Helicobacter　pylori　(H.　pylori),　a　common　pathogen　residing　in　the　gastrointestinal　tract,　has　been　well　characterized　in　stomach　cancer,while　its　correlation　with　esophageal　cancer　remains　poorly　understood.　In　this　study,　we　aim　to　assess　the　relationship　between　esophageal　intraepithelial　H.　pylori　invasion　and　inflammation　as　well　as　atypical　hyperplasia　in　esophageal　squamous　epithelial　tissues.　Esophageal　squamous　cell　carcinoma　(ESCC)　tissue　samples　from　196　individuals　from　both　southern　and　northern　esophageal　carcinoma　high-risk　areas　in　China　were　examined　(125　from　northern　high-risk　areas,　71　from　southern　high-risk　area),　while　additional　30　samples　were　collected　adjacent　to　the　esophageal　squamous　cell　carcinoma　(A-ESCC).　H.　pylori　infection　was　identified　by　Giemsa　staining,　immuno-histochemical　staining,　and　H.　pylori　16S　rRNA-based　PCR.　A　significant　increase　of　H.　pylori　infection　was　found　in　tumor　tissues　(including　ESCC　and　A-ESCC　samples)　compared　to　that　of　non-tumor　tissues　(p＜0.05).　The　positive　rate　of　H.　pylori　16S　rRNA　in　ESCC,　A-ESCC,　and　normal　groups　were　62.5,　74.1,　and　26.7%,　respectively.　The　PCR　results　showed　that　the　positive　incidence　of　the　H.　pylori　virulence　factor　CagA　gene　in　tumor　(ESCC　and　A-ESCC)　and　normal　groups　was　54.9　and　20%,　respectively　(p＜0.05).　To　explore　the　possible　causes　of　CagA+　H.　pylori　infection　leading　to　carcinogenesis,　we　found　that　CagA+　H.　pylori　filtrate　induced　DNA　strand　breaks　in　esophageal　epithelial　NE3　cells,　suggesting　that　H.　pylori　infection　may　be　an　original　cause　leading　to　atypical　hyperplasia　of　esophageal　squamous　epithelial　tissues　and　contributed　to　pathological　carcinogenesis　of　ESCC.　What＇s　new?　The　bacteria　H.　pylori　has　been　extensively　studied　in　conjunction　with　gastric　cancer,　but　scientists　haven＇t　yet　pinned　down　its　role　in　esophageal　squamous　cell　cancer.　In　this　study,　the　authors　looked　at　how　often　esophageal　cancers　coincided　with　H.　pylori　infection.　They　found　the　bacteria　far　more　often　in　tumor　tissues　than　non-tumor.　Cell　culture　experiments　also　revealed　that　H.　pylori　can　break　esophageal　DNA,　suggesting　a　mechanism　for　how　it　could　spur　cancer　development.