Schistosomiasis and malignancy.

L B Lemmer; P J Fripp

Home/Archive/PubMed

PubMed · 7974044

Schistosomiasis and malignancy.

L B Lemmer·P J Fripp

View original source ↗Export metadata ↓

Abstract

It is generally accepted that schistosomiasis, if not causative, is at least associated with malignancy. In this review, the epidemiology of schistosomiasis and bladder carcinoma, as well as the role of chronic bladder infection, are discussed together with known carcinogenic factors, possible abnormal vitamin metabolism and/or deficiencies and factors that influence conjugated carcinogens. Experimental evidence is briefly examined and recent work from the Far East on schistosomiasis and colon carcinoma reviewed.

Explore related subjects

Colorectal Neoplasms Cystitis Female Humans Incidence Male Schistosomiasis Urinary Bladder Neoplasms Journal Article Review

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

L B Lemmer, P J Fripp. 1994. Schistosomiasis and malignancy.. https://pubmed.ncbi.nlm.nih.gov/7974044/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2026

Co-targeting Deregulated WNT and MAPK Signaling Pathways Limits Phenotypic Reprogramming of Intestinal Stem Cell Progeny in KRAS-Hyperactivated Colorectal Cancer.

In their recent article, Moore and colleagues demonstrate that, upon KRAS hyperactivation, colorectal cancer growth is driven by a reprogramming of Lgr5+ intestinal stem cell (ISC) progeny towards the acquisition of a regenerative phenotype. They find that this phenotype is regulated by a balance between WNT-related ISCs and MAPK-related regenerative and proliferative transcriptional programs. By targeting both pathways, they are able to suppress this dynamic plasticity and achieve tumor regression in cell line and mouse models. The antagonistic relationship between these central pathways defined here provides key insights into genomic patterns of colorectal cancer and targeted therapy strategies.

Colorectal Neoplasms↗

PubMed2026

Identification and validation of a previously missed mutational signature in colorectal cancer.

Mutational signature analysis has enhanced our understanding of mutagenic processes. In a recent study, we analyzed 802 microsatellite-stable colorectal cancers (CRC) and identified a de novo signature, SBS_D, which was decomposed into SBS18. Here, we re-evaluate this decomposition and provide evidence that SBS_D represents a distinct mutational process from SBS18. Through an analysis of 2,616 CRCs across three independent cohorts, we demonstrate that SBS_D is consistently present, suggesting this signature may have been previously overlooked. We illustrate that the pattern of SBS_D better aligns with signatures associated with deficiencies in DNA repair, despite evidence that SBS_D is not driven by canonical defects in these DNA repair pathways. Overall, this study identifies a previously unrecognized mutational signature in DNA repair-proficient CRC and proposes that its etiology may be linked to DNA repair infidelity emerging late in tumor development. SBS_D has been submitted to the COSMIC database and provisionally designated as SBS111.

Colorectal Neoplasms↗

PubMed2026

Mapping micrometastatic seeds of relapse.

In this issue of Cancer Cell, Liu et al. apply spatial multi-omics to map colorectal cancer micrometastases across primary tumors and matched liver and lung metastases, revealing liver micrometastases as an early evolved, stem-like, immune-suppressed residual disease state linked to a six-gene recurrence signature.

Colorectal Neoplasms↗