{'fraction_non_alphanumeric': 0.05565978736710444, 'fraction_numerical': 0.05128205128205128, 'mean_word_length': 5.324110671936759, 'pattern_counts': {'":': 0, '<': 1, '<?xml version=': 0, '>': 1, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Relations of TGF‐beta1 with HIF‐1alpha, GLUT‐1 and longer survival of colorectal cancer patients

Aims and Methods: During colorectal carcinogenesis, transforming growth factor beta 1 (TGF‐β1) undergoes a functional change from suppression of cancer cell proliferation to inhibition of T cell mediated anti‐cancer immunity. We aimed to evaluate relations among TGF‐β1 and cancer cell survival factors hypoxia inducible factor‐1 alpha (HIF‐1α) and glucose transporter 1 (GLUT‐1) by immunohistochemistry in 108 colorectal cancers. Results: TGF‐β1 was detected in 87% (94/108), HIF‐1α in 85% (92/108), and GLUT‐1 in 65% (70/108) of colorectal cancers. Not only did TGF‐β1 accumulate in cytoplasm of cancer cells but also there was strong immunoreactivity to TGF‐β1 in adjacent inflammatory cells. GLUT‐1 was visualised in a membranous fashion while HIF‐1 was expressed in a paranuclear pattern and occasionally in nuclei of malignant cells. Cancer immunoreactivities to TGF‐β1 correlated with HIF‐1α (p < 0.001, r = 0.516) and GLUT‐1 (p > 0.001, r = 0.355) in general and subgroups of different clinicopathological traits. TGF‐β1 expressions of inflammatory infiltrates correlated with longer patient survival (p = 0.05, r = 0.449) and immunoreactivities to HIF‐1α of cancer cells (p = 0.008, r = 0.254) particularly in node positive and deeply invading cancers but failed to associate significantly with GLUT‐1. Conclusions: HIF‐1α and GLUT‐1 could cooperate with TGF‐β1, and TGF‐β1 might mediate cross‐talk between the inflammatory environment and tumour with a favourable impact on patient survival.