Immunohistochemical expression of matrix metalloproteinase-7 in human colorectal adenomas using specified automated cellular image analysis system: A clinicopathological study

Qasim, Ban J.; Ali, Hussam Hasson

doi:10.4103/1319-3767.105916

Cited by 13 publications

(8 citation statements)

References 12 publications

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“…MMP-7 breaks down the ECM by degrading casein, fibronectin, or collagen types I, II, IV and V [105]. MMP-7 has the ability to promote lung colonization of chondrosarcomas in vivo [106], was shown to be overexpressed in advanced colorectal polyps with severe dysplasia, and to facilitate their conversion to malignant cells [107]. MMP-7 appears to contribute to tumor aggressiveness as it is overexpressed at the invasion front of the tumor [108].…”

Section: In Vitro and In Vivo Evidencementioning

confidence: 99%

Somatic Mutation Theory - Why it's Wrong for Most Cancers

Brücher¹,

Jamall

2016

Cell Physiol Biochem

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Hysteron proteron reverses both temporal and logical order and this syllogism occurs in carcinogenesis and the somatic mutation theory (SMT): the first (somatic mutation) occurs only after the second (onset of cancer) and, therefore, observed somatic mutations in most cancers appear well after the early cues of carcinogenesis are in place. It is no accident that mutations are increasingly being questioned as the causal event in the origin of the vast majority of cancers as clinical data show little support for this theory when compared against the metrics of patient outcomes. Ever since the discovery of the double helical structure of DNA, virtually all chronic diseases came to be viewed as causally linked to one degree or another to mutations, even though we now know that genes are not simply blueprints, but rather an assemblage of alphabets that can, under non-genetic influences, be used to assemble a business letter or a work of Shakespearean literature. A minority of all cancers is indeed caused by mutations but the SMT has been applied to all cancers, and even to chemical carcinogenesis, in the absence of hard evidence of causality. Herein, we review the 100 year story of SMT and aspects that show why genes are not just blueprints, how radiation and mutation are associated in a more nuanced view, the proposed risk of cancer and bad luck, and the in vitro and in vivo evidence for a new cancer paradigm. This paradigm is scientifically applicable for the majority of non-heritable cancers and consists of a six-step sequence for the origin of cancer. This new cancer paradigm proclaims that somatic mutations are epiphenomena or later events occurring after carcinogenesis is already underway. This serves not just as a plausible alternative to SMT and explains the origin of the majority of cancers, but also provides opportunities for early interventions and prevention of the onset of cancer as a disease.

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Section: In Vitro and In Vivo Evidencementioning

confidence: 99%

Somatic Mutation Theory - Why it's Wrong for Most Cancers

Brücher¹,

Jamall

2016

Cell Physiol Biochem

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“…Secondly, from the clinical practice viewpoint, MMP-7 inhibitors can potentially be applied to control the invasive capacity of cancers (34). Thirdly, MMP-7 was found to be highly expressed in advanced colorectal adenomatous and involved in converting colorectal adenomas into malignant state and facilitating the cancer growth (35). According to the highlights above, it is reasonable that hereditary genomic information coded by various polymorphisms on MMP-7 may determine differential responses and personal susceptibility to CRC in the processes in inflammation, tumor initiation, invasion and metastasis.…”

Section: Discussionmentioning

confidence: 99%

The Contribution of MMP-7 Genotypes to Colorectal Cancer Susceptibility in Taiwan

Yueh

Hung

Chang

et al. 2018

CGP

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“…In clinical practice, MMP7 inhibitors can potentially be applied to control the invasive capacity of cancer cells (30,(32)(33)(34). In 2013, MMP7 was found to be highly expressed in advanced colorectal adenomatous and involved in converting colorectal adenomas into a malignant state and facilitating the cancer growth (35). In the literature, the A-181G genotype of MMP7 was studied for association with solid cancer such as oral, esophageal, gastric, colorectal, lung, breast and ovarian cancer, and renal cell carcinoma (21,22).…”

Section: Discussionmentioning

confidence: 99%