PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
33994742-12	2021	p53 was overexpressed in smokers (80.95%) and those consuming alcohol (60%).	Alcohols	62-69	tumor protein p53	Homo sapiens	0-3	
33290139-9	2020	Conclusion: The p53 rs1042522 arg allele together with tobacco smoking and alcohol drinking, was associated with an increased risk, for gastric cancer and EC, but not the survival among northwestern Chinese patients.	Alcohols	75-82	tumor protein p53	Homo sapiens	16-19	
33560536-4	2021	TP53 mutations are highly prevalent in OPSCC driven by mutagens in tobacco and alcohol.	Alcohols	79-86	tumor protein p53	Homo sapiens	0-4	
29351612-10	2018	This alcohol consumption signature was also observed in liver cancer and head and neck squamous cell carcinoma, and its mutational activity was substantially higher in samples with mutations in TP53.	Alcohols	5-12	tumor protein p53	Homo sapiens	194-198	
31786674-6	2020	This increased risk of death observed for alcohol consumers was more evident in patients with normal p53 expression, GLUT-1 positive or CD-8 positive tumors.	Alcohols	42-49	tumor protein p53	Homo sapiens	101-104	
20301488-16	1993	Agents/circumstances to avoid: People with germline TP53 pathogenic variants should: (1) avoid known carcinogens including sun exposure, tobacco use, occupational exposures, and excessive alcohol use; and (2) minimize exposure to diagnostic and therapeutic radiation.	Alcohols	188-195	tumor protein p53	Homo sapiens	52-56	
30057300-5	2018	Further experimental testing demonstrated that Michael acceptors, aldehydes, imines, and primary alcohols can promote thermodynamic stabilization of mutant p53.	Alcohols	97-105	tumor protein p53	Homo sapiens	156-159	
30057300-6	2018	Moreover, mild thiol reactivity, often coupled with combined chemical functional groups, such as in imines, aldehydes, and primary alcohols, can stimulate mutant p53 refolding.	Alcohols	131-139	tumor protein p53	Homo sapiens	162-165	
28369097-0	2017	p53 pathway determines the cellular response to alcohol-induced DNA damage in MCF-7 breast cancer cells.	Alcohols	48-55	tumor protein p53	Homo sapiens	0-3	
28799801-0	2017	Cross-generational effects of alcohol dependence in humans on HRAS and TP53 methylation in offspring.	Alcohols	30-37	tumor protein p53	Homo sapiens	71-75	
28799801-1	2017	AIM: We hypothesized that cross-generational effects of alcohol exposure could alter DNA methylation and expression of the HRAS oncogene and TP53 tumor suppressor gene that drive cancer development.	Alcohols	56-63	tumor protein p53	Homo sapiens	141-145	
28799801-4	2017	CONCLUSION: The results suggest that ancestral exposure to alcohol can have enduring effects that impact epigenetic processes such as DNA methylation that controls expression of genes that drive cancer development such as HRAS and TP53.	Alcohols	59-66	tumor protein p53	Homo sapiens	231-235	
28369097-4	2017	The impact of alcohol on p53 is recognized, yet the role of p53 in alcohol-induced mammary carcinogenesis remains poorly defined.	Alcohols	67-74	tumor protein p53	Homo sapiens	60-63	
28369097-6	2017	p53 activity and target gene expression after alcohol exposure were determined using p53 luciferase reporter assay, qPCR, and Western blotting.	Alcohols	46-53	tumor protein p53	Homo sapiens	0-3	
28369097-6	2017	p53 activity and target gene expression after alcohol exposure were determined using p53 luciferase reporter assay, qPCR, and Western blotting.	Alcohols	46-53	tumor protein p53	Homo sapiens	85-88	
28369097-9	2017	A p53-dependent signaling cascade was stimulated by alcohol-induced DNA damage.	Alcohols	52-59	tumor protein p53	Homo sapiens	2-5	
28369097-2	2017	Alcohol is known to induce oxidative stress and DNA damage; likewise, p53 is a critical modulator of the DNA repair pathway and ensures genomic integrity.	Alcohols	0-7	tumor protein p53	Homo sapiens	70-73	
28369097-10	2017	Moderate to high concentrations of alcohol (0.1-0.8% v/v) induced p53 activation, as indicated by increased p53 phosphorylation, reporter gene activity, and p21/Bax gene expression, which led to G0/G1 cell cycle arrest.	Alcohols	35-42	tumor protein p53	Homo sapiens	66-69	
28369097-10	2017	Moderate to high concentrations of alcohol (0.1-0.8% v/v) induced p53 activation, as indicated by increased p53 phosphorylation, reporter gene activity, and p21/Bax gene expression, which led to G0/G1 cell cycle arrest.	Alcohols	35-42	tumor protein p53	Homo sapiens	108-111	
28357076-7	2017	However, interactions between p53 codon 72 SNP and smoking, alcohol consumption and HBV infection may increase the risk of HCC [smoking odds ratio (OR), 2.00; 95% confidence interval (CI), 1.21-3.29; alcohol consumption OR, 1.87; 95% CI, 1.08-3.26; HBV infection OR, 1.84; 95% CI, 1.10-3.08].	Alcohols	200-207	tumor protein p53	Homo sapiens	30-33	
28369097-13	2017	Our study suggests that functional p53 plays a critical role in cellular responses to alcohol-induced DNA damage, which protects the cells from DNA damage associated with breast cancer risk.	Alcohols	86-93	tumor protein p53	Homo sapiens	35-38	
18242117-3	2008	As mutations in the tumour suppressor gene TP53 are the most common genetic alterations involved in human cancers, especially esophageal tumours, the aim of this work was to establish the mutational pattern induced by acetaldehyde in vitro on the TP53 gene, and to compare this pattern with that found in human alcohol-related tumours.	Alcohols	311-318	tumor protein p53	Homo sapiens	43-47	
24935359-10	2014	The combined p53 with p16(INK4a) profiles were significantly correlated with alcohol consumption in younger patients (p=0.006).	Alcohols	77-84	tumor protein p53	Homo sapiens	13-16	
21468597-7	2011	We found that the TP53 Pro/Pro genotype compared to the Arg/Arg genotype had a profound effect on pancreatic cancer risk among males, particularly among heavy smokers and excessive alcohol drinkers.	Alcohols	181-188	tumor protein p53	Homo sapiens	18-22	
20228093-5	2010	We observed significantly higher mean intakes of alcohol, total meat and red meat, in the group with p53 mutations and advanced Dukes" stage disease (daily alcohol intake was 7 and 12 g for p53- and p53+ cases, respectively, P = 0.04; daily total meat intake was 69 and 100 g for p53- and p53+ cases, respectively, P = 0.03 and daily red meat intake was 39 and 75 g for p53- and p53+ cases, respectively, P = 0.01).	Alcohols	49-56	tumor protein p53	Homo sapiens	101-104	
19948747-0	2010	Study of p53 codon 72 polymorphism and codon 249 mutations in Southern India in relation to age, alcohol drinking and smoking habits.	Alcohols	97-104	tumor protein p53	Homo sapiens	9-12	
24521534-6	2014	Although p53 mutations were associated with tobacco smoking and alcohol drinking, this association disappeared in virus-unrelated HNSCC.	Alcohols	64-71	tumor protein p53	Homo sapiens	9-12	
24435975-7	2014	However, in a multivariate analysis adjusted for alcohol consumption, smoking, ethnicity, and number of pregnancies, the interaction between the genotypes TP53 Arg/Arg (rs1042522) and MDM2 TT (rs2279744) showed to be associated to RPL, increasing the risk for this condition (OR = 2.58, 95% CI: 1.31-5.07, p = 0.006).	Alcohols	49-56	tumor protein p53	Homo sapiens	155-159	
21159183-9	2010	There were indications of p53 aberrations being associated with the combined effect of smoking, alcohol and work history.	Alcohols	96-103	tumor protein p53	Homo sapiens	26-29	
21072901-1	2010	AIM: To investigate p53 mutations in esophageal cancer in a high-risk population, and correlate them with smoking, alcohol consumption and betel chewing.	Alcohols	115-122	tumor protein p53	Homo sapiens	20-23	
18331287-6	2008	RESULTS: p53 expression was significantly higher in users of tobacco and alcohol than in non-users.	Alcohols	73-80	tumor protein p53	Homo sapiens	9-12	
18242117-3	2008	As mutations in the tumour suppressor gene TP53 are the most common genetic alterations involved in human cancers, especially esophageal tumours, the aim of this work was to establish the mutational pattern induced by acetaldehyde in vitro on the TP53 gene, and to compare this pattern with that found in human alcohol-related tumours.	Alcohols	311-318	tumor protein p53	Homo sapiens	247-251	
16477330-2	2006	This study investigated the genotype distribution of p53 codon 72 polymorphism in hypopharyngeal cancer patients and non-cancer controls matched for age, gender, alcohol consumption and smoking habit.	Alcohols	162-169	tumor protein p53	Homo sapiens	53-56	
16318864-7	2006	The incidence of p53 overexpression was additively increased with environmental exposure to cigarette smoke, alcohol, and areca quid.	Alcohols	109-116	tumor protein p53	Homo sapiens	17-20	
17599946-6	2007	We conclude that the TP53 R72P polymorphism may contribute to the etiology of colorectal cancer in the Chinese population, particularly among alcohol consumers.	Alcohols	142-149	tumor protein p53	Homo sapiens	21-25	
16326430-9	2005	The levels of p53, bcl-2, and 8-OHdG were concomitantly changed by alcohol and acetaldehyde treatment in midbrain cells.	Alcohols	67-74	tumor protein p53	Homo sapiens	14-17	
16277102-4	2005	RESULTS: P53 alteration occurred in 20 of 45 tumors (44%) and was more common among younger patients (58% versus 36% for younger versus older patients, respectively) and those lacking tobacco/alcohol exposure (53% versus 40% for "no-risk" and "risk" groups, respectively), but the differences were not statistically significant.	Alcohols	192-199	tumor protein p53	Homo sapiens	9-12	
16271069-12	2005	Noticeably, alcohol consumption could enhance this peculiar spectrum of p53 mutation in ESCC.	Alcohols	12-19	tumor protein p53	Homo sapiens	72-75	
12837832-5	2003	Association of clinical and pathologic variables (e.g., alcohol consumption, sex, age, pathologic stage) with mutation of the p53 gene was determined by logistic regression.	Alcohols	56-63	tumor protein p53	Homo sapiens	126-129	
14742318-0	2004	Diet and alcohol consumption in relation to p53 mutations in breast tumors.	Alcohols	9-16	tumor protein p53	Homo sapiens	44-47	
15069555-7	2004	While the results suggest that the p53 codon 72 polymorphism may contribute to gastric cancer susceptibility, further larger studies are needed to substantiate our findings and to explore a possible interaction between p53 codon 72 polymorphism and alcohol in the etiology of gastric cancer.	Alcohols	249-256	tumor protein p53	Homo sapiens	35-38	
15023836-0	2004	Association between p53 gene mutations and tobacco and alcohol exposure in laryngeal squamous cell carcinoma.	Alcohols	55-62	tumor protein p53	Homo sapiens	20-23	
15023836-1	2004	OBJECTIVES: To analyze the relationship between p53 gene mutations, tobacco smoke, and alcohol consumption in patients with laryngeal squamous cell carcinoma.	Alcohols	87-94	tumor protein p53	Homo sapiens	48-51	
16054986-4	2005	One cellular consequence of sustained oxidative stress and redox imbalance resulting from the combined actions of alcohol and iron is lipid peroxidation, resulting in the production of aldehydic products such as 4-hydroxy-2-nonenal, which has been linked to site-specific mutations of the p53 gene.	Alcohols	114-121	tumor protein p53	Homo sapiens	289-292	
14742318-8	2004	Our data were consistent with increased likelihood of tumors with p53 mutations for premenopausal breast cancer with increased alcohol intake 10 or 20 years previous; for intake of 16 or more drinks per month in the period 20 years before the interview compared with non-drinkers, the OR was 5.25, 95% CI 1.48-18.58.	Alcohols	127-134	tumor protein p53	Homo sapiens	66-69	
14742318-12	2004	For premenopausal women, alcohol consumption in the past was associated with p53 mutations.	Alcohols	25-32	tumor protein p53	Homo sapiens	77-80	
12401821-7	2002	p53 immunoexpression in more than 25% of the neoplastic cells was significantly associated with smoking but not with alcohol consumption.	Alcohols	117-124	tumor protein p53	Homo sapiens	0-3	
12772781-5	2003	The incidence of p53 mutation in hepatocellular cancer patients with chronic liver disease due to hepatitis B virus infection was significantly higher than in those with chronic liver disease due to alcohol, indicating that not alcohol but hepatitis B virus, in fact induces the mutations in p53 gene.	Alcohols	228-235	tumor protein p53	Homo sapiens	17-20	
12750239-10	2003	After adjustment for age, cigarette smoking, areca quid chewing, and alcohol drinking, the Gln/Gln genotype still showed an independent association with the frequency of p53 mutation (odd ratio, 4.50; 95% confidence interval, 1.52-13.36).	Alcohols	69-76	tumor protein p53	Homo sapiens	170-173	
11857392-7	2002	TP53 mutations, mainly transversions, were more frequently found in heavy smokers (p = 0.03), with the same tendency after chronic alcohol consumption.	Alcohols	131-138	tumor protein p53	Homo sapiens	0-4	
11771346-6	2001	Moreover, there was also an interesting correlation between the degree of positivity to p53 and exposure to smoke, and to a lesser extent to alcohol, in the oncological patients.	Alcohols	141-148	tumor protein p53	Homo sapiens	88-91	
11914604-5	2002	Thus, use of both alcohol and cigarettes is clearly associated with a high frequency of p53 protein accumulation in multiple oesophageal squamous cell carcinoma present at the same time.	Alcohols	18-25	tumor protein p53	Homo sapiens	88-91	
11564575-1	2001	Tobacco smoking and alcohol drinking are the principal factors associated with p53 expression in oral squamous cell carcinomas (OSCC) in the west, whereas betel quid chewing and smokeless tobacco are important factors in the east.	Alcohols	20-27	tumor protein p53	Homo sapiens	79-82	
11564575-5	2001	Multivariate modelling showed that lifetime exposure to alcohol drinking was significantly positively associated with p53 expression (likelihood ratio P value 0.01).	Alcohols	56-63	tumor protein p53	Homo sapiens	118-121	
11532872-2	2001	In this study, we used PCR-single strand conformation polymorphism and DNA sequencing to analyze the conserved regions of the p53 gene (exons 5-9) in OSCC tumor specimens from 187 patients with varied histories of betel quid, tobacco and alcohol use.	Alcohols	238-245	tumor protein p53	Homo sapiens	126-129	
11532872-5	2001	However, alcohol drinkers exhibited a significantly higher incidence (57/101, 56.44%) of p53 mutations than non-users (39.53%, 34/86) (P = 0.02).	Alcohols	9-16	tumor protein p53	Homo sapiens	89-92	
11532872-6	2001	The effect of alcohol on the incidence of p53 mutations was still statistically significant (RR = 2.24; 95% CI, 1.21-4.15) after adjustment for cigarette smoking and betel quid (BQ) chewing.	Alcohols	14-21	tumor protein p53	Homo sapiens	42-45	
11323100-1	2001	In esophageal squamous cell carcinoma (SCC), we used immunohistochemical analysis to further elucidate the correlation of p53 protein expression with clinicopathological factors, as well as with risk factors, such as tobacco smoking, alcohol consumption and a family history of cancer, using odds ratios (ORs).	Alcohols	234-241	tumor protein p53	Homo sapiens	122-125	
11323100-6	2001	The esophageal SCC in either smokers or alcohol users was 4.67-5.83 times more likely to express p53 protein, while the likelihood of p53 expression in patients who use both tobacco and alcohol was more than 14.0 times.	Alcohols	40-47	tumor protein p53	Homo sapiens	97-100	
11323100-6	2001	The esophageal SCC in either smokers or alcohol users was 4.67-5.83 times more likely to express p53 protein, while the likelihood of p53 expression in patients who use both tobacco and alcohol was more than 14.0 times.	Alcohols	186-193	tumor protein p53	Homo sapiens	134-137	
11323100-9	2001	In contrast, tobacco smoking and alcohol consumption were shown to be strongly associated with p53 mutations in esophageal carcinogenesis.	Alcohols	33-40	tumor protein p53	Homo sapiens	95-98	
10866304-0	2000	Alcohol consumption and cigarette smoking increase the frequency of p53 mutations in non-small cell lung cancer.	Alcohols	0-7	tumor protein p53	Homo sapiens	68-71	
10866304-6	2000	p53 mutations were more common in patients who used alcohol than in patients who consumed less than one drink per day (72 versus 39%; P = 0.003), and were detected more often smokers than nonsmokers (58% versus 10%, P = 0.02).	Alcohols	52-59	tumor protein p53	Homo sapiens	0-3	
10866304-7	2000	Mutations in the p53 gene were present more often (P = 0.01) in alcohol drinkers who smoked cigarettes [76% (31 of 41)], than in nondrinkers (<1 drink per day) who smoked cigarettes [42% (20 of 48)] or in nondrinkers who did not smoke [14% (1 of 7)].	Alcohols	64-71	tumor protein p53	Homo sapiens	17-20	
10866304-8	2000	In conclusion, alcohol consumption and tobacco use are both associated with p53 mutations in non-small cell lung cancer.	Alcohols	15-22	tumor protein p53	Homo sapiens	76-79	
10866304-9	2000	The link between exposure to both alcohol and tobacco and p53 mutations raises the possibility that alcohol may enhance the mutagenic effects of cigarette smoke in the lung.	Alcohols	34-41	tumor protein p53	Homo sapiens	58-61	
10866304-9	2000	The link between exposure to both alcohol and tobacco and p53 mutations raises the possibility that alcohol may enhance the mutagenic effects of cigarette smoke in the lung.	Alcohols	100-107	tumor protein p53	Homo sapiens	58-61	
10839309-0	2000	Alcohol consumption and cigarette smoking in relation to high frequency of p53 protein accumulation in oesophageal squamous cell carcinoma in the Japanese.	Alcohols	0-7	tumor protein p53	Homo sapiens	75-78	
10839309-2	2000	A significantly larger proportion of heavy alcohol drinkers and cigarette smokers was evident in the p53-positive group.	Alcohols	43-50	tumor protein p53	Homo sapiens	101-104	
10619896-6	1999	A correlation was found between alcohol intake and p53 expression.	Alcohols	32-39	tumor protein p53	Homo sapiens	51-54	
10754498-8	2000	Interestingly, heavy drinking had a significant positive correlation with the p53 mutation, but heavy smoking did not, suggesting that prolonged exposure to alcohol is more related to p53 mutation in oropharyngeal SCC than to tobacco consumption.	Alcohols	157-164	tumor protein p53	Homo sapiens	78-81	
10754498-8	2000	Interestingly, heavy drinking had a significant positive correlation with the p53 mutation, but heavy smoking did not, suggesting that prolonged exposure to alcohol is more related to p53 mutation in oropharyngeal SCC than to tobacco consumption.	Alcohols	157-164	tumor protein p53	Homo sapiens	184-187	
10398108-7	1999	Abuse of alcohol, an additional factor in these HNSCC patients, together with the abuse of tobacco, might play a role in the development of the p53-positive clusters.	Alcohols	9-16	tumor protein p53	Homo sapiens	144-147	
9158397-18	1997	Paucity of p53 mutations may be explained by the absence of exposure to tobacco smoke or alcohol.	Alcohols	89-96	tumor protein p53	Homo sapiens	11-14	
10895614-7	1998	p53 tumour suppressor gene mutations are the most frequently found genetic errors in oral cancer and the p53 gene is a likely target for tobacco and alcohol.	Alcohols	149-156	tumor protein p53	Homo sapiens	0-3	
10895614-7	1998	p53 tumour suppressor gene mutations are the most frequently found genetic errors in oral cancer and the p53 gene is a likely target for tobacco and alcohol.	Alcohols	149-156	tumor protein p53	Homo sapiens	105-108	
9790097-7	1998	p53 staining following microwave enhancement of alcohol-fixed tissue showed a significant incidence of conversion of negative results to positive and of positive staining in unexpected tissue components.	Alcohols	48-55	tumor protein p53	Homo sapiens	0-3	
9158397-17	1997	CONCLUSIONS: Our results suggest that p53 gene mutations are less frequent in squamous carcinomas occurring in nonsmoking young patients who do not drink alcohol than in young smokers or in the general population.	Alcohols	154-161	tumor protein p53	Homo sapiens	38-41	
9891551-2	1998	The aim of this study was to establish the status of p53 gene and p53-regulated proteins (Bax, Bcl-2 and Waf-1) expression in head and neck simultaneous preneoplastic and invasive lesions from patients with chronic alcohol and tobacco exposure.	Alcohols	215-222	tumor protein p53	Homo sapiens	53-56	
9891551-2	1998	The aim of this study was to establish the status of p53 gene and p53-regulated proteins (Bax, Bcl-2 and Waf-1) expression in head and neck simultaneous preneoplastic and invasive lesions from patients with chronic alcohol and tobacco exposure.	Alcohols	215-222	tumor protein p53	Homo sapiens	66-69	
9366703-12	1997	A significant correlation existed with both p53 gene mutation status and HPV status with respect to alcohol and tobacco use.	Alcohols	100-107	tumor protein p53	Homo sapiens	44-47	
9366703-13	1997	The presence of the p53 gene mutation positively correlated with increased tobacco and alcohol use, whereas infection with HPV predicted a significantly lower rate of alcohol and tobacco consumption.	Alcohols	87-94	tumor protein p53	Homo sapiens	20-23	
9366703-15	1997	Conversely, there is a strong association between heavy alcohol and tobacco use and mutation of the p53 gene.	Alcohols	56-63	tumor protein p53	Homo sapiens	100-103	
7896460-0	1995	Analysis of the p53 gene in relation to tobacco and alcohol in cancers of the upper aero-digestive tract.	Alcohols	52-59	tumor protein p53	Homo sapiens	16-19	
8960021-8	1996	The association we found between alcohol intake and mutant p53 expression may deserve further investigation.	Alcohols	33-40	tumor protein p53	Homo sapiens	59-62	
8645592-2	1996	Alcohol use as well as medication with hydralazine-containing antihypertensive drugs, but not heredity were associated with p53 staining.	Alcohols	0-7	tumor protein p53	Homo sapiens	124-127	
7734291-8	1995	Our data suggest that subjects with increased susceptibility to carcingogens after exposure to tobacco or alcohol are at higher risk for multiple cancers in which one of the most common genetic events is aberrant p53 expression.	Alcohols	106-113	tumor protein p53	Homo sapiens	213-216	
7854378-2	1995	We performed a molecular analysis to determine the pattern of mutations in the p53 gene in neoplasms from patients with squamous-cell carcinoma of the head and neck and a history of tobacco or alcohol use.	Alcohols	193-200	tumor protein p53	Homo sapiens	79-82	
7854378-9	1995	CONCLUSIONS: In our study, a history of tobacco and alcohol use was associated with a high frequency of p53 mutations in patients with squamous-cell carcinoma of the head and neck.	Alcohols	52-59	tumor protein p53	Homo sapiens	104-107	
11706422-0	1993	Relationship of tobacco/alcohol use to p53 expression in patients with lingual squamous cell carcinomas.	Alcohols	24-31	tumor protein p53	Homo sapiens	39-42	
7848689-1	1994	BACKGROUND AND METHODS: p53 protein expression was studied immunohistochemically in 73 colorectal adenocarcinomas, using monoclonal antibody D07 in alcohol fixed, paraffin embedded tissue.	Alcohols	148-155	tumor protein p53	Homo sapiens	24-27	
8076382-0	1994	p53 expression and mutations in squamous cell carcinoma of the head and neck: expression correlates with the patients" use of tobacco and alcohol.	Alcohols	138-145	tumor protein p53	Homo sapiens	0-3	
11706422-1	1993	This study examined p53 expression immunocytochemically in 40 lingual squamous cell carcinomas from Dutch patients with known histories of smoking and/or drinking alcohol.	Alcohols	163-170	tumor protein p53	Homo sapiens	20-23	
11706422-4	1993	25% (3/12) of p53-positive neoplasms and 71.4% (20/28) of p53-negative neoplasms were found in patients who had been exposed to both alcohol and tobacco.	Alcohols	133-140	tumor protein p53	Homo sapiens	14-17	
11706422-4	1993	25% (3/12) of p53-positive neoplasms and 71.4% (20/28) of p53-negative neoplasms were found in patients who had been exposed to both alcohol and tobacco.	Alcohols	133-140	tumor protein p53	Homo sapiens	58-61	
11706422-5	1993	A similar negative association with p53 reactivity was also found when either tobacco or alcohol were used in isolation.	Alcohols	89-96	tumor protein p53	Homo sapiens	36-39	
11706422-6	1993	The results contrast with previous observations in head/neck and oral carcinomas and indicate that the association of alcohol/tobacco and p53 expression remains open to question.	Alcohols	118-125	tumor protein p53	Homo sapiens	138-141	
1731521-8	1992	This is the first demonstration of widespread p53 overexpression in alcohol-fixed, embedded tissue and confirms the major role played by p53 in human malignancies.	Alcohols	68-75	tumor protein p53	Homo sapiens	46-49