of pituitary tumors. Farrell, W.E., Clayton, R.N. Frontiers in neuroendocrinology. (2000) [Pubmed]
  3. Deregulation of the p14ARF/MDM2/p53 pathway is a prerequisite for human astrocytic gliomas with G1-S transition control gene abnormalities. Ichimura, K., Bolin, M.B., Goike, H.M., Schmidt, E.E., Moshref, A., Collins, V.P. Cancer Res. (2000) [Pubmed]
  4. Human glioblastomas with no alterations of the CDKN2A (p16INK4A, MTS1) and CDK4 genes have frequent mutations of the retinoblastoma gene. Ichimura, K., Schmidt, E.E., Goike, H.M., Collins, V.P. Oncogene (1996) [Pubmed]
  5. Concurrent inactivation of RB1 and TP53 pathways in anaplastic oligodendrogliomas. Watanabe, T., Yokoo, H., Yokoo, M., Yonekawa, Y., Kleihues, P., Ohgaki, H. J. Neuropathol. Exp. Neurol. (2001) [Pubmed]
  6. RB1 and TP53 pathways in radiation-induced sarcomas. Gonin-Laurent, N., Hadj-Hamou, N.S., Vogt, N., Houdayer, C., Gauthiers-Villars, M., Dehainault, C., Sastre-Garau, X., Chevillard, S., Malfoy, B. Oncogene (2007) [Pubmed]
  7. The DNA sequence and analysis of human chromosome 13. Dunham, A., Matthews, L.H., Burton, J., Ashurst, J.L., Howe, K.L., Ashcroft, K.J., Beare, D.M., Burford, D.C., Hunt, S.E., Griffiths-Jones, S., Jones, M.C., Keenan, S.J., Oliver, K., Scott, C.E., Ainscough, R., Almeida, J.P., Ambrose, K.D., Andrews, D.T., Ashwell, R.I., Babbage, A.K., Bagguley, C.L., Bailey, J., Bannerjee, R., Barlow, K.F., Bates, K., Beasley, H., Bird, C.P., Bray-Allen, S., Brown, A.J., Brown, J.Y., Burrill, W., Carder, C., Carter, N.P., Chapman, J.C., Clamp, M.E., Clark, S.Y., Clarke, G., Clee, C.M., Clegg, S.C., Cobley, V., Collins, J.E., Corby, N., Coville, G.J., Deloukas, P., Dhami, P., Dunham, I., Dunn, M., Earthrowl, M.E., Ellington, A.G., Faulkner, L., Frankish, A.G., Frankland, J., French, L., Garner, P., Garnett, J., Gilbert, J.G., Gilson, C.J., Ghori, J., Grafham, D.V., Gribble, S.M., Griffiths, C., Hall, R.E., Hammond, S., Harley, J.L., Hart, E.A., Heath, P.D., Howden, P.J., Huckle, E.J., Hunt, P.J., Hunt, A.R., Johnson, C., Johnson, D., Kay, M., Kimberley, A.M., King, A., Laird, G.K., Langford, C.J., Lawlor, S., Leongamornlert, D.A., Lloyd, D.M., Lloyd, C., Loveland, J.E., Lovell, J., Martin, S., Mashreghi-Mohammadi, M., McLaren, S.J., McMurray, A., Milne, S., Moore, M.J., Nickerson, T., Palmer, S.A., Pearce, A.V., Peck, A.I., Pelan, S., Phillimore, B., Porter, K.M., Rice, C.M., Searle, S., Sehra, H.K., Shownkeen, R., Skuce, C.D., Smith, M., Steward, C.A., Sycamore, N., Tester, J., Thomas, D.W., Tracey, A., Tromans, A., Tubby, B., Wall, M., Wallis, J.M., West, A.P., Whitehead, S.L., Willey, D.L., Wilming, L., Wray, P.W., Wright, M.W., Young, L., Coulson, A., Durbin, R., Hubbard, T., Sulston, J.E., Beck, S., Bentley, D.R., Rogers, J., Ross, M.T. Nature (2004) [Pubmed]
  8. Further characterization of retinoblastoma gene-mediated cell growth and tumor suppression in human cancer cells. Zhou, Y., Li, J., Xu, K., Hu, S.X., Benedict, W.F., Xu, H.J. Proc. Natl. Acad. Sci. U.S.A. (1994) [Pubmed]
  9. Truncating mutations of RB1CC1 in human breast cancer. Chano, T., Kontani, K., Teramoto, K., Okabe, H., Ikegawa, S. Nat. Genet. (2002) [Pubmed]
  10. A retinoblastoma-binding protein that affects cell-cycle control and confers transforming ability. Woitach, J.T., Zhang, M., Niu, C.H., Thorgeirsson, S.S. Nat. Genet. (1998) [Pubmed]
  11. Loss of the retinoblastoma tumor-suppressor gene in parathyroid carcinoma. Cryns, V.L., Thor, A., Xu, H.J., Hu, S.X., Wierman, M.E., Vickery, A.L., Benedict, W.F., Arnold, A. N. Engl. J. Med. (1994) [Pubmed]
  12. Human pituitary adenomas infrequently contain inactivation of retinoblastoma 1 gene and activation of cyclin dependent kinase 4 gene. Honda, S., Tanaka-Kosugi, C., Yamada, S., Sano, T., Matsumoto, T., Itakura, M., Yoshimoto, K. Endocr. J. (2003) [Pubmed]
  13. A fumagillin derivative angiogenesis inhibitor, AGM-1470, inhibits activation of cyclin-dependent kinases and phosphorylation of retinoblastoma gene product but not protein tyrosyl phosphorylation or protooncogene expression in vascular endothelial cells. Abe, J., Zhou, W., Takuwa, N., Taguchi, J., Kurokawa, K., Kumada, M., Takuwa, Y. Cancer Res. (1994) [Pubmed]
  14. Activation of cyclin D1-Cdk4 and Cdk4-directed phosphorylation of RB protein in diabetic mesangial hypertrophy. Féliers, D., Frank, M.A., Riley, D.J. Diabetes (2002) [Pubmed]
  15. Androgens repress Bcl-2 expression via activation of the retinoblastoma (RB) protein in prostate cancer cells. Huang, H., Zegarra-Moro, O.L., Benson, D., Tindall, D.J. Oncogene (2004) [Pubmed]
  16. Cell-permeable ceramide inhibits the growth of B lymphoma Raji cells lacking TNF-alpha-receptors by inducing G0/G1 arrest but not apoptosis: a new model for dissecting cell-cycle arrest and apoptosis. Kuroki, J., Hirokawa, M., Kitabayashi, A., Lee, M., Horiuchi, T., Kawabata, Y., Miura, A.B. Leukemia (1996) [Pubmed]
  17. Deletions of the short arm of chromosome 3 in solid tumors and the search for suppressor genes. Kok, K., Naylor, S.L., Buys, C.H. Adv. Cancer Res. (1997) [Pubmed]
  18. Presence and location of TP53 mutation determines pattern of CDKN2A/ARF pathway inactivation in bladder cancer. Markl, I.D., Jones, P.A. Cancer Res. (1998) [Pubmed]
  19. CpG island methylation in sporadic and neurofibromatis type 2-associated schwannomas. Gonzalez-Gomez, P., Bello, M.J., Alonso, M.E., Lomas, J., Arjona, D., Campos, J.M., Vaquero, J., Isla, A., Lassaletta, L., Gutierrez, M., Sarasa, J.L., Rey, J.A. Clin. Cancer Res. (2003) [Pubmed]
  20. Understanding urothelial carcinoma through cancer pathways. Schulz, W.A. Int. J. Cancer (2006) [Pubmed]
  21. Frequent disruption of the RB1 pathway in diffuse large B cell lymphoma: prognostic significance of E2F-1 and p16INK4A. Møller, M.B., Kania, P.W., Ino, Y., Gerdes, A.M., Nielsen, O., Louis, D.N., Skjødt, K., Pedersen, N.T. Leukemia (2000) [Pubmed]
  22. Molecular control of the cell cycle in cancer: biological and clinical aspects. Møller, M.B. Danish medical bulletin. (2003) [Pubmed]
  23. Multiple functions of D-type cyclins can antagonize pRb-mediated suppression of proliferation. Baker, G.L., Landis, M.W., Hinds, P.W. Cell Cycle (2005) [Pubmed]
  24. Genetic and epigenetic alteration profiles for multiple genes in salivary gland carcinomas. Kishi, M., Nakamura, M., Nishimine, M., Ikuta, M., Kirita, T., Konishi, N. Oral Oncol. (2005) [Pubmed]
  25. Mutations and altered expression of p16INK4 in human cancer. Okamoto, A., Demetrick, D.J., Spillare, E.A., Hagiwara, K., Hussain, S.P., Bennett, W.P., Forrester, K., Gerwin, B., Serrano, M., Beach, D.H. Proc. Natl. Acad. Sci. U.S.A. (1994) [Pubmed]
  26. Induction of a retinoblastoma phosphatase activity by anticancer drugs accompanies p53-independent G1 arrest and apoptosis. Dou, Q.P., An, B., Will, P.L. Proc. Natl. Acad. Sci. U.S.A. (1995) [Pubmed]
  27. Dual mechanisms for the inhibition of E2F binding to RB by cyclin-dependent kinase-mediated RB phosphorylation. Knudsen, E.S., Wang, J.Y. Mol. Cell. Biol. (1997) [Pubmed]
  28. The retinoblastoma protein binds the promoter of the survival gene bcl-2 and regulates its transcription in epithelial cells through transcription factor AP-2. Decary, S., Decesse, J.T., Ogryzko, V., Reed, J.C., Naguibneva, I., Harel-Bellan, A., Cremisi, C.E. Mol. Cell. Biol. (2002) [Pubmed]
  29. The interaction of RB with E2F coincides with an inhibition of the transcriptional activity of E2F. Hiebert, S.W., Chellappan, S.P., Horowitz, J.M., Nevins, J.R. Genes Dev. (1992) [Pubmed]
  30. Disruption of BRCA1 LXCXE motif alters BRCA1 functional activity and regulation of RB family but not RB protein binding. Fan, S., Yuan , R., Ma, Y.X., Xiong, J., Meng, Q., Erdos, M., Zhao, J.N., Goldberg, I.D., Pestell, R.G., Rosen, E.M. Oncogene (2001) [Pubmed]
  31. Complex interplay among apoptosis factors: RB, p53, E2F, TGF-beta, cell cycle inhibitors and the bcl2 gene family. Chiarugi, V., Magnelli, L., Cinelli, M. Pharmacol. Res. (1997) [Pubmed]
  32. Retinoblastoma protein complexes with C/EBP proteins and activates C/EBP-mediated transcription. Charles, A., Tang, X., Crouch, E., Brody, J.S., Xiao, Z.X. J. Cell. Biochem. (2001) [Pubmed]
  33. The retinoblastoma tumor suppressor protein targets distinct general transcription factors to regulate RNA polymerase III gene expression. Hirsch, H.A., Gu, L., Henry, R.W. Mol. Cell. Biol. (2000) [Pubmed]
  34. Interferon-alpha inhibits cyclin E- and cyclin D1-dependent CDK-2 kinase activity associated with RB protein and E2F in Daudi cells. Zhang, K., Kumar, R. Biochem. Biophys. Res. Commun. (1994) [Pubmed]
  35. Biochemical characterizations reveal different properties between CDK4/cyclin D1 and CDK2/cyclin A. Kim, D.M., Yang, K., Yang, B.S. Exp. Mol. Med. (2003) [Pubmed]
  36. FMS (CSF-1 receptor) prolongs cell cycle and promotes retinoic acid-induced hypophosphorylation of retinoblastoma protein, G1 arrest, and cell differentiation. Yen, A., Sturgill, R., Varvayanis, S., Chern, R. Exp. Cell Res. (1996) [Pubmed]
  37. Molecular determinants of UCN-01-induced growth inhibition in human lung cancer cells. Usuda, J., Saijo, N., Fukuoka, K., Fukumoto, H., Kuh, H.J., Nakamura, T., Koh, Y., Suzuki, T., Koizumi, F., Tamura, T., Kato, H., Nishio, K. Int. J. Cancer (2000) [Pubmed]
  38. Phosphorylation site mutated RB exerts contrasting effects on apoptotic response to different stimuli. Masselli, A., Wang, J.Y. Oncogene (2006) [Pubmed]
  39. Functional interaction between E2F-4 and p130: evidence for distinct mechanisms underlying growth suppression by different retinoblastoma protein family members. Vairo, G., Livingston, D.M., Ginsberg, D. Genes Dev. (1995) [Pubmed]
  40. The APC tumor suppressor controls entry into S-phase through its ability to regulate the cyclin D/RB pathway. Heinen, C.D., Goss, K.H., Cornelius, J.R., Babcock, G.F., Knudsen, E.S., Kowalik, T., Groden, J. Gastroenterology (2002) [Pubmed]
  41. Inhibition of cyclin D-CDK4/CDK6 activity is associated with an E2F-mediated induction of cyclin kinase inhibitor activity. Khleif, S.N., DeGregori, J., Yee, C.L., Otterson, G.A., Kaye, F.J., Nevins, J.R., Howley, P.M. Proc. Natl. Acad. Sci. U.S.A. (1996) [Pubmed]
  42. Interaction between the retinoblastoma protein and the oncoprotein MDM2. Xiao, Z.X., Chen, J., Levine, A.J., Modjtahedi, N., Xing, J., Sellers, W.R., Livingston, D.M. Nature (1995) [Pubmed]
  43. Overcoming cellular senescence in human cancer pathogenesis. Yeager, T.R., DeVries, S., Jarrard, D.F., Kao, C., Nakada, S.Y., Moon, T.D., Bruskewitz, R., Stadler, W.M., Meisner, L.F., Gilchrist, K.W., Newton, M.A., Waldman, F.M., Reznikoff, C.A. Genes Dev. (1998) [Pubmed]
  44. Control of cell cycle progression in human natural killer cells through redox regulation of expression and phosphorylation of retinoblastoma gene product protein. Yamauchi, A., Bloom, E.T. Blood (1997) [Pubmed]
  45. Differential specificity for binding of retinoblastoma binding protein 2 to RB, p107, and TATA-binding protein. Kim, Y.W., Otterson, G.A., Kratzke, R.A., Coxon, A.B., Kaye, F.J. Mol. Cell. Biol. (1994) [Pubmed]
  46. Molecular alterations of the RB1, TP53, and MDM2 genes in primary and xenografted human osteosarcomas. Pellín, A., Boix-Ferrero, J., Carpio, D., López-Terrada, D., Carda, C., Navarro, S., Peydró-Olaya, A., Triche, T.J., Llombart-Bosch, A. Diagn. Mol. Pathol. (1997) [Pubmed]
  47. RB1CC1 suppresses cell cycle progression through RB1 expression in human neoplastic cells. Kontani, K., Chano, T., Ozaki, Y., Tezuka, N., Sawai, S., Fujino, S., Saeki, Y., Okabe, H. Int. J. Mol. Med. (2003) [Pubmed]
  48. Frequent loss of 9p21 (p16(INK4A)) and other genomic imbalances in human malignant fibrous histiocytoma. Simons, A., Schepens, M., Jeuken, J., Sprenger, S., van de Zande, G., Bjerkehagen, B., Forus, A., Weibolt, V., Molenaar, I., van den Berg, E., Myklebost, O., Bridge, J., van Kessel, A.G., Suijkerbuijk, R. Cancer Genet. Cytogenet. (2000) [Pubmed]
  49. Altered retinoblastoma protein expression and prognosis in early-stage non-small-cell lung carcinoma. Xu, H.J., Quinlan, D.C., Davidson, A.G., Hu, S.X., Summers, C.L., Li, J., Benedict, W.F. J. Natl. Cancer Inst. (1994) [Pubmed]
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