Preparing the tumour for sequencing.
© Charité | Linda Ambrosius
Creationist mode: 
When cells within a single tumour differ in terms of their genetic makeup, this is referred to as intratumour heterogeneity. Researchers from Charité – Universitätsmedizin Berlin and the Max Delbrück Center for Molecular Medicine (MDC) have been able to reconstruct the process by which this genetic heterogeneity develops in neuroblastoma, a type of cancer which primarily affects young children. According to their findings, the genetic makeup of individual tumours shows marked spatial and temporal variability. Results from this study have been published in Nature Communications.
The brilliance of this design is only just being appreciated by medical science since it makes it very difficult to treat and control the growth of these malignant cancers which are especially common in young children, accounting for 15% of cancer-related child deaths. It enables the tumour to quickly evolve to escape any drug therapies because these don't work against all the cell variations in the tumour, enabling some to survive the treatment and grow back. It also means some of the cells can break off from the original tumour and migrate to other parts of the body to start new tumours which will also carry this ability to evade treatment with them.
According to information provided by Charité and MDC in their press release:
In our study, we were able to show that the genetic changes typically associated with neuroblastoma can both disappear and emerge over the course of the disease. These mutations are not evenly distributed throughout the tumor; rather, they occur in distinct sections or even in individual cells, giving the tumor a mosaic-like appearance.
Dr. Karin Schmelz, First author
Charité’s Department of Pediatric Oncology and Hematology
Charité’s Department of Pediatric Oncology and Hematology
Tumors are heterogeneous, which means that different parts of the same tumor can be genetically distinct. This phenomenon, known as intratumor heterogeneity, is steadily gaining in significance within the field of cancer research. Cellular and molecular differences within the same tumor play an important role in many different cancers due to their implications for diagnosis and the use of targeted therapies.What should be obvious to any devotee of this divine malevolence is the considerable lengths it has gone to to ensure as many children die of this awful disease as possible by creating the cancers so they can evade the treatments medical science is able to offer.
[…]
Cancer cells undergo constant genetic change; they are engaged in a fight for survival, including against other cancer cells. Each cancer has its own phylogenetic tree, which depicts the way in which a tumor evolves; some cancer cells become metastatic, while others develop treatment resistance.
Cancer is driven by evolutionary processes. The process of recording detailed spatial and temporal changes in the copy numbers of specific genes is extremely complex.The researchers analyzed a total of 140 neuroblastoma samples. The biopsy samples were collected from 10 pediatric patients at various points during the clinical course and covered multiple tumor regions. Sample analysis involved the use of multiple modern sequencing techniques followed by computer-assisted evaluation.
We have now been able to extend this to neuroblastoma, where we were able to show in detail how the cancer genome undergoes structural changes.
Dr. Roland Schwarz, co-author.
Group Leader of the MDC’s Evolutionary and Cancer Genomics research group
The researchers focused their analysis on the neuroblastoma-associated genes ALK, MYCN and FGFR1, which play an important role in both clinical course and treatment. According to their results, changes in the ALK and MYCN genes were not present continuously throughout the course of the disease, nor were they found in all tumor cells. Changes in the ALK and FGFR1 genes can offer useful treatment targets, particularly in relapsed patients.We are now in a better position to understand how neuroblastoma cells behave. This knowledge is essential in relation to patients who suffer a recurrence of their disease because their treatment often requires the use of personalized and targeted therapies. When a tumor presents as genetically heterogeneous, targeted molecular therapy may well capture a majority of the abnormal tissue but, crucially, will not capture all of the affected cells. The cancer will then be able to regrow from those remaining cells.The researchers found that, in some patients, ALK mutations which were present at the time of diagnosis had disappeared by the time the tumor was surgically removed. Furthermore, changes in the FGFR1 gene were only found in distinct tumor regions. The researchers were also able to identify an instability in the number of gene copies present in neuroblastoma cells. In some cases, cancer cell clones showed early divergence from the primary tumor, breaking away to infiltrate other organs where they formed metastases.
Our findings have less relevance for neuroblastoma diagnosis and therapy selection. This is because diagnosis is already reliable, thanks to technologies that have undergone decades of testing, such as imaging, urine testing and single tissue biopsies, and because chemotherapy targeting fast-growing cells remains the treatment of choice for the primary tumor. However, if the disease recurs following treatment, targeted treatment options become particularly important. Treatment selection which is based on a single tissue biopsy from a single tumor region is unlikely to adequately address the tumor’s genetic heterogeneity. When a relapse occurs, we should therefore consider using state-of-the-art sequencing techniques to analyze tumor tissue samples harvested from multiple regions. This would provide us with as much detail as possible about the disease, enabling us to further improve the decision-making process pertaining to the selection of personalized therapies.
Prof. Dr. Angelika Eggert, co-author
Head of Charité’s Department of Pediatric Oncology and Hematology
Creationist mode: 
What is not obvious to normal people though is why Creationists prefer to present this putative designer as a malevolent sadist who designs things like childhood cancers and makes it so difficult for medical science to treat them and reduce the suffering, rather than to accept what the scientists involved in this study say - that these tumours are the result of an evolutionary process where the initial mistakes in genetic replication result in competing cell types, so driving the evolutionary process.
In the abstract to their open access paper in Nature Communications, the authors say:
AbstractWhy is it so difficult to accept the blatantly obvious as revealed by science, while insisting that the designer of these monstrosities is a loving god worthy of worship? Their inability to see this putative designer god for what it would need to be to design things like childhood cancers says more about its followers and worshippers than it does about the imaginary magic designer.
Intratumour heterogeneity is a major cause of treatment failure in cancer. We present in-depth analyses combining transcriptomic and genomic profiling with ultra-deep targeted sequencing of multiregional biopsies in 10 patients with neuroblastoma, a devastating childhood tumour. We observe high spatial and temporal heterogeneity in somatic mutations and somatic copy-number alterations which are reflected on the transcriptomic level. Mutations in some druggable target genes including ALK and FGFR1 are heterogeneous at diagnosis and/or relapse, raising the issue whether current target prioritization and molecular risk stratification procedures in single biopsies are sufficiently reliable for therapy decisions. The genetic heterogeneity in gene mutations and chromosome aberrations observed in deep analyses from patient courses suggest clonal evolution before treatment and under treatment pressure, and support early emergence of metastatic clones and ongoing chromosomal instability during disease evolution. We report continuous clonal evolution on mutational and copy number levels in neuroblastoma, and detail its implications for therapy selection, risk stratification and therapy resistance.
Schmelz, Karin; Toedling, Joern; Huska, Matt; Cwikla, Maja C.; Kruetzfeldt, Louisa-Marie; Proba, Jutta; Ambros, Peter F.; Ambros, Inge M.; Boral, Sengül; Lodrini, Marco; Chen, Celine Y.; Burkert, Martin; Guergen, Dennis; Szymansky, Annabell; Astrahantseff, Kathy; Kuenkele, Annette; Haase, Kerstin; Fischer, Matthias; Deubzer, Hedwig E.; Hertwig, Falk; Hundsdoerfer, Patrick; Henssen, Anton G.; Schwarz, Roland F.; Schulte, Johannes H.; Eggert, Angelika
Spatial and temporal intratumour heterogeneity has potential consequences for single biopsy-based neuroblastoma treatment decisions
Nature Communications 12, 6804 (2021). DOI: 10.1038/s41467-021-26870-z
Copyright: © 2021 The authors. Published by Springer Nature Ltd.
Open access
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)
Until they are prepared to confront this imaginary god, as Stephen Fry said he would do if he died and found it really existed, with, "Childhood cancers? What's that all about? How dare you create a world with such evil in it?", then they have no claim to occupy the moral highground or dictate to others how they should live their lives or what control over their own bodies they should be permitted to have.
No wonder these same people by and large follow preachers of hate who espose extreme, self-centred libertarianism and violence against minorities and advocate policies which result in the deaths of hundreds of thousands of people from the nasty viruses they also believe their divine malevolence created, while using their religion as an excuse for their odious personalities.
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