Rapid degradation of the human DNA forces science to use gene editing architectures

Gene editing of human embryos yields early results

Excerpt: "Scientists have long sought a strategy for curing genetic diseases, but — with just a few notable exceptions — have succeeded only in their dreams. Now, though, researchers in China and Texas have taken a step toward making the fantasies a reality for all inherited diseases.

Using the gene-editing tool known as CRISPR/Cas9, the researchers have successfully edited disease-causing mutations out of viable human embryos. Other Chinese groups had previously reported editing human embryos that could not develop into a baby because they carried extra chromosomes, but this is the first report involving viable embryos.

In the new work, reported March 1 in Molecular Genetics and Genomics, Jianqiao Liu of Guangzhou Medical University in China and colleagues used embryos with a normal number of chromosomes. The embryos were created using eggs and sperm left over from in vitro fertilization treatments. In theory, the embryos could develop into a baby if implanted into a woman’s uterus.

Researchers in Sweden and England are also conducting gene-editing experiments on viable human embryos, but those groups have not yet reported results. 

Human germline editing wasn’t realistic until CRISPR/Cas9 and other new gene editors came along, says R. Alta Charo, a bioethicist at the University of Wisconsin Law School in Madison. “We’ve now gotten to the point where it’s possible to imagine a day when it would be safe enough” to be feasible. Charo was among the experts on a National Academies of Sciences and Medicine panel that in February issued an assessment of human gene editing. Altering human embryos, eggs, sperm or the cells that produce eggs and sperm would be permissible, provided there were no other alternatives and the experiments met other strict criteria, the panel concluded.

Scientists design guide RNAs so that they will carry Cas9 to only one stretch of about 20 bases (the information-carrying subunits of DNA) out of the entire 6 billion base pairs that make up the human genetic instruction book, or genome. But most 20-base locations in the human genome aren’t particularly distinctive. They are like Starbucks coffee shops: There are a lot of them and they are often similar enough that a GPS might get confused about which one you want to go to, says Edgell. Similarly, guide RNAs sometimes direct Cas9 to cut alternative, or “off-target,” sites that are a base or two different from the intended destination. Off-target cutting is a problem because such edits might damage or change genes in unexpected ways. (My comment: This is because one gRNA might have hundreds of target genes it regulates. But anyway, scientists have found the RNA-addressing system.)


My comment: Modern science has already found about 200,000 disease-causing genetic mutations in the human DNA. 400,000 children with (new) developmental disorders born each year globally. About 10,000 new genetic mutations are discovered annually in the human DNA.

Conclusions are crystal clear: Evolution is not happening. So called natural selection is not able to filter out genetic errors. Human genome is rapidly deteriorating and serious science is forced to make their best efforts in editing the human DNA.


Goodbye junk-dna!

'Jumping genes' and transposons are cut or silenced by clever mechanisms

Eukaryotic cells are able to produce even thousands of different proteins from one gene. This is why there are even two millions of different proteins in a human body, although there are only about 19,600 protein coding genes used for human cells to produce the huge number of different proteins. This clever mechanism is called alternative splicing. RNA-mediated mechanism uses a gene like a library; it makes a template and modifies it by several ways. Cutting, pasting, recombining, moving, removing etc.

Sometimes some strands (rna-like retrotransposos) needed for the alternative splicing mechanism are inserted into the genome by mistake. These genomic parasites can be harmful for genomic stability and integrity. Especially in germline cells they can cause serious troubles, even cell death. That's why there are mechanisms designed in the cell, that silence or remove those erroneous genetic sequences. The mechanism is described here:


Excerpt: "The researchers have found that small pieces of RNA get stitched together into a loop. The investigators were interested in the unicellular ciliate, Paramecium tetraurelia, because they identified small RNA molecules that excise pieces of Paramecium DNA. Looking deeper, there was a kind of feedback loop operating in the excision of DNA segments. Junk DNA was being cut out of the genome, and it is then transcribed into RNA before getting degraded by cellular machinery. The transcribed RNAs act to help cut out even more DNA, building up the RNA production from these excised pieces. However, the resulting RNA pieces are quite small; they are too tiny to be read by normal cellular machinery.

The scientists had to keep digging to learn more about what as happening. "It was an interesting detective work," Nowacki remembers. They had a suspect -- all they needed was to pin it down. "We were not actually looking for the unknown, because we soon had an idea, and then it was all about testing that idea." What they found was that the RNAs were strung together, into strands or concatemers that are about 200 base pairs long and then closed into a loop.

The evidence continues to mount that so-called junk DNA has important functions, likely in the regulation of gene expression and who knows what else. Nowacki suggested that this is the first time, a precise mechanism has been identified whereby deleted, junk DNA is transcribed. That could mean it will finally shed its junky nickname.

Nowacki's lab is working on the NCCR "RNA & Disease -- The Role of RNA Biology in Disease Mechanisms" project, which aims to reveal more about the role of RNA in disease. RNA is a crucial part of gene expression, and disruptions in that system have been linked to cancer, diseases of the heart and brain, and metabolic disorders. Swiss researchers that study different aspects of the function and characteristics of RNA work together at the NCCR, coordinating research using a variety of models like plants, yeast, roundworms, mice and human cells."

My comment: The cell uses mistakes for finding more mistakes! An incredible mechanism! There are no selfish genes or jumping genes. Unchecked, unremoved or unsilenced transposons typically cause diseases. Modern science has just found out the link between the ALS disease and unsilenced dna-transposons:


There are no mechanisms for assumed evolution. Life is not driven by gene sequences. Genes are driven by lifestyle. Don't get lost.


Human traits and Epigenetics

Human traits are determined by epigenetic control of gene expression

Excerpt: "Genome‐wide SNP analyses have identified genomic variants associated with adult human height. However, these only explain a fraction of human height variation, suggesting that significant information might have been systematically missed by SNP sequencing analysis. A candidate for such non‐SNP‐linked information is DNA methylation. Regulation by DNA methylation requires the presence of CpG islands in the promoter region of candidate genes. Seventy two of 87 (82.8%), height‐associated genes were indeed found to contain CpG islands upstream of the transcription start site (USC CpG island searcher; validation: UCSC Genome Browser), which were shown to correlate with gene regulation. Consistent with this, DNA hypermethylation modules were detected in 42 height‐associated genes, versus 1.5% of control genes (P = 8.0199e−17), as were dynamic methylation changes and gene imprinting. Epigenetic heredity thus appears to be a determinant of adult human height. Major findings in mouse models and in human genetic diseases support this model. Modulation of DNA methylation are candidate to mediate environmental influence on epigenetic traits. This may help to explain progressive height changes over multiple generations, through trans‐generational heredity of progressive DNA methylation patterns."

Excerpt: "Visel's team was particularly interested in the portion of the genome that does not encode for proteins – until recently nicknamed "junk" DNA – but which comprises around 98% of our genomes. In experiments using embryonic tissue from mice, where the structures that make up the face are in active development, Visel's team identified more than 4,300 regions of the genome that regulate the behaviour of the specific genes that code for facial features. These "transcriptional enhancers" tweak the function of hundreds of genes involved in building a face. Some of them switch genes on or off in different parts of the face, others work together to create, for example, the different proportions of a skull, the length of the nose or how much bone there is around the eyes."

3. Skull morphogenesis

Excerpt: "Histone deacetylases (Hdacs) are transcriptional repressors with crucial roles in mammalian development. Here we provide evidence that Hdac8 specifically controls patterning of the skull by repressing a subset of transcription factors in cranial neural crest cells. Global deletion of Hdac8 in mice leads to perinatal lethality due to skull instability, and this is phenocopied by conditional deletion of Hdac8 in cranial neural crest cells. Hdac8 specifically represses the aberrant expression of homeobox transcription factors such as Otx2 and Lhx1. These findings reveal how the identity and patterning of vertebrate-specific portions of the skull are epigenetically controlled by a histone deacetylase."

4. Hair color


5. Skin and eye color

My comment: Traits are not determined by gene sequences. There are no mechanisms for evolution. Everything points to Design and Creation. Don't get misled.


The DNA methylation revealed a much stronger link to survival than point mutations

The DNA methylation revealed a much stronger link to survival than point mutations


Excerpt: "Various chemical modifications in the genome determine whether genes are read or deactivated. Methyl labels in the DNA play a key role in this "epigenetic" regulation of gene activity. Life style and environmental factors influence the methylation in the genome. Scientists have already well documented links between the methylation status of specific positions in the genome and cancer as well as other diseases....The DNA methylation revealed a much stronger link to survival than all other previously studied alterations in individual DNA building blocks (SNPs, single nucleotide polymorphisms). The epigenetic risk profile thus proved to be a more accurate indicator for lifespan than all other previously established genetic risk profiles that are based on alterations in DNA building blocks.

"We were surprised that the methylation status of only ten positions of our genome correlates so strongly with all-cause mortality," commented Brenner. "We found even stronger links to mortality from cardiovascular diseases. Now it is important to find out which prevention measures are most effective to achieve a beneficial impact on the methylation profile and mortality."

My comment: Point mutations are results of bad life habits, poor nutrition, stress and environmental factors. Aberrant methylation patterns trigger sequence alterations, which usually are genetic errors. The DNA methylation is an important element in your genome. It stabilizes the whole DNA, activates/silences genes, keeps faulty genes silenced and is used as an analog information layer on top of genes and histones. Methylation patterns are altered when an organism adapts into different type of diet, climate and other environmental factors. Cancer and other serious diseases and health problems are typically caused by disrupted methylation patterns. These epigenetic layers are often transgenerationally inheritable genomic elements. You can take care of your epigenome by eating healthy food, avoiding smoking, alcohol and other toxins.

Changes in gene sequences alone will never lead to evolution or adaptation. Genes are networked by several grammar-complex information layers and they need epigenetic markers for correct functions. Genes are just RAW libraries for RNA directed cellular mechanisms. The evolutionary theory is a major lie. Don't get lost.


How diet impacts our genome

Dietary anti-cancer compound may work by influence on cellular genetics


Excerpt: "Researchers have discovered one of the reasons why broccoli may be good for your health.

They found that sulforaphane, a dietary compound from broccoli that's known to help prevent prostate cancer, may work through its influence on long, non-coding RNAs. This is another step forward in a compelling new area of study on the underlying genetics of cancer development and progression.

The findings were published by researchers from Oregon State University in the Journal of Nutritional Biochemistry.

The research provides more evidence for how these lncRNAs, which were once thought to be a type of "junk DNA" of no particular value or function, may instead play a critical role in triggering cells to become malignant and spread.

Growing evidence shows that lncRNAs, which number in the thousands, have a major role in cell biology and development, often by controlling what genes are turned on, or "expressed" to carry out their genetic function. Scientists now believe that when these lncRNAs are dysregulated they can contribute to multiple disease processes, including cancer.

The lncRNAs are also of special interest, researchers say, because they are so highly cell- and tissue-specific.

Unlike many chemotherapeutic drugs that affect healthy cells as well as malignant ones and can cause undesired side effects, the control of lncRNAs may offer a new way to specifically prevent or slow the progression of malignant cells.
"This could be a turning point in our understanding of how cancer may be triggered and spreads," said Emily Ho, the endowed director of the Moore Family Center for Whole Grain Foods, Nutrition and Preventive Health at OSU, a professor in the College of Public Health and Human Sciences and principal investigator with the Linus Pauling Institute.

"It's obviously of interest that this dietary compound, found at some of its highest levels in broccoli, can affect lncRNAs. This could open the door to a whole range of new dietary strategies, foods or drugs that might play a role in cancer suppression or therapeutic control."

In particular, this research showed that one lncRNA, called LINC01116, is upregulated in a human cell line of prostate cancer, but can be decreased by treatment with sulforaphane. The data "reinforce the idea that lncRNAs are an exciting new avenue for chemoprevention research, and chemicals derived from diet can alter their expression," the scientists wrote in their study.

"We showed that treatment with sulforaphane could normalize the levels of this lncRNA," said Laura Beaver, a research associate in the Linus Pauling Institute and College of Public Health and Human Sciences, and lead author on the study. "This may relate to more than just cancer prevention. It would be of significant value if we could develop methods to greatly slow the progress of cancer, help keep it from becoming invasive."

The impact of diet on lncRNA expression has been largely unknown until now, the researchers said. In this study, they identified a four-fold decrease in the ability of prostate cancer cells to form colonies when LINC01116 was disrupted.

Among men, prostate cancer is the second most frequently diagnosed cancer globally, and the second leading cause of cancer-related deaths in the United States. Worth noting, the researchers said, is that an increased consumption of cruciferous vegetables such as broccoli, which are high in sulforaphane, appears to be associated with a lower risk of developing prostate cancer.

That same lncRNA, they noted, is also overexpressed in studies of several other types of cancer, including brain, lung and colon cancer. Some other lncRNAs have been found at higher levels in breast, stomach, lung, prostate cancer and chronic lymphocytic leukemia.

In other research, a knockout of the gene that encodes one type of lncRNA in mice conferred some resistance to obesity caused by a high-fat diet.

"Taken together, this literature and our own study begin to paint a picture of the important and previously unappreciated role of lncRNAs in the body's response to diet," the researchers wrote in the study. "These discoveries illustrate that lncRNAs can play important roles in cancer development and may be useful targets for cancer prevention, detection and treatment." "

My comment: Broccoli contains sulphoraphane (
C6H11NOS2) which is broken down into methyl groups and other important compounds in the gut. Both short and long non-coding RNA-molecules need these CH3 groups for their epigenetic markers. These are used for correct and successful gene expression and several regulatory functions in most organisms. Lack of methyl is linked to unsuccessful cellular differentiation and malignant cellular behavior. This means cancer.

Here we have a perfect example of functioning non-coding RNA, that is not junk. We also have a perfect example of actual reason for most cancers, poor nutrition. Did you know that poor diet is associated with 45% of all deaths from heart disease, stroke and diabetes? Scientists should look at the epitranscriptome when trying to find reasons for cancers and other health problems.


Take care of your genome. Life is not driven by genes. Genes are driven by lifestyle.


Protein coding genes are just raw data

An astonishing similarity of protein coding genes in humans, pigs, mice, dolphins, kangaroos, spiders etc.


Excerpt: "The human genome contains about 21,000 protein-encoding genes, but the total number of proteins in human cells is estimated to be between 250,000 to one MILLION."

My comment: Newest studies have confirmed the number of human protein coding genes to be about 19,000. RNA-directed cellular mechanisms are able to build thousands of different proteins by using raw data of one gene, without changing the gene's sequence. Mechanism is called alternative mRNA splicing. Based on DSCAM gene in Drosophila Melanogaster, the fruit fly's cell is able to build even 38,016 different proteins, without changing the sequence. The way of how the cell uses protein coding genes tells us that genes are not drivers. Instead, they are just raw data, libraries for RNA-directed mechanisms.

The alternative splicing is the most significant mechanism inducing the ecological adaptation and organisms' variation. The clever question arises: how come variation of organisms happen if the sequences of protein coding genes are not to be changed? Mutations in protein coding genes could be extremely harmful and they would cause a huge mess in genomic stability and integrity.

Serious science has the answer:
Epigenetic Control of Gene Expression. The alternative splicing mechanism is regulated by several epigenetic factors. The three main regulators are:

1. The DNA methylation.

By the way, did you know that the C. Elegans, a tiny multicellular nematode worm, that is assumed to be a simple type of organism, has 20,450 protein coding genes? More than us! It is not a simple life form! It also uses the alternative splicing machinery for regulating its proteins in 1031 cells it has.

Protein coding genes are very similar in most animals. For example, human and mice genomes differ only at 2.5%.


Human and pig genomes are also extremely similar.


"We took the human genome, cut it into 173 puzzle pieces and rearranged it to make a pig,” explains animal geneticist Lawrence Schook. “Everything matches up perfectly. The pig is genetically very close to humans."

Human protein coding genes are 
also very similar to kangaroos, dolphins, spiders etc. These are very inconvenient facts for believers of the evolutionary theory that is misleading people by maintaining the heresy of human-chimp genomic similarity. They don't tell you that the famous 98% is true only with these protein coding genes. But when we compare the alternative splicing mechanism and epigenomes, the differences are quite remarkable.

Everything points to Design and Creation. Don't get misled.


Plant Epigenetics points to Design

Plant diversity and epigenetic mechanisms


Excerpt from Jef Akst | February 1, 2017

"There are three different types of DNA methylation in plants: CG, CHH (where H is any base except G), and CHG. In Arabidopsis, CG methylation is found on some genes, but primarily on repeat sequences that make up transposons, as well as other repeat sequences in the genome. CHH methylation is found only where there is CG methylation and often near transposable elements, though some evidence points to CHH methylation on some silenced genes as well. CHG methylation is typically found with the CHH variety.


Every time a cell divides, it must replicate its genome and its epigenome. Plants have diverse pathways overseeing the faithful passage of the methylome to daughter cells.

CG methylation

Copying CG methylation patterns to the two daughter strands is relatively straightforward. That’s because this type of methylation is symmetrical: the complementary strand is also CG (reading from 5’ to 3’), and that cytosine is also methylated. So when the parent DNA strand splits, the two daughter strands that form will have methylation on the parent-strand side, and that methylation can guide the addition of a methyl group to the newly replicated strands’ CG cytosine as DNA is being copied.

CHH methylation

CHH methylation is inherently asymmetrical, because the H is any base except guanine. CHH methylation is passed on to both daughter genomes using a process called RNA-directed DNA methylation, which involves small RNAs that guide RNA interference machinery to methylate complementary regions of DNA.

CHG methylation

Although CHG methylation is symmetrical and thus could in principle use the same methylation maintenance pathway as CG methylation, it also relies on RNA-directed DNA methylation (not pictured below). In addition, this type of methylation is paired with methylation of lysine 9 on histone H3 (H3K9). The histomethyltransferase that methylates H3K9 regions binds to methylated CHG. Conversely, the CHG-methylating enzyme binds to H3K9, then methylates nearby CHG sites, forming a positive feedback loop between the two types of methylation.


Arabidopsis pollen grains have three haploid cells: one vegetative cell that helps produce the pollen tube and two sperm. One sperm fertilizes the egg to make the embryo, while the other fuses with the female’s central cell to form the supportive tissue known as endosperm.

During reproduction, certain types of DNA methylation are reprogrammed in the pollen."

My comment: About 95% of most plants' genes are methylated and thus silenced. This explains the huge variation potential within plants. Traits of plants are based on these epigenetic markers just like within other eukaryotic organisms. Removing epigenetic markers from the plant cell turns the cell into a pluripotent stem cell, an undifferentiated cell that has no task or mission. The most incredible mechanism within plant epigenetics is RNA-directed reprogramming that occurs in the pollen. This means that short RNA molecules guide the reprogrammming procedure by transmitting information and energy for correct epigenetic marking. The principle of this mechanism is similar to other eukaryotic organisms. This explains why gene sequence changes are only errors and noise in this signal of Intelligence.

Everything points to Design and Creation. Don't get lost.


Muntjacs fight pseudoscience

Rapid 'speciation' and chromosome loss don't support the theory of evolution

Excerpt: "The Red Muntjac has the lowest diploid chromosomal number in mammals (2n = 6 for females and 7 for males) whereas Reeves' Muntjac has 2n = 46 in both sexes (remarkably, these two species can produce viable F1 hybrids in captivity)."

My comment: Despite the huge difference in chromosome count (2n=6 and 2n=46), those two breeds of Muntjac are able to get viable offspring. Such interesting cases of hybridization can be observed in captivity, for example in zoos.

Chromosomes of the Red Muntjacs are tightly packaged because of huge areas of heterochromatin. Telomeres are also very strong indicating large areas of faulty genes.
I also found an interesting phenomenon regarding the number of chromosomes. Because shifting diet causes genetic mutations, the heavy loss of chromosomes has driven the Red Muntjac into omnivory. This finding needs a lot of further study to be confirmed.

There are no mechanisms for evolution. We can't even use the term 'micro evolution' because how come could anyone call information loss as evolution? Micro devolution is a better expression.

Organisms experience variation very rapidly. Five new Muntjac 'species' were 'discovered' in 1990's. My claim is that they were not only discovered, they were actually new variations of that kind. Rapid variation is a scientific fact:

Rapid 'evolution' in real time. New lizard 'species' in 15 years:

Many new primate 'species' in the 2000's

New mammal 'species' arisen in 2000's

A new 'species' is evolving right before our eyes

Watching new 'species' 'evolve' (adapt) in real time

Meet the 20,000 new 'species' we discovered in a single year

A new fish 'species' from Lake Victoria

New bird 'species' in 19 years

New butterfly 'species' in USA:

New fish species:

New species just in front of our eyes:

New butterfly species in four years:

Six new species from Madeira mouse in 500 years

Thousands of new fish species:

Morphological differences in 10 000 years:

Mice 'evolution'

New sparrow race under 50 years

Mites 'evolved' rapidly

Six new snake 'species'

Everything points to Biblical Creation and Design. Don't get misled.


GMO corn causes genetic mutations

Genetically modified corn leads to oxidative stress and genetic mutations


Excerpt: "In-depth analysis of types of proteins (“proteomics”) and small biochemical molecules (“metabolomics”) revealed major compositional differences between NK603 and its non-GMO parent. The results obtained show not only disturbances in energy utilisation and oxidative stress (damage to cells and tissues by reactive oxygen), but worryingly large increases in certain substances (polyamines).

Polyamines found to be present in increased amounts in GMO NK603 corn include putrescine and cadaverine, which can produce various toxic effects. For example, they enhance the effects of histamine, thus heightening allergic reactions, and both have been implicated in the formation of carcinogenic substances called nitrosamines.

Overall, the findings of this study disprove industry and regulatory agency claims that NK603 is ‘substantially equivalent’ to its non-GMO counterpart and suggest that a more thorough evaluation of the safety of consuming products derived from this GMO corn on a long term basis should be undertaken.


1. A total of 117 proteins and 91 small molecule biochemicals (metabolites) were found to be statistically significantly altered in NK603 corn by the GM transformation process.

2. The GM transformation process was the major contributor to variation in the protein and metabolite profiles, rather than environmental factors such as the spraying of the Roundup weedkiller or the growing season.

3. Alteration in the protein profile revealed by the proteomics analysis was reflective of an imbalance in energy utilisation and oxidative stress (damage to cells and tissues by reactive oxygen).

4. Small molecule biochemical profile differences revealed by metabolomics mostly consisted of an increase in a class of compounds known as polyamines; the levels of potentially toxic putrescine and especially cadaverine were markedly increased in the GM NK603 corn."
My comment: Scientists should be extremely careful when modifying genomes of organisms. Plants are designed to provide all necessary nutrients for animals and humans. Removing or modifying plants' genes leads to disruption of proteins and non-coding RNA-molecules that play a significant role in metabolic mechanisms within animals and humans. Modern scientists already understand that oxidative stress leads to genetic mutations and genomic degradation. Population genetics has provided false doctrine of mutation driven evolution for decades. 


How the cell uses cytokines as knobs instead of switches

Epigenetic layers function as analog information regulators


Excerpt: "Conventional wisdom has held that cytokines are “digital,” in that they either bind to a cellular receptor — triggering a cascade of signals within the cell — or they don’t. If a mutation prevents perfect binding, no cascade. There is no middle ground.

But maybe there is. A rare case of a rare disease has led an international research team headed by Broad Institute of Harvard and MIT associate member Vijay Sankaran of Dana-Farber/Boston Children’s Cancer and Blood Disorders Center, postdoctoral fellow Ah Ram Kim, and Yale University’s Daryl Klein to propose an “analog” view of cytokine function. It may be, as they show in Cell, that cytokine mutations that affect not whether a protein and receptor interact, but the quality of that interaction, can tune a cell’s biochemical response, triggering some signals and not others.

This insight could give researchers an opening to develop cytokine-based therapeutics tailored to elicit particular activities — potentially a boon for people suffering forms of cancer, kidney disease, blood disorders, and more.

...In addition to explaining the child’s grave disease, the findings suggest something new: a different way to think about adapting cytokines therapeutically.

“In hematology and immunology, people tend to think about cytokines as working like on and off switches,” Sankaran said. Doctors commonly use or manipulate EPO and other cytokines to treat cancer, autoimmunity, immunodeficiencies, and other conditions, he said. “But what we’re learning is that maybe they can be tuned."

My comment: Population genetics has provided these pseudoscientific claims about genetic mutations for decades. Cytokine production is regulated by epigenetic control of gene expression. The most significant factors inducing this clever fine-tuning of cytokines are methylation levels of the (EPO) gene and miRNA control of the alternative splicing of pre-mRNA.

This kind of gradient tuning of protein production together with several other mechanisms needs perfect Design. Organisms are replete with this kind of regulatory mechanisms with tunable analog knobs. I have told about them in my previous posts:


Epigenetics is opening scientists' eyes to see the incredible complexity of the cell. Epigenetics will not save the theory of evolution. Everything points to Design and Creation. Don't get lost.

A lack of methyl groups in the gene body may develop cancer

A lack of methyl groups in the gene body may develop cancer


Excerpt: "Every cell in our body contains the complete DNA library. So-called methyl groups regulate that in body tissues only the genetic information is expressed that is indeed needed in this tissue. Now, for the first time, researchers from the Leibniz Institute on Aging in Jena, Germany, verified that a lack of methyl groups in the gene body leads to an incorrect gene activation and, as a consequence, may lead to the emergence of cancer. The stunning results were published in the journal Nature on February 22, 2017.

Each cell in the body contains the basic building plan of our entire organism. It is written in the "DNA" and comprises single genes which determine specific individual attributes. Gene expression is strictly regulated in order to build tissue-specific cells with tissue-specific attributes. For example in an intestinal cell, the genetic information is activated that forms the cell's identity as intestinal cell. In this strictly regulated process, methyl groups play an important role. If they are enzymatically bound to a gene's starting point, known as the promoter, the respective gene is inactivated. In this case, the DNA is "methylated." During aging as well as during the development of age-induced diseases like cancer, the activation of genetic information is increasingly defective. However, as of yet, the detailed processes of these errors and the role that DNA methylation has in these processes have only poorly been understood.

A lack of methyl groups in the gene body may develop cancer

It was known for some time that DNA methylation at the promoters of a gene fulfills the function of an on/off switch. One of the big open questions in Epigenetics is why DNA within the gene body (where the important genetic information is located) is methylated as well. This question was now addressed by scientist Francesco Neri from the Leibniz Institute on Aging -- Fritz Lipmann Institute (FLI) in Jena, Germany, and his colleagues from the Human Genetics Foundation and the Torino University, Italy. They proved that genes are also aberrantly activated if -- beyond promoters -- DNA methylation is missing within the gene body. As a consequence, aberrant proteins are produced, which impinge on the cell structure. Thus, the function and identity of a cell are massively disrupted: cells degrade, cancer may emerge.

..."This new knowledge that a lack of DNA methylation at the gene body may lead to the production of aberrant proteins, might offer a new target for cancer therapy. If we succeed to find a way to traffic methyl groups to non-methylated DNA sequences of cancer cells, we could possibly stop proliferation of these cells," Dr. Neri hopes. But there is still a long way to go."
My comment: Aberrant methylation patterns trigger sequence changes. These are genetic errors that need to get hided by cellular mechanisms. Factors like poor diet, stress, toxins etc. lead to weakened and disrupted methylation patterns which means we can influence the condition of our own epigenomes and also prevent most genetic mutations from occurring. For example vitamin C is very efficient at balancing the methylation patterns.


Modern scientists are now realizing the true reasons for successful cellular differentiation and unsuccessful cellular differentiation. Hopefully this discovery helps them understand that variation we can observe in nature is also based on epigenetic factors.

These clever mechanisms point to Design and Creation. Don't get misled.


Signs of human chromosome loss

Mutations are leading to heavy loss of biological information

• A 1984 report describes a family with 3 adult siblings who had 44 chromosomes, #s 13 and 14 combined.
• A 1988 report tells of 3 distantly-related families in Finland, also involving #s 13 and 14, whose Rob chromosome passed in carriers through at least 9 generations, appearing in at least one homozygote.
• A 1989 paper describes a Rob between #s 14 and 21 in a homozygote whose carrier parents were related.
Trickling into the headlines was a case report from 2013 of a 25-year-old healthy Chinese man who has 44 chromosomes because each 14 joins a 15 – a combo not seen before.

"In a recent article, a doctor in China has identified a man who has 44 chromosomes instead of the usual 46. Except for his different number of chromosomes, this man is perfectly normal in every measurable way."

My comment: Genetic mutations are caused by aberrant and disrupted methylation patterns due to poor nutrition, toxins, smoking, alcohol, lack of exercise etc. SNPs are genetic errors that are not allowed to end up into transcription machinery. That's why cellular mechanisms hide and silence those erroneous genes by methylating histones. Dense areas of tightly packaged areas of chromatin consume the energy and that's why the cell tries to get rid of them. This can happen during both mitosis and meiosis, although the meiotic chromosomal recombination procedure is a very complex phenomenon. The final result can be observed as smaller or lost chromosomes. This happens rapidly all over nature, for example:


"On Madeira, one species may have evolved into six in the space of just 500 years.
Britton-Davidian, an evolutionary biologist at Université Montpellier II in Montpellier, France, showed that populations of Maderian mice have between 22 and 30 chromosomes, even though their ancestors, who first arrived with the Portugese in the 15th century, had 40."

It's very likely that the number of human chromosomes has been much higher 500 years ago. That's why claims about human/chimp chromosome fusion are false science.

Mutations lead to a chromosome loss during individual's lifetime, this is a scientific fact:


We can only observe loss of information in nature. That's why the evolutionary theory is the biggest lie ever. Don't get misled.


Three basic tenets of the Evolutionary theory refuted by a single study

In addition to mutations in genes, aberrant enhancer element activity at non-coding regions of the genome is a key driver of tumorigenesis


Excerpt from abstract: "In addition to mutations in genes, aberrant enhancer element activity at non-coding regions of the genome is a key driver of tumorigenesis. Here, we perform epigenomic enhancer profiling of a cohort of more than forty genetically diverse human colorectal cancer (CRC) specimens. Using normal colonic crypt epithelium as a comparator, we identify enhancers with recurrently gained or lost activity across CRC specimens. Of the enhancers highly recurrently activated in CRC, most are constituents of super enhancers, are occupied by AP-1 and cohesin complex members, and originate from primed chromatin. Many activate known oncogenes, and CRC growth can be mitigated through pharmacologic inhibition or genome editing of these loci. Nearly half of all GWAS CRC risk loci co-localize to recurrently activated enhancers. These findings indicate that the CRC epigenome is defined by highly recurrent epigenetic alterations at enhancers which activate a common, aberrant transcriptional programme critical for CRC growth and survival."

My comment: This study just shot down three basic pseudoscientific claims of the theory of evolution: We've been taught that random mutations and natural selection are key drivers of evolution and that at least 97% of our DNA is junk.

However, modern science has found that:

1. Mutations will not lead to evolution because they are genetic errors. There are 200,000 disease-causing genetic mutations in the human DNA. The so called natural selection is not able to filter them out.

2. Mutations are not random changes. They are caused by poor nutrition, smoking, alcohol, stress, toxins, radiation, lack of exercise etc. Mutations are results of our lifestyles. Variation in nature is caused by epigenetic factors.


3. We shouldn't use the term 'junk-dna' anymore. Non-coding regions of the genome are crucial regulatory areas for gene expression, cellular backup mechanisms and survival strategies for our heart, brain and other important organs.

There are no mechanisms for evolution. We've been created. Don't get misled.

Cells are guiding each other

Why cloning using a DNA sample will not be successful? Why genetically identical twins might have different colors of eys, hair and skin?


Excerpt: "Stem cells from an adult mouse have been used to grow a structure resembling a mouse embryo in vitro for the first time.

The ability to study the early stages of embryo development outside the womb may one day help explain why a significant number of human pregnancies fail. This breakthrough in developmental research originated from the same team at University of Cambridge which recently developed a technique that allows human embryos to develop in the lab up to the legal limit of 14 days in the UK.

'We are very optimistic that this will allow us to study key events of this critical stage of human development without actually having to work on (IVF) embryos,' said lead researcher Professor Magdalena Zernicka-Goetz of the University of Cambridge.

The development of a fertilised egg into a fetus is a complex and poorly understood process of self-assembly and intricate cell-to-cell interaction. In a few days a small ball of undifferentiated cells develops into a blastocyst consisting of three different types of embryonic stem cell. Previous attempts to grow embryos using only one kind of stem cell proved unsuccessful because the cells would not assemble into their correct positions.

The researchers placed both placental and embryonic stem cells into a three-dimensional scaffold and discovered that within 96 hours the cells had begun to communicate, forming two distinct clusters of cells at each end and a cavity in the middle.

'We knew that interactions between the different types of stem cell are important for development, but the striking thing that our new work illustrates is that this is a real partnership – these cells truly guide each other,' said Professor Zernicka-Goetz."

My comment: Gene sequences in the embryo's DNA are not sufficient for guiding cellular differentiation. Information for embryonic development is given by exosomes shared from neighbouring cells. Exosomes are carriers for short non-coding RNA molecules which are responsible for epigenetic reprogramming, the procedure when epigenetic markers are established on the genome.

There are thousands of different types of microRNAs and other short RNA molecules in human sperm, for example. They are used for epigenetic reprogramming. Complex traits of an vertebrate organism are based on this mechanism which reprograms the epitranscriptome.

So, having a DNA sample of a Mammoth will not make it possible to clone a Mammoth. We'd need living cells from a Mammoth. The evolutionary story lacks a mechanism for assumed evolution of multicellularity. Information for cellular differentiation is shared from top to down, not from down to top, as evolutionists claim. The whole theory of evolution is upside down when reflected to observations of real life.

Everything points to Intelligent Design and Creation. Don't get lost.


Salt flats are remnants of a mega-flood in Mars

Every salt flat on Earth is located close to a volcano


Excerpt: "A combination of volcanism, tectonics, collapse and subsidence in the Tharsis region led to several massive groundwater releases from Echus Chasma, which subsequently flooded the Kasei Valles region around 3.6–3.4 billion years ago. These ancient mega-floods have left their mark on the features seen today."


Excerpt: "The 18-square-mile chloride salt deposit is similar to Utah's Bonneville Salt Flats, they say."

My comment: It's obvious that the Earth's salt flats are also remnants of a mega-flood. It's not a coincidence that every salt flat or saline lake of the Earth is located close to a volcano, a caldera or a tectonic crossroad.

The origin of salt is under the crust. Other planets and moons have pretty similar structure as the Earth. Look at the Ganymede cross section:

Compare the salt layer of the Ganymede with the Earth's thick salt layers. The erratic salt layers point to a catastrophy.

How does secular science explain the salt flats, like Bonneville in Utah? "The Salt Flats were formed when ancient Lake Bonneville dried up", say scientists. But what a coincidence, an 'ancient' supervolcano is located pretty close to the Utah salt flats. There is also a volcano close to the largest salt flats of the Earth, Salar de Uyuni, Bolivia.

There's a small inactive volcano In Ethiopia called El Sod. Over a hundred meters of salt in that small crater proves that the origin of salt is under the crust.


Salt flats and saline lakes are remnants of a Biblical flood. Don't get misled.