Lara Lipton
A5020220461- Genetic factors in colorectal cancer
- Colorectal Cancer Treatments and Studies
- Cancer Genomics and Diagnostics
- Pancreatic and Hepatic Oncology Research
- Colorectal Cancer Screening and Detection
- Gastric Cancer Management and Outcomes
- Inflammatory mediators and NSAID effects
- Lung Cancer Treatments and Mutations
- Estrogen and related hormone effects
- DNA Repair Mechanisms
- Multiple and Secondary Primary Cancers
- Synthesis of β-Lactam Compounds
- Neuroendocrine Tumor Research Advances
- BRCA gene mutations in cancer
- Tumors and Oncological Cases
- Hepatocellular Carcinoma Treatment and Prognosis
- Cancer, Lipids, and Metabolism
- Renal cell carcinoma treatment
- Helicobacter pylori-related gastroenterology studies
- Cancer-related Molecular Pathways
- RNA modifications and cancer
- Cholangiocarcinoma and Gallbladder Cancer Studies
- Genomic variations and chromosomal abnormalities
- Pancreatitis Pathology and Treatment
- Genetic Associations and Epidemiology
Cabrini Hospital
2013-2024
Peter MacCallum Cancer Centre
2011-2024
Sunshine Hospital
2017-2024
Footscray Hospital
2008-2023
Western Hospital
2010-2023
Ludwig Cancer Research
2007-2023
The Royal Melbourne Hospital
2011-2022
Western Health
2015-2022
Walter and Eliza Hall Institute of Medical Research
2013-2022
The University of Melbourne
2011-2019
Germ-line mutations in the base-excision–repair gene MYH have been associated with recessive inheritance of multiple colorectal adenomas. Tumors from affected persons displayed excess somatic transversions a guanine–cytosine pair to thymine–adenine (G:C→T:A) APC gene.
PURPOSE: Colorectal cancer prognosis is currently predicted from pathologic staging, providing limited discrimination for Dukes stage B and C disease. Additional markers outcome are required to help guide therapy selection individual patients. EXPERIMENTAL DESIGN: A multisite single-platform microarray study was done on 553 colorectal cancers. Gene expression changes were identified between D tumors (three training sets) assessed as a signature in (independent test external validation sets)....
Activation of the canonical TGF-β signaling pathway provides growth inhibitory signals in normal intestinal epithelium. Colorectal cancers (CRCs) frequently harbor somatic mutations members TGFBR2 and SMAD4, but to what extent SMAD2 or SMAD3 contribute tumorigenesis is unclear. A cohort 744 primary CRCs 36 CRC cell lines were sequenced for SMAD2, analyzed allelic loss by single-nucleotide polymorphism (SNP) microarray analysis. Mutation spectra compared between genes, pathogenicity was...
Background Surgical management of colon cancer for patients with Lynch syndrome who carry a mismatch repair (MMR) gene mutation is controversial. The decision to remove more or less the involves consideration relatively high risk metachronous colorectal (CRC) impact extensive surgery. Objective To estimate and compare risks CRC undergoing either segmental (subtotal total) resection first cancer. Design Risk was estimated 382 MMR carriers (172 MLH1 , 167 MSH2 23 MSH6 20 PMS2 ) from Colon...
Lynch syndrome is a highly penetrant cancer predisposition caused by germline mutations in DNA mismatch repair (MMR) genes. We estimated the risks of primary cancers other than colorectal following diagnosis mutation carriers. obtained data from Colon Cancer Family Registry for 764 carriers an MMR gene (316 MLH1, 357 MSH2, 49 MSH6, and 42 PMS2), who had previous cancer. The Kaplan–Meier method was used to estimate their cumulative risk 10 20 years after age-, sex-, country- calendar...
Purpose We evaluated the activity of regorafenib, an oral multikinase inhibitor, in advanced gastric adenocarcinoma. Patients and Methods conducted international (Australia New Zealand, South Korea, Canada) randomized phase II trial which patients were randomly assigned at a two-to-one ratio stratified by lines prior chemotherapy for disease (one v two) region. Eligible received best supportive care plus regorafenib 160 mg or matching placebo orally on days 1 to 21 each 28-day cycle until...
BRAF(V600E) mutations are found in 10% of colorectal cancers (CRCs). The low frequency this mutation therefore makes it a challenging target for drug development, unless subsets patients with higher rates can be defined. Knowledge the concordance between primary-metastasis pairs and impact on outcome would also assist optimal development. We selected primary CRCs from 525 (stages I-IV) evenly matched age (<70 ≥70), gender tumor location (right, left rectum), 81 pairs. BRAF(V600E), KRAS...
Genome-wide association studies (GWAS) have identified 14 tagging single nucleotide polymorphisms (tagSNPs) that are associated with the risk of colorectal cancer (CRC), and several these tagSNPs near bone morphogenetic protein (BMP) pathway loci. The penalty multiple testing implicit in GWAS increases attraction complementary approaches for disease gene discovery, including candidate gene- or pathway-based analyses. strongest loci additional predisposition SNPs arguably those already known...
Oncogene mutations contribute to colorectal cancer development. We searched for differences in oncogene mutation profiles between metastases from different sites and evaluated these as markers site of relapse.One hundred were screened 19 oncogenes, further 61 87 matched primary cancers analyzed genes with identified mutations. Mutation prevalence was compared (a) liver (n = 65), lung 50), brain 46), (b) cancers, (c) an independent cohort 604). Mutations differing metastasis relapse 859...
Microsatellite instability (MSI) is an established marker of good prognosis in colorectal cancer (CRC). Chromosomal (CIN) strongly negatively associated with MSI and has been shown to be a poor small number studies. However, substantial group "double-negative" (MSI-/CIN-) CRCs exists. The these patients unclear. Furthermore, CIN are each specific molecular changes, such as mutations KRAS BRAF, that have prognosis. It not known which MSI, CIN, the gene primary predictors survival.
PIK3CA and PTEN mutations are prevalent in colorectal cancer potential markers of response to mitogen-activated protein/extracellular signal-regulated kinase inhibitors anti-EGF receptor antibody therapy. Relationships between phosphoinositide 3-kinase (PI3K) pathway mutation, clinicopathologic characteristics, molecular features, prognosis remain controversial.A total 1,093 stage I-IV cancers were screened for (exons 9 20), KRAS (codons 12-13), BRAF (codon 600) mutations, microsatellite...
Succinate dehydrogenase-deficient gastrointestinal stromal tumors (SDH-deficient GISTs) are a unique class of GIST defined by negative immunohistochemical staining for succinate dehydrogenase B (SDHB). SDH-deficient GISTs show distinctive clinical and pathologic features including absence KIT PDGFRA mutations, exclusive gastric location, common lymph node metastasis, prognosis not predicted size mitotic rate, indolent behavior metastases. They may be syndromal with some being associated the...
Abstract Mendelian-like inheritance of germline DNA methylation in cancer susceptibility genes has been previously reported. We aimed to scan the genome for heritable marks associated with breast by studying 25 Australian multiple-case families. Here we report genome-wide measured 210 peripheral blood samples provided family members using Infinium HumanMethylation450. develop and apply a new statistical method identify based on complex segregation analysis. estimate carrier probabilities...
DNA-methylation changes in human cancer are complex and vary between the different types of cancer. Capturing this epigenetic variability an atlas will be beneficial for basic research as well translational medicine. Hypothesis-free approaches that interrogate methylation patterns genome-wide have already generated promising results. However, these methods still limited by their quantitative accuracy number CpG sites can assessed individually. Here, we use a unique approach to measure set...
Familial adenomatous polyposis (FAP) is a dominantly inherited colorectal tumor predisposition that results from germ-line mutations in the APC gene (chromosome 5q21). FAP shows substantial phenotypic variability: classical patients develop more than 100 adenomas, whereas those with attenuated (AAPC) have fewer adenomas. A further group of individuals, so-called “multiple” adenoma patients, phenotype like AAPC, 3–99 polyps throughout colorectum, but mostly no demonstrable mutation. Routine...