Luís NunesOslo University Hospital · Institute for Cancer Research
Luís Nunes
Doctor of Philosophy
Postdoctoral Researcher in Molecular Oncology
About
25
Publications
1,999
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Introduction
Luís Nunes, biologist, PhD. He defended his PhD at Uppsala University focusing on cancer genetics, specifically prognostic and predictive biomarkers for colorectal cancer. He's particularly interested in using sequencing methodologies, programming, and statistical analyses in genetic research. By combining these complementary approaches, he aims to contribute to the understanding of the factors influencing the development of genetic diseases, and enhance their detection and treatment.
Education
November 2018 - April 2023
September 2013 - August 2016
Publications
Publications (25)
Background: Co-occurring mutations in pairs of genes can pinpoint clinically relevant subgroups of cancer. Most colorectal cancers (CRCs) are microsatellite stable (MSS) and have few frequent mutations. Large patient cohorts and broad genomic coverage are needed for comprehensive co-mutation profiling.
Methods: Co-mutations were identified in a po...
Introduction: Properties of tumor angiogenesis impact on tumor growth and composition of the tumor microenvironment. Tumor vessels are composed of pericytes and other mural cells. Detailed characterization of the cellular composition of the microvasculature can suggest functional vessel and case properties relevant for outcome, response to treatmen...
Colorectal cancer is caused by a sequence of somatic genomic alterations affecting driver genes in core cancer pathways¹. Here, to understand the functional and prognostic impact of cancer-causing somatic mutations, we analysed the whole genomes and transcriptomes of 1,063 primary colorectal cancers in a population-based cohort with long-term follo...
Introduction: Subsets of cancer-associated fibroblasts (CAFs) in colorectal cancer remain poorly characterized preventing their use as biomarkers and drug targets.
Results: Integrated scRNA seq profiling and multiplex staining identified four human CAF subsets These were A1 (PDGFRA+/FAP-/TF), PDGFRAhighA2 (PDGFRA+/FAP+/TF-), PDGFRAlowA2 (PDGFRA-/FA...
Rectal cancer poses challenges in preoperative treatment response, with up to 30% achieving a complete response (CR). Personalized treatment relies on accurate identification of responders at diagnosis. This study aimed to unravel CR determinants, overall survival (OS), and time to recurrence (TTR) using clinical and targeted sequencing data. Analy...
Simple Summary
Analysis of mutant DNA, leaking from tumors into blood plasma, can be used to detect tumor recurrence. We demonstrate that a novel, multiplex method termed superRCA is useful to analyze plasma for somatic hotspot mutations prevalent in solid cancer genomes to detect the recurrence of colorectal cancer.
Abstract
Mutation analysis of...
Mutation analysis of circulating tumor DNA (ctDNA) has applications in monitoring of colorectal cancer (CRC) patients for recurrence. Considering the low tumor fraction of ctDNA in cell-free DNA (cfDNA) isolated from blood plasma, the sensitivity of the detection method is important. Here, plasma DNA collected at diagnosis and follow-up from 25 CRC...
Background
Ephrin (EPH) receptors have been implicated in tumorigenesis and metastasis, but the functional understanding of mutations observed in human cancers is limited. We previously demonstrated reduced cell compartmentalisation for somatic EPHB1 mutations found in metastatic colorectal cancer cases. We therefore integrated pan-cancer and pan-E...
BRAF‐V600E mutation (mt) is a strong negative prognostic and predictive biomarker in metastatic colorectal cancer (mCRC). Non‐V600Emt, designated atypical BRAFmt (aBRAFmt) are rare, and little is known about their frequency, co‐mutations and prognostic and predictive role. These were compared between mutational groups of mCRC patients collected fro...
Mutational analyses of tumor DNA guide the use of targeted therapies and checkpoint inhibitors in management of solid tumors. Reducing false positive mutation calls without compromising sensitivity as gene panels increase in size, and whole exome and genome sequencing enters clinical use, remains a major challenge. Aiming for robust somatic mutatio...
Background: Ephrin (EPH) receptors have been implicated in tumorigenesis and metastasis, but the functional understanding of mutations observed in human cancers is limited. We previously demonstrated reduced cell compartmentalisation for somatic EPHB1 mutations found in metastatic colorectal cancer cases. We therefore integrated pan-cancer and pan-...
Colorectal cancer (CRC) is caused by a sequence of somatic genomic alterations affecting driver genes in core cancer pathways. To understand the functional and prognostic impact of cancer-causing somatic mutations, we analysed the whole genomes and transcriptomes of 1,063 primary CRCs in a population-based cohort with long-term follow-up. From the...
Ephrin (EPH) receptors have been implicated in tumorigenesis and metastasis, but the functional understanding of mutations observed in human cancers is limited. We previously demonstrated reduced cell compartmentalisation for somatic EPHB1 mutations found in metastatic colorectal cancer cases. We, therefore, integrated pan-cancer and pan-EPH mutati...
Background:
KRAS mutations, present in over 40% of metastatic colorectal cancer (mCRC), are negative predictive factors for anti-EGFR therapy. Mutations in KRAS-G12C have a cysteine residue for which drugs have been developed. Published data on this specific mutation are conflicting; thus, we studied the frequency and clinical characteristics in a...
Background:
Tumour-infiltrating CD3, CD8 lymphocytes and CD68 macrophages are associated with favourable prognosis in localised colorectal cancer, but the effect in metastatic colorectal cancer (mCRC) is not established.
Methods:
A Scandinavian population-based cohort of non-resectable mCRC patients was studied. Tissue microarrays (n = 460) were...
Canaries changing colors
Many animals are sexually dimorphic, with different phenotypes in males and females. To identify the genetic basis of sexual differences in bird coloration, Gazda et al. investigated red coloration in mosaic canaries and related species (see the Perspective by Chen). Using a combination of genetic crosses, genomic mapping,...
Background: We have reported that BRAF V600E mutations and microsatellite instability-high (MSI-H) are more prevalent in a population-based cohort of metastatic colorectal cancer (mCRC) patients than has been reported from clinical trials or hospital-based patient groups. The aim was to explore if other mutations in mCRC differ in prevalence betwee...
Questions
Question (1)
Hi everyone,
I’d like to raise a point of discussion around something that I find confusing in molecular oncology papers: the inconsistent use of italics for gene family names, particularly the RAS family.
According to the HGNC, the RAS family is a subset of the RAS small GTPase superfamily that includes the well-known proto-oncogenes HRAS, NRAS, and KRAS. Now, the HGNC guidelines are crystal clear when it comes to italicizing genes, alleles, and RNAs (to keep them separate from proteins). But when it comes to gene families like just RAS, things get…unclear.
For example, in the HGNC guideline paper (), they mention gene families like "cytochrome P450" or "HLA and KIR gene families" – and none of those are italicized. This made me assume in my mind that family names like RAS shouldn't get the italics either. Yet, when you look at the papers, some researchers use it in italic, while others don’t, and I couln't find any explanation for the different usage.
Here’s my take on the issue: RAS shouldn’t be italicized, because it’s not a single official human gene name – it’s a whole crew of related genes. If we italicize it, we risk confusing readers, especially those new to the field, who might think it’s a singular gene rather than a collection of them.
I’m interested in hearing what do you think, or if you can pinpoint me to places that have adressed this before that I have just missed it!
Looking forward for the discussion! :)
