|Year : 2012 | Volume
| Issue : 1 | Page : 23-25
Helicobacter pylori in colorectal neoplasms of Kashmiri patients: What is the prevalence?
Aga Syed Sameer1, Safiya Abdullah2, Saniya Nissar2, Roohi Rasool2, Shahid Mudassir Baba2, Mushtaq A Siddiqi2
1 Department of Immunology and Molecular Medicine, Sher-I-Kashmir Institute of Medical Sciences, Soura; Department of Biochemistry, Medical College, Sher-I-Kashmir Institute of Medical Sciences, Bemina, Srinagar, Kashmir, India
2 Department of Immunology and Molecular Medicine, Sher-I-Kashmir Institute of Medical Sciences, Soura, Srinagar, Kashmir, India
|Date of Web Publication||13-Apr-2012|
Aga Syed Sameer
Department of Biochemistry, Medical College, Sher-I-Kashmir Institute of Medical Sciences, Bemina, Srinagar, Kashmir
Source of Support: None, Conflict of Interest: None
Background: The purpose of the present study was to detect the presence of Helicobacter pylori in colorectal cancer (CRC) patients in Kashmiri population. Materials and Methods: A total of 86 CRC samples were studied. Samples were taken from tissues suitable for DNA amplification by polymerase chain reaction (PCR). DNA was extracted and H. pylori detection was carried out by PCR amplification of glmM gene. Results: Out of 86 samples, only eight were H. pylori-positive for amplification glmM gene of a 294 bp DNA fragment. Conclusion: H. pylori is not the prominent risk factor for the development of colorectal cancer in Kashmiri population.
Keywords: Colorectal cancer, Helicobacter pylori, Kashmir
|How to cite this article:|
Sameer AS, Abdullah S, Nissar S, Rasool R, Baba SM, Siddiqi MA. Helicobacter pylori in colorectal neoplasms of Kashmiri patients: What is the prevalence?. Clin Cancer Investig J 2012;1:23-5
|How to cite this URL:|
Sameer AS, Abdullah S, Nissar S, Rasool R, Baba SM, Siddiqi MA. Helicobacter pylori in colorectal neoplasms of Kashmiri patients: What is the prevalence?. Clin Cancer Investig J [serial online] 2012 [cited 2019 Oct 20];1:23-5. Available from: http://www.ccij-online.org/text.asp?2012/1/1/23/95015
| Introduction|| |
Helicobacter pylori is one of the most genetically diverse bacterial species.  Some strains may be substantially more virulent than others. The virulent strains have a unique CagA pathogenicity island, a 40 kilobase-pair segment of DNA comprising a collection of approximately 30 genes. CagA gene codes for the cytotoxic protein, which is one of the important virulence factors of H. pylori. 
A number of studies have been carried out on colorectal cancer to assess the role of H. pylori in carcinogenesis. In many of these studies, high prevalence of infection was found in these tissues, ,, while other study reported the non-association. 
Kashmir valley, located in the northern division of India, surrounded by Himalayas, has an unique ethnic population living in temperate environmental conditions, having distinctive food habits, which play an overwhelming role in the development of gastro intestinal tract (GIT) cancers over the genetic factors. , Colorectal cancer (CRC) is the fourth most common cancer in men and the third most common cancer in women worldwide.  In Kashmir valley, CRC represents the third most common GIT cancer after esophageal and gastric. ,,
In the present study, we assessed the prevalence of H. pylori infection in colorectal cancer patients using polymerase chain reaction (PCR) detection method.
| Materials and Methods|| |
This study included 86 consecutive primary CRC patients. All CRC patients were recruited from Department of Surgery, Sher-I-Kashmir Institute of Medical Science, from March 2008 to August 2009. Tumor types and stages were determined by two experienced pathologists. The mean age was 52 years old, and 56 of the patients were >50 years old; see [Table 1] for details.
Data on all CRC patients were obtained from personal interviews with patients and or guardians, medical records and pathology reports. The data collected included sex, age, dwelling, tumor location, Dukes stage, lymph node status, pesticide exposure and bleeding per rectum (PR). All patients and/or guardians were informed about the study, and their will to participate in this study was taken on predesigned questionnaire (available on request). The collection and use of tumor and blood samples for this study was previously approved by the appropriate Institutional Ethics Committee.
DNA extraction and polymerase chain reaction-restriction fragment length polymorphism
DNA extraction was performed using ammonium acetate method. Each sample was examined by two different researchers in separate PCRs. Primers (F: 5'-AAGCTTTTAGGGGTGTTAGGGGTTT-3' R: 5'-AAGCTTACTTTCTAACACTAACGC-3') used in this study were designed for glmM gene (294 bp) as described previously to be most sensitive to detect presence of H. pylori infection in biopsy samples. 
PCR was carried out in a final volume of 25 μL containing 50 ng genomic DNA template, 1X PCR buffer (Biotools) with 2 mM MgCl 2 , 0.8 μM of each primer (Genescript), 50 μM dNTPs (Biotools), and 0.5 U DNA polymerase (Biotools). For PCR amplification, the standard program was used as follows: one initial denaturation step at 94°C for 7 min, followed by 35 denaturation cycles of 1 min at 94°C, 1 min of annealing at 55°C, and 1 min of extension at 72°C, followed by a final elongation cycle at 72°C for 10 min.
PCR mixture was electrophoresed through a 2-3% agarose gel for resolution. A positive control for each PCR was used as an internal control for amplification.
| Results and Discussion|| |
A total of 86 colorectal cancer patients were included in this study. The patients comprised 49 males and 37 females (M/F ratio = 1.32). Mean age in patients was 52 years. Furthermore, out of 86 confirmed cases of CRC, 59 were rural and 27 urban; 36 cases had carcinoma in colon and 50 in rectum; and 55 were smokers and 31 non smokers [Table 1].
|Table 1: Frequency distribution analysis of selected demographics and risk factors in colorectal cancer cases|
Click here to view
The PCR method of detection of H. pylori infection in the tumor samples revealed very low prevalence of H. pylori in CRC in our population. Out of 86 samples that were screened, only eight tumors (9.3%) had H. pylori infection. Seven of the eight positive tumor samples were of higher grade (Duke's C+D Stage) [Table 2]. Another important finding of this study was that one of the H. pylori infected tumor was of a familial adenomatous polyposis patient.
|Table 2: The clinico-pathological features of colorectal cancer patients having H. pylori infection|
Click here to view
Although H. pylori infection is one of the most common bacterial infections in man, known to cause gastritis and increase the risk of gastric cancer,  there are conflicting reports about the presence of H. pylori infection and colorectal cancer. ,,,
In this study, we found very low prevalence of the H. pylori infection in CRC patients in our ethnic population, which was in tune with other studies. , These results suggest that H. pylori has a very small role in causing the CRC malignancy in our population.
| Conclusion|| |
In our study, we detected the presence of H. pylori genomic material by PCR reaction in colorectal cancer. However, we conclude that there is very less frequency of H. pylori infection in our CRC patients.
| References|| |
|1.||Alm RA, Ling LS, Moir DT, King BL, Brown ED, Doig PC, et al. Genomic-sequence comparison of two unrelated isolates of the human gastric pathogen. Helicobacter pylori. Nature 1999;397:176-80. |
|2.||Shmuely H, Passaro D, Figer A, Niv Y, Pitlik S, Samra Z, et al. Relationship between helicobacter pylori CagA status and colorectal cancer. Am J Gastroenterol 2001;96:3406-10. |
|3.||Breuer-Katschinski B, Nemes K, Marr A, Rump B, Leiendecker B, Breuer N, et al. Helicobacter pylori, and the risk of colonic adenomas. Colorectal Adenoma Study Group. Digestion 1999;60:210-5. |
|4.||Muszynsky J, Dzierzanowska D, Sieminska J, Bogdanska M, Vogt E, Ehrmann A. Is helicobacter pylori infection a real risk factor for gastric carcinoma? Scand J Gastroenterol 1995;30:647-51. |
|5.||Rudi J, Müller M, von Herbay A, Zuna I, Raedsch R, Stremmel W, et al. Lack of association of helicobacter pylori seroprevalence and gastric cancer in a population with low gastric cancer incidence. Scand J Gastroenterol 1995;30:958-63. |
|6.||Moss SF, Neugt AI, Garbowsky GC, Wang MR, Treat MR, Forde KA. Helicobacter pylori and colorectal neoplasia: Evidence against association. Gastroenterology 1995;108:A511. |
|7.||Sameer AS, Chowdri NA, Syeed N, Banday MZ, Shah ZA, Siddiqi MA. SMAD4 - Molecular gladiator of the TGF-â signaling is trampled upon by mutational insufficiency in Colorectal Carcinoma of Kashmiri population: An analysis with relation to KRAS proto-oncogene. BMC Cancer 2010;10:300. |
|8.||Sameer AS, Shah ZA, Syeed N, Banday MZ, Bashir SM, Bhat BA, et al. TP53 Pro47Ser and Arg72Pro polymorphisms and colorectal cancer predisposition in an ethnic Kashmiri population. Genet Mol Res 2010;9:651-60. |
|9.||Center MM, Jemal A, Smith RA, Ward E. Worldwide variations in colorectal cancer. CA Cancer J Clin 2009;59:366-78. |
|10.||Javid G, Zargar SA, Rather S, Khan AR, Khan BA, Yattoo GN, et al. Incidence of colorectal cancer in Kashmir valley, India. Indian J Gastroenterol 2011;30:7-11. |
|11.||Lu JJ, Perng CL, Shyu RY, Chen CH, Lou Q, Chong SK, et al. Comparison of five PCR methods for detection of Helicobacter pylori DNA in gastric tissues. J Clin Microbiol 1999;37:772-4. |
|12.||Meucci G, Tatarella M, Vecchi M, Ranzi ML, Biguzzi E, Beccari G, et al. High prevalence of Helicobacter pylori infection in patients with colonic adenomas and carcinomas. J Clin Gastroenterol 1997;25:605-7. |
|13.||Jones M, Helliwell P, Pritchard C, Tharakan J, Mathew J. Helicobacter pylori in colorectal neoplasms: Is there an aetiological relationship? World J Surg Oncol 2007;5:51. |
|14.||Bulajic M, Stimec B, Jesenofsky R, Kecmanovic D, Ceranic M, Kostic N, et al. Helicobacter pylori in colorectal carcinoma tissue. Cancer Epidemiol Biomarkers Prev 2007;16:631-3. |
|15.||Grahn N, Hmani-Aifa M, Fransén K, Söderkvist P, Monstein HJ. Molecular identification of Helicobacter DNA present in human colorectal adenocarcinomas by 16S rDNA PCR amplification and pyrosequencing analysis. J Med Microbiol 2005;54:1031-5. |
[Table 1], [Table 2]