Y chromosome abnormality in human stomach and lung cancer

Sex chromosome abnormalities in human stomach and lung cancers from 33 male patients were examined by Southern blot hybridization with pDP34 DNA probe, which recognizes X and Y chromosome-linked restriction fragment length polymorphisms (RFLPs). Contrary to the recent cytogenetic observations showing high incidence of loss of the Y chromosome in solid tumors, loss of the Y chromosome was observed in only 3 of 21 stomach cancers and 2 of 12 lung cancers. Gain of the Y chromosome was found in one of 12 lung cancers, but not in any of the stomach cancers. No X chromosome abnormality was found in any of these 33 stomach cancers and lung cancers.     

尿嘧啶核苷磷酸化酶基因在胃癌、肺癌和结肠癌组织中的表达水平及其临床意义

目的分析尿嘧啶核苷磷酸化酶基因的表达水平与胃癌、肺癌和结肠癌临床病理因素之间的关系.方法采用RT-PCR法检测了28例胃癌,12例肺癌和20例结肠癌组织中尿嘧啶核苷磷酸化酶基因(UPase)的表达.结果与正常组织相比,UPase基因在胃癌组织中的表达水平增高,而在肺癌和结肠癌组织中的表达无明显差异.胃癌组织中UPase基因表达增高患者的生存率较表达正常或降低患者的生存率稍高,但无统计学意义(P＞0.05);肺癌和结肠癌组织中UPase基因表达增高患者的生存率与表达降低患者的生存率相比无明显差异(P＞0.05).UPase基因表达水平与胃癌、肺癌和结肠癌的临床期别、病理分级、淋巴结转移无相关性.结论UPase基因在胃癌、肺癌、结肠癌中表达水平不同,在胃癌组织中呈高表达状态,其高表达可能与胃癌患者的高生存率有关.     

Mutation of the DNA methyltransferase (DNMT) 1 gene in human colorectal cancers

Alteration of DNA methylation is one of the most consistent epigenetic changes in human cancers. DNA methyltransferase (DNMT) 1 is a major enzyme that determines genomic methylation patterns. In order to understand the significance of mutations of the DNMT1 gene during human carcinogenesis, we performed polymerase chain reaction-single strand conformation polymorphism analysis using 46 oligonucleotide primer sets for all 40 coding exons and the 5'-flanking region (450 bp) of the DNMT1 gene in 29 colorectal cancers, 32 stomach cancers, 40 hepatocellular carcinomas (HCCs) and a corresponding sample of non-cancerous tissue from each case. Mutations in coding exons of the DNMT1 gene were detected in two (7%) of the colorectal cancers: they consisted of one-base deletion resulting in deletion of the whole catalytic domain and a point mutation resulting in a single amino acid substitution. No stomach cancers or HCCs showed mutations in the coding exons of the DNMT1 gene. No mutation in the 5'-flanking region of the DNMT1 gene was detected in any of the colorectal and stomach cancers or HCCs. These data suggest that mutational inactivation of the DNMT1 gene that potentially causes a genome-wide alteration of DNA methylation status may be a rare event during human carcinogenesis.     

K-ras mutation: early detection in molecular diagnosis and risk assessment of colorectal, pancreas, and lung cancers--a review

Multiple genomic alterations are involved in the development of most human cancers. They include alterations in oncogenes, tumor suppressor genes, DNA mismatch repair and excision repair genes. Genetic testing for susceptibility has been a part of the management of patients with well-defined but uncommon hereditary cancers in which certain susceptible gene mutations are determined in the germ line. However, a molecular diagnostic approach to sporadic cancers, which comprise the vast majority of malignant tumors in human beings, is still under development. One of the best characterized tumor-related genes is K-ras, which somatically mutates in several types of sporadic human cancers. Since mutations of this gene occur exclusively in three hot spots (codons 12, 13 and 61), and are frequently detected and well characterized in colorectal, pancreas and lung cancers, molecular diagnosis and susceptibility (risk) assessment targeting K-ras mutations are being developed. For this purpose, sample collection methods that reflect the state of the entire affected organ are important. Clinical samples used for molecular diagnosis and risk assessment include stool and lavage fluid, pancreatic and duodenal juices, and sputum and lavage fluids for colorectal, pancreas and lung cancers, respectively. The reported incidence of K-ras mutations detected in these samples ranges from 7% to 80% for colorectal cancers, 25% to 87% for pancreatic cancers, and 25% to 48% for lung cancers. Incidence of mutations clearly depends on the sensitivity of the method for detecting the mutant K-ras allele, as well as the nature and the quality of the clinical samples. Various methods including plaque hybridization, dot blot hybridization, combined PCR and RFLP or SSCP, and sensitive PCR have been used, and they exhibited high specificity (75 to 100%) in detecting mutations. Molecular analysis is demonstrating promise in assessing susceptibility to, or risk of developing, sporadic cancers.     

Isolation of an amplified DNA sequence in stomach cancer

By use of the in-gel DNA renaturation method, the presence of amplified DNA sequences was demonstrated in KATO-III, a cell line established from a signet ring cell carcinoma of the stomach. A DNA fragment from one of these amplified regions in KATO-III cells was cloned and designated SAM0.2; the locus containing the SAM0.2 fragment was referred to as SAM. The SAM locus was shown to be amplified not only in KATO-III cells, but also in three of 24 surgical specimens of stomach cancers and in two of 13 xenografts of human stomach cancers, all of these specimens being poorly differentiated adenocarcinoma or mucinous adenocarcinoma of the stomach. The SAM locus was not amplified in 14 cell lines of cancers of other organs or in 42 surgical specimens of lung cancers.     

Methylation and Expression of Human Pepsinogen Genes in Normal Tissues and Their Alteration in Stomach Cancer

In normal human tissues, pepsinogen A mRNA was expressed only in the fundic mucosa of the stomach, whereas pepsinogen C mRNA was expressed in all regions of the stomach mucosa and also in the proximal duodenal mucosa. The distributions of these mRNAs were consistent with those of pepsinogens A and C in the gastroduodenal mucosa. Methylation analysis of DNAs from normal tissues with methylation-sensitive restriction enzymes, Hpa II and Hha I, revealed that pepsinogen A and C genes are hypomethylated in tissues producing pepsinogens A and C, suggesting a role of DNA methylation in the regulation of the differential expression of the genes for the two human pepsinogens during normal differentiation. In stomach cancer tissues and cancer cell lines, the expressions of the pepsinogen genes were decreased or lost, in good accordance with their pepsinogen productions. No gross structural changes of the pepsinogen genes were observed in these cancers, but the methylation patterns of the pepsinogen genes were found to be altered in different ways in different cancers. The functional significance of the altered methylation is unknown; however, these results suggest that considerable heterogeneity of the methylation patterns occurs in human stomach cancers.     

Methylation and expression of human pepsinogen genes in normal tissues and their alteration in stomach cancer

In normal human tissues, pepsinogen A mRNA was expressed only in the fundic mucosa of the stomach, whereas pepsinogen C mRNA was expressed in all regions of the stomach mucosa and also in the proximal duodenal mucosa. The distributions of these mRNAs were consistent with those of pepsinogens A and C in the gastroduodenal mucosa. Methylation analysis of DNAs from normal tissues with methylation-sensitive restriction enzymes, HpaII and HhaI, revealed that pepsinogen A and C genes are hypomethylated in tissues producing pepsinogens A and C, suggesting a role of DNA methylation in the regulation of the differential expression of the genes for the two human pepsinogens during normal differentiation. In stomach cancer tissues and cancer cell lines, the expressions of the pepsinogen genes were decreased or lost, in good accordance with their pepsinogen productions. No gross structural changes of the pepsinogen genes were observed in these cancers, but the methylation patterns of the pepsinogen genes were found to be altered in different ways in different cancers. The functional significance of the altered methylation is unknown; however, these results suggest that considerable heterogeneity of the methylation patterns occurs in human stomach cancers.     

Isolation of an Amplified DNA Sequence in Stomach Cancer

By use of the in-gel DNA renaturation method, the presence of amplified DNA sequences was demonstrated in KATO-III, a cell line established from a signet ring cell carcinoma of the stomach. A DNA fragment from one of these amplified regions in KATO-III cells was cloned and designated SAM_0.2; the locus containing the SAM_0.2 fragment was referred to as SAM. The SAM locus was shown to be amplified not only in KATO-III cells, but also in three of 24 surgical specimens of stomach cancers and in two of 13 xenografts of human stomach cancers, all of these specimens being poorly differentiated adenocarcinoma or mucinous adenocarcinoma of the stomach. The SAM locus was not amplified in 14 cell lines of cancers of other organs or in 42 surgical specimens of lung cancers.     

发达与发展中国家癌症发病率与死亡率的比较与分析

  目的  分析发达国家与发展中国家的常见癌症发病情况与死亡率, 并将中国的癌症现状与之比较, 明确我国面临的主要癌症负担类型。  方法  各国家常见肿瘤的发病人数、发病率、死亡率及世界标化发病率等数据均来源于GLOBOCAN 2008。  结果  发达国家和发展中国家的恶性肿瘤发病第1位均是肺癌, 其次发达国家为结直肠癌、乳腺癌、前列腺癌, 发展中国家的胃癌、乳腺癌和肝癌; 发达国家死亡率最高的分别依次为肺癌、结直肠癌、乳腺癌、前列腺癌, 发展中国家为肺癌、肝癌、胃癌、食管癌。中国的肺癌发病率和死亡率均居第1位, 胃癌、肝癌发病及死亡率均高于发展中国家和发达国家, 乳腺癌的死亡率远低于发达国家亦低于其他发展中国家。预计到2020年, 中国新增发病和死亡人数最多的癌症是肺癌、胃癌和肝癌。  结论  不同国家的癌谱不同, 中国癌谱具有发达国家和发展中国家的双重特征。肺癌、胃癌及肝癌是威胁我国居民健康的主要恶性肿瘤, 并且未来十几年其增长速度较快, 是我国恶性肿瘤防控的重点。      

Genetic pathways and mutation profiles of human cancers: site- and exposure-specific patterns

Cancer is a complex disease that involves the accumulation of both genetic and epigenetic alterations of numerous genes. Data in the Genetic Alterations in Cancer database for gene mutations and allelic loss [loss of heterozygosity (LOH)] in human tumors (e.g. lung, oral, esophagus, stomach and colon/rectum) were reviewed. Results for the genes and pathways implicated in tumor development at these sites are presented. Mutation incidence, spectra and codon specificity are described for lung, larynx and oral tumors. LOH occurred more frequently than gene mutations in tumors from all sites examined. The cell cycle gene, TP53 (all sites), and cell signaling gene, APC (colorectal and gastric cancers), were the only genes with similar incidences of LOH and mutation. Alterations of one or more cell cycle and cell signaling genes were reported for tumors from each site. Site-specific activation was apparent in the cell signaling mitogen-activated protein kinase oncogenes (KRAS in lung, HRAS in oral cancers and BRAF in esophageal and colorectal cancers). Analysis of genetic changes in lung tumors showed that the incidence of mutations in the TP53 and KRAS genes and the incidence of LOH in the FHIT gene were significantly greater in smokers versus non-smokers (P < 0.01). In lung and oral cancers, the TP53 GC --> TA transversion frequency increased with tobacco smoke exposure (P < 0.05). Furthermore, the TP53 mutational hot spots for lung and laryngeal cancers from smokers included codons 157, 245 and 273, whereas for oral tumors included codons 280 and 281.     

Dietary Habits and Cancer Mortality Among Middle Aged and Older Japanese Living in Hokkaido,Japan by Cancer Site and Sex

Dietary factors are thought to be closely associated with the development of human cancers and hence numerous studies ‍in this area have already been conducted in the United States and other Western countries. Comparatively few prospective ‍studies have been published in Japan, especially for Hokkaido people. The present investigation was therefore performed to ‍assess links between four leading cancers and some of the Japanese common dietary factors through a cohort study (1984- ‍2002) in Hokkaido by analyzing 1,524 men and 1,634 women separately aged 40 and over. Adjusted Cox proportional ‍hazard regression was used to calculate the relative risk (RR) for each dietary factor. For men, two dietary factors, miso ‍soup (RR=0.2, 95% confidence interval (95%CI)=0.1-0.8) and pickled vegetables (RR=0.2, 95%CI=0.1-0.8) were associated ‍with lower risk for stomach and colorectal cancer respectively. For women, three factors, namely salty confectionary (RR=3.5, ‍95%CI=1.1-10.9), black tea (RR=3.8, 95%CI=1.1-13.6), and carbonated drink/juice (RR=3.9, 95% CI=1.4-11.1) appeared ‍related to an elevated risk of stomach cancer. However, further analysis simultaneously with all other adjusted factors ‍indicated only carbonated drink/juice (RR=3.1, 95%CI=1.1-8.9) to present a significant risk factor for stomach cancer. One ‍factor, namely wild edible plants (RR=3.3, 95%CI=1.1-9.8), increased the risk for colorectal cancer in women. None of the ‍dietary components were significantly associated with lung or pancreatic cancers. This study also indicated a wide variation ‍in the impact of dietary factors by sex and cancer site, in line with earlier work, poonting to a necessity for careful interpretation. ‍Further epidemiological investigations by sex with more study subjects and confounding factors will be useful for determining ‍the contribution of individual dietary factors to development of human cancers in Hokkaido, Japan.     

Structural expression of bovine milk and meat factors in tissues of colorectal,lung and pancreatic cancer patients

Chronic inflammation, linked to the presence of bovine milk and meat factors (BMMFs) and specific subsets of macrophages, results in oxygen radical synthesis and induction of mutations in DNA of actively replicating cells and replicating single stranded DNA. Cancers arising from this process have been characterized as indirect carcinogenesis by infectious agents (without persistence of genes of the agent in premalignant or cancers cells). Here, we investigate structural properties of pleomorphic vesicles, regularly identified by staining peritumor tissues of colorectal, lung and pancreatic cancer for expression of BMMF Rep. The latter represents a subgroup of BMMF1 proteins involved in replication of small single-stranded circular plasmids of BMMF, but most likely also contributing to pleomorphic vesicular structures found in the periphery of colorectal, lung and pancreatic cancers. Structurally dense regions are demonstrated in preselected areas of colorectal cancer, after staining with monoclonal antibodies against BMMF1 Rep. Similar structures were observed in human embryonic cells (HEK293TT) overexpressing Rep. These data suggest that Rep or Rep isoforms contribute to the structural formation of vesicles.     

Analysis of the candidate target genes for mutation in microsatellite instability-positive cancers of the colorectum, stomach, and endometrium

Microsatellite instability (MSI) in human carcinoma DNA is a characteristic phenotype observed in hereditary non-polyposis colorectal cancer and also in some human sporadic cancers including multiple primary carcinomas. In this study, we analyzed mutations in the hCHK1, E2F4, hMSH3, and hMSH6 genes in MSI+ human cancers arising in colorectum, stomach and endometrium. The E2F4 and hMSH3 genes were mutated in all tumor types. Interestingly, the hMSH6 gene was mutated in colorectal and gastric cancers but not in endometrial cancer; this is similar to the TGFbetaRII gene. It is notable that the mutation status of the secondary mutators, hMSH3 and hMSH6, did not influence slippage-related frameshift mutations in genes harboring simple tandem-repeats, which suggests that the MSI phenotype may be affected mainly by abnormalities in the primary mutator genes, not by the secondary mutator genes. No mutations were observed in the cell cycle checkpoint gene hCHK1; mutations of this gene are thought to have a limited role, if any, in at least the tumor types analyzed in this study.     

Searching for microsatellite mutations in coding regions in lung, breast, ovarian and colorectal cancers

RepX represents a new informatics approach to probe the UniGene database for potentially polymorphic repeat sequences in the open reading frame (ORF) of genes, 56% of which were found to be actually polymorphic. We now have performed mutational analysis of 17 such sites in genes not found to be polymorphic (<0.03 frequency) in a large panel of human cancer genomic DNAs derived from 31 lung, 21 breast, seven ovarian, 21 (13 microsatellite instability (MSI)+ and eight MSI-) colorectal cancer cell lines. In the lung, breast and ovarian tumor DNAs we found no mutations (<0.03-0.04 rate of tumor associated open reading frame mutations) in these sequences. By contrast, 18 MSI+ colorectal cancers (13 cancer cell lines and five primary tumors) with mismatch repair defects exhibited six mutations in three of the 17 genes (SREBP-2, TAN-1, GR6) (P<0.000003 compared to all other cancers tested). We conclude that coding region microsatellite alterations are rare in lung, breast, ovarian carcinomas and MSI (-) colorectal cancers, but are relatively frequent in MSI (+) colorectal cancers with mismatch repair deficits.     

Cancer Incidence Rates in Turkey in 2006: A Detailed Registry Based Estimation

Purpose: The purpose of this study is to provide a detailed report on cancer incidence in Turkey, a relativelylarge country with a population of 72 million. We present the estimates of the cancer burden in Turkey for2006, calculated using data from the eight population based cancer registries which have been set up in selectedprovinces representative of sociodemographic patterns in their regions. Methods: We calculated age specificand age adjusted incidence rates (AAIR–world standard population) for each of registries separately. Weassigned a weighting coefficient for each registry proportional to the population size of the region which theregistry represents. Results: We pooled a total of 24,428 cancers (14,581 males, 9,847 females). AAIRs per 100000 were: 210.1 in men and 129.4 in women for all cancer sites excluding non-melanoma skin cancer. The AAIRper 100 000 men was highest for lung cancer (60.3) followed by prostate (22.8), bladder (19.6), stomach (16.3)and colo-rectal (15.4) cancers. Among women the rate per 100 000 was highest for breast cancer (33.7) followedby colorectal (11.5), stomach (8.8), thyroid (8.8) and lung (7.7). The most striking findings about the cancerincidence in the provinces were the high incidence rates for stomach and esophageal cancers in Erzurum andhigh stomach cancer incidence rates in Trabzon for both sexes. Conclusions: We are thus able to present themost accurate and realistic estimations for cancer incidence in Turkey so far. Lung, prostate, bladder, stomach,colorectal, larynx cancers in men and breast, colorectal, stomach, thyroid, lung, corpus uteri cancers in womenare the leading cancers respectively. This figure shows us tobacco related cancers, lung, bladder and larynx,predominate in men. Concurrently, we analyzed the data for each province separately, giving us the opportunityto present the differences in cancer patterns among provinces. The high incidences of stomach and esophagealcancers in East and high incidence of stomach cancer in Northeast regions are remarkable.     

Immunohistochemical demonstration of fluoropyrimidine-metabolizing enzymes in various types of cancer

Fluoropyrimidines [5-Fluorouracil (5-FU) and its prodrugs] have been widely used in the treatment of solid cancers. The anticancer effects primarily depend on intratumoral levels of enzymes metabolizing the drugs, such as dihydropyrimidine dehydrogenase (DPD), orotate phosphoribosyltransferase (OPRT), thymidine phosphorylase (TP), and thymidylate synthase (TS). In order to know the tumor types susceptible to respective fluoropyrimidines, we investigated the expression of DPD, OPRT, TP and TS in various types of cancer with the immunoperoxidase method. These four enzymes existed in all of the cancer types studied, such as pulmonary, gastric, colorectal, hepatic, cholecystic, pancreatic, renal, urocystic, and mammary cancers. Respective types of cancers presented characteristic immunohistochemical features as follows: pulmonary adenocarcinoma, DPD- and TP-high; pulmonary squamous cell carcinoma, TS- and TP-high; intestinal-type gastric adenocarcinoma, TP-high; diffuse-type gastric adenocarcinoma, DPD-low and TS-high; colorectal adenocarcinoma, DPD- and TP-low, hepatocellular carcinoma, DPD-high, and TS- and OPRT-low; cholecystic adenocarcinoma, DPD- and TS-high; renal cell carcinoma, DPD-low, and OPRT- and TP-high; urocystic transitional cell carcinoma, DPD-high and OPRT-low; and mammary ductal carcinoma, OPRT-low, and TS- and TP-high. The enzyme expression pattern in cancer tissue was generally similar to that of their normal counterparts. However, TP immunoreactivity in adenocarcinomas of the lung, stomach and gallbladder, and urothelial carcinoma of the urinary bladder was stronger, and DPD immunoreactivity in adenocarcinoma of the breast was weaker, when compared with normal epithelial cells. Non-epithelial cells were also positive for these enzymes. These results indicated that the key enzymes influencing the effects of fluoropyrimidines differ from cancer to cancer. Fluoropyrimidine treatment may be selected, based on the simultaneous immunohistochemical evaluation of the fluoropyrimidine metabolic enzymes.     

Analysis of human cancer DNA's for DNA sequence of human adenovirus serotypes 3, 7, 11, 14, 16, and 21 in group B1

We have investigated whether Group B human adenoviruses (Ad) (Ad3, Ad7, Ad11, Ad14, Ad16, and Ad21), which are widespread in the human population and are tumorigenic in hamsters, may play a role in human cancer. Hybridization of Ad7-radiolabeled DNA with DNA's from an Ad7-induced primary hamster tumor and from two cell lines (5728 and Ad7 P-cell) established from Ad7-induced hamster tumors indicated multiple copies per cell of 17, 30 to 36, and 20%, respectively of the Ad7 genome. Thus, cells transformed by Group B Ads resemble cells transformed by Group C and Group A Ad's in that they retain multiple copies of a variable fraction of the viral genome. These model studies suggest that possible Group B Ad-induced human cancer cells should contain one or more copies of virus DNA per cell. Therefore, we assayed human cancer DNA's for Ad sequences, by highly sensitive "saturation-hybridization" reactions with Ad7 or Ad11 DNA (4 X 10(6) to 2.1 x 10(8) cpm/microgram). We concentrated on cancers of the respiratory and digestive systems, because these systems are the most common sites of infection by Group B Ad's. In 8 independent experiments, no Ad7 sequences were detected in DNA's from 16 normal lung tissues, 18 normal tissues of the digestive system, 34 cancers of the respiratory system, 19 cancers of the digestive system, 11 cancers of the urinary system, 5 cancers of the genital system, 3 cancers of the breast, and 6 Hodgkin's lymphomas. Reconstruction controls with added Ad7 DNA indicated that about 0.05 to 0.1 copy of Ad7 DNA per cell should be detected. Ad11 is strongly implicated as a cause of acute hemorrhagic cystitis. In two independent experiments, no Ad11 sequences were detected in DNA's from 9 carcinomas of bladder, 10 carcinomas of prostate, 24 carcinomas of kidney, 3 hypernephromas, 3 Wilms' tumors, or 2 normal kidneys. Reconstruction experiments indicated that the cancer DNA assays had a sensitivity of 0.05 to 0.1 copy of Ad11 DNA per cell. The DNA's of Group B Ad's are greater than 85% homologous by hybridization; thus, these results are applicable to all Group B serotypes. Our data provide evidence (but not formal proof) that none of the human cancers that we analyzed were induced by Group B Ad's. These tumors represent about 50% of the tumors that affect humans. The possible involvement of Group B Ad's in other less common forms of human cancers is under investigation in our laboratory.     

Differential expression of matrilysin and cyclooxygenase-2 in intestinal and colorectal neoplasms

Both the matrix metalloproteinase matrilysin and the prostaglandin H synthase cyclooxygenase-2 (Cox-2), are thought to play key roles in colorectal carcinogenesis. These enzymes are overexpressed in 85-90% of human colorectal cancers. Furthermore, mice carrying an adenomatous polyposis coli germline mutation that are also nullizygous for either matrilysin or Cox-2 display a significant reduction in tumor multiplicity. To determine if there is a direct link between matrilysin and Cox-2, their expression was characterized in two mouse models of intestinal carcinogenesis and in human colorectal tumor samples. Both matrilysin and Cox-2 expression was increased in the mouse models and in the human colorectal cancers; however, immunohistochemistry and in situ hybridization indicated that their localization within the tumors was different. In the mouse models, Cox-2 was expressed in the superficial stroma, whereas matrilysin expression was localized exclusively to the neoplastic epithelium. In contrast, in human colorectal cancers, both Cox-2 and matrilysin were expressed in the neoplastic epithelium. Although over 80% of the specimens expressed both matrilysin and Cox-2, the levels and localization of matrilysin and Cox-2 expression were distinct. Cox-2 expression was strongest in well-differentiated areas, and matrilysin immunostaining was strongest in the more dysplastic and invasive regions of the tumor. These results indicate that these two important modulators of colorectal tumorigenesis are differentially expressed and imply that the therapeutic benefit may be improved by combination therapy utilizing selective Cox-2 and matrilysin inhibitors.     

Presence of Human Papillomavirus DNA in Colorectal Cancer Tissues in Shiraz,Southwest Iran

Background: Colorectal cancer is one of the most common cancers worldwide. Viruses including human papillomavirus (HPV) have been reported to be associated with different cancers but any association with colorectal cancers remains controversial. Aim: To evaluate any association between HPV infection and adenocarcinoma of the colon and adenomatous polyps. Materials and Methods: Paraffin-embedded tissue specimens of 70 colorectal adenocarcinomas, 70 colorectal adenomatous polyps, and 70 colorectal normal tissues were subjected to DNA extraction. The quality of the extracted DNA was confirmed by amplification of a β-globin fragment using polymerase chain reaction (PCR). PCR using specific primers were performed to detect HPV DNA. Specific primers targeting the E6 region of the HPVs 16 and 18 were used for genotyping. Results: HPV DNA was detected in 2 (2.85%) out of 70 adenocarcinoma colorectal tissues and 4 (5.71 %) out of 70 adenomatous colorectal tissues. All normal colorectal tissues were negative for HPV DNA. HPV-16 was the most predominant genotype (5 sample) followed by HPV-18 (4 sample). Despite the above observations, statistical analyses indicated no significant differences in the frequencies of HPV positive subjects between the cancerous and normal samples. Conclusions: Although the differences observed in the frequencies of HPV positive cases in our study was not significant relative to those of control subjects, the fact of 6 positive samples among cancerous tissues, may still suggest a role of HPV in colorectal carcinogenesis. The study collectively indicated that some colorectal cancerous tissues are infected with high risk HPV genotype. The findings merit more investigation.