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. 2013 Jul 22;202(2):295–309. doi: 10.1083/jcb.201210099

Table 4.

p53 status in K243R/+ tumors

Tumor Sex Age Mutationa Mutanta Effect p_domainb
wk
Hepatocellular carcinoma 1 Male 61 c.163ins_T STOP 55 Insertion TAD
Hepatocellular carcinoma 2 Male 117 c.242C>Tc.301C>T p.A81Vp.Q101X MissenseNonsense PRDDBD
Sarcoma 1 Male 69 c.163ins_Tc.296ins_A STOP 55STOP 99 InsertionInsertion TADDBD
Sarcoma 2 Female 122 c.296ins_Ac.467C>T STOP 99p.A156V InsertionMissense DBDDBD
B cell lymphoma 1 Female 62 c.359-365del7 STOP 128 Deletion DBD
B cell lymphoma 2 Female 119 c.109T>C;980T>Cc.429G>A p.S37P;L327Pp.W143X MissenseNonsense TAD, 4DDBD
B cell lymphoma 3 Female 139 c.443C>T p.P148L Missense DBD
Leukemia 1 Female 57 c.1064A>Gc.841A>G p.E355Gp.T281A MissenseMissense DBDDBD
a

Mutation nomenclatures follow the Human Genome Variation Society recommendations. c, coding sequence; ins, insertion; del, deletion; p, protein sequence. p53 status was determined by the nucleotide sequencing of four to five clones derived from each tumor.

b

Protein domain with mutation indicated. TAD, transactivation domain; PRD, proline-rich domain; DBD, DNA-binding domain; 4D, tetramerization domain.