In conclusion, TP53 mutation was observed in as high as 40% of B-precursor ALL cell lines, but was significantly less frequent among Ph1 and t(17;19)-positive ALL cell lines. TP53 mutation might be associated with the functional significance of the fusion gene product derived from translocation in the p53 pathway. (KOPN-30bi, 257bi, 266bi, 272bi, YAMN-73, 283bi, and 291) , 4 t(17;19)-ALL cell lines [11] (UOC-B1, HAL01 [14] , YCUB-2 [15] , Endo-kun), and 5 other ALL cell lines including 1 with t(12;21) (Reh) [16] and 4 with others (Nalm6, KOPN-32 [13] , 235 [13] , and 261 [17] ). Total RNA was extracted using the Trizol reagent (Invitrogen, Carlsbad, CA), reverse transcription was performed using random hexamer (Amersham Bioscience, Buckinghamshire, United Kingdom) by Superscript II reverse transcriptase (Invitrogen), and then incubated with RNase (Invitrogen). The state of the TP53 gene was tested by the yeast functional assay [12] as described previously [22, 23] . In brief, RT-PCR amplified TP53 cDNAs were cotransfected with a linealized gap vector carrying the 5 0 and 3 0 ends of the gene into the yIG397 strain containing an integrated plasmid with the ADE2 open reading frame under the control of TP53-responsive promoter. Yeast containing the mutant TP53 cDNA fails to transcribe ADE mRNA and formed red colonies, whereas yeast expressing the wild-type TP53 forms white colonies. Thus, the status of the TP53 gene is quantitatively analyzed by the color of colonies. When functional assay demonstrated the TP53 mutation, sequences of We describe here the clinical manifestations of 37 patients with combined coagulation factor (F) V and FVIII deficiency, which is the commonest multiple coagulation factor deficiency state. Only a few cases are reported in the literature from India. Prolonged bleed post injury/ surgery (62%) is the commonest manifestation in our series, and epistaxis (19%) is rare in our patients in comparison to other series described in the literature. Although the frequency of bleeding manifestations differs among various reports, there is no evidence for increased bleeding manifestation due to combined deficiency of two coagulation factors as against a single coagulation factor. To the best of our knowledge, this is the largest series of this disorder described so far. Combined Factor (F) V and VIII is the commonest combined hereditary coagulation factor deficiency with a prevalence of 1:1,000,000 [1] . It is an autosomal recessive disorder of blood coagulation [2] and the frequency of such autosomal recessive disorders increases 8-10-folds in populations where consanguinity is common. It is caused by a defect in lectin mannose binding protein 1 (LMAN 1) gene or in multiple coagulation factor deficiency (MCFD) gene 2 [3] [4] [5] . It was initially described by Oeri et al. [6] in 1954 and so far about 150 patients have been described from around the world [7] [8] [9] [10] [11] . The largest of these studies so far, describe the clinical manifestations of this disorder in 27 patients of Iranian origin [7] . Patients who are homozygous for this combined factor deficiency state maintain a factor level between 4% and 30% [12, 13] . We present herewith the clinical and phenotypic data of combined FV and FVIII deficiency in a large series of 37 patients of Indian origin seen at our center.