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Do you know how far genetic research has come?

Skeptic Ginger

Nasty Woman
Joined
Feb 14, 2005
Messages
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I'm discussing once again the topic of evolution and I have to wonder sometimes if a person I am talking to really knows how advanced genetic research has come? These are skeptics who are fully convinced and knowledgeable about evolution theory, I'm not talking about people who are poorly informed about it. But I'm never sure if they really know that what is currently going on in genetic research is mind boggling.

I know there are several board members whose field this is. I am a lowly infectious disease practitioner. I don't have that background. But I read enough microbiology to know this field is incredibly advanced. The genetic coding of proteins and how they fold, all sorts of mechanisms for turning genes on and off, genomes galore decoded, genes transferred from rabbits to fruit flies and still function properly, the molecular pathways that that run from one species to another, not just how their skeletons morphed... all these things and tons more are discussed in the literature which I come across all the time.

Yet I'm not sure all the skeptics I discuss evolution with are completely aware of how advanced this research is.

So I put together a random sample of current research from university professors' pages to genetics journals to news stories just to give people a flavor of how much we really know about the genetic mechanisms of evolution work. We know a lot! There is no order here, just stuff that looked relevant to genetic science and evolution theory which came up in a Google search for, "extent genetic research evolution". The point is just to check, were you aware they were looking at genetics in this much detail? This is only a teeny tiny fraction of the research which is currently going on.

Please post any additions you come across that boggled your mind as well that we were looking at genetics at such an incredible level of understanding.



john hawks weblog - paleoanthropology, genetics, and evolution
The cost of determining a person’s complete genetic blueprint is about to plummet again — to $5,000.

That is the price that a start-up company called Complete Genomics says it will start charging next year for determining the sequence of the genetic code that makes up the DNA in one set of human chromosomes. The company is set to announce its plans on Monday. ...

[T]he cost of DNA sequencing has dropped by a factor of 10 every year for the last four years, a faster rate of decline than even for computers, Dr. [George] Church said.

The genetic basis of modularity in the development and evolution of the vertebrate dentition.
The construction of organisms from units that develop under semi-autonomous genetic control (modules) has been proposed to be an important component of their ability to undergo adaptive phenotypic evolution. The organization of the vertebrate dentition as a system of repeated parts provides an opportunity to study the extent to which phenotypic modules, identified by their evolutionary independence from other such units, are related to modularity in the genetic control of development.

Genetic Variation: We're More Different Than We Thought
This discovery of the extent of genetic variation, by Howard Hughes Medical Institute (HHMI) international research scholar Stephen W. Scherer, and colleagues, is expected to change the way researchers think about genetic diseases and human evolution....

...To get a better picture of exactly how important this type of variation is for human evolution and disease, Scherer's team compared DNA from 270 people with Asian, African, or European ancestry that had been compiled in the HapMap collection and previously used to map the single nucleotide changes in the human genome. Scherer's team mapped the number of duplicated or deleted genes, which they call copy number variations (CNVs). They reported their findings in the November 23, 2006, issue of the journal Nature.

Scherer, a geneticist at the Hospital for Sick Children and the University of Toronto, and colleagues searched for CNVs using microarray-based genome scanning techniques capable of finding changes at least 1,000 bases (nucleotides) long. A base, or nucleotide, is the fundamental building block of DNA. They found an average of 70 CNVs averaging 250,000 nucleotides in size in each DNA sample. In all, the group identified 1,447 different CNVs that collectively covered about 12 percent of the human genome and six to 19 percent of any given chromosome--far more widespread than previously thought.

Genetic Variants & Evolution
Genetic Variants & Evolution...

...Wray sees the MMP3 story as an important example of the power of rapid evolutionary change. Traditionally, important alleles are thought to change very slowly. However, Wray points out that when the environment changes rapidly, organisms with genes that can also evolve rapidly may have an advantage. The rapid rise of the European MMP3 allele suggests that that may have been the case 20,000 years ago.

Archaeal Genomics
1- What are the mechanisms for the repair of DNA lesions in Archaea?

We use a combination of genomic and genetic methods to identify proteins involved in the repair of DNA double-strand breaks and oxidative DNA damage in the Archaea and to elucidate the regulatory networks underlying the stress response to DNA damage.

2- What is the extent of genetic diversity in natural microbial populations and what generates and maintains that diversity?

We use environmental genomics and molecular tools to characterize the genotypic diversity of natural populations from extreme environments.

Evolution and multilevel optimization of the genetic code
The discovery of the genetic code was one of the most important advances of modern biology. But there is more to a DNA code than protein sequence; DNA carries signals for splicing, localization, folding, and regulation that are often embedded within the protein-coding sequence. In this issue, Itzkovitz and Alon show that the specific 64-to-20 mapping found in the genetic code may have been optimized for permitting protein-coding regions to carry this extra information and suggest that this property may have evolved as a side benefit of selection to minimize the negative effects of frameshift errors.

The mitochondrial genome sequence of the Tasmanian tiger (Thylacinus cynocephalus)
We report the first two complete mitochondrial genome sequences of the thylacine (Thylacinus cynocephalus), or so-called Tasmanian tiger, extinct since 1936. The thylacine's phylogenetic position within australidelphian marsupials has long been debated, and here we provide strong support for the thylacine's basal position in Dasyuromorphia, aided by mitochondrial genome sequence that we generated from the extant numbat (Myrmecobius fasciatus). Surprisingly, both of our thylacine sequences differ by 11%–15% from putative thylacine mitochondrial genes in GenBank, with one of our samples originating from a direct offspring of the previously sequenced individual.

Sequencing human–gibbon breakpoints of synteny reveals mosaic new insertions at rearrangement sites
The gibbon genome exhibits extensive karyotypic diversity with an increased rate of chromosomal rearrangements during evolution. In an effort to understand the mechanistic origin and implications of these rearrangement events, we sequenced 24 synteny breakpoint regions in the white-cheeked gibbon (Nomascus leucogenys, NLE) in the form of high-quality BAC insert sequences (4.2 Mbp). While there is a significant deficit of breakpoints in genes, we identified seven human gene structures involved in signaling pathways (DEPDC4, GNG10), phospholipid metabolism (ENPP5, PLSCR2), β-oxidation (ECH1), cellular structure and transport (HEATR4), and transcription (ZNF461), that have been disrupted in the NLE gibbon lineage. Notably, only three of these genes show the expected evolutionary signatures of pseudogenization. Sequence analysis of the breakpoints suggested both nonclassical nonhomologous end-joining (NHEJ) and replication-based mechanisms of rearrangement. A substantial number (11/24) of human–NLE gibbon breakpoints showed new insertions of gibbon-specific repeats and mosaic structures formed from disparate sequences including segmental duplications, LINE, SINE, and LTR elements. Analysis of these sites provides a model for a replication-dependent repair mechanism for double-strand breaks (DSBs) at rearrangement sites and insights into the structure and formation of primate segmental duplications at sites of genomic rearrangements during evolution.

Whole population, genome-wide mapping of hidden relatedness
We present GERMLINE, a robust algorithm for identifying segmental sharing indicative of recent common ancestry between pairs of individuals. Unlike methods with comparable objectives, GERMLINE scales linearly with the number of samples, enabling analysis of whole-genome data in large cohorts. Our approach is based on a dictionary of haplotypes that is used to efficiently discover short exact matches between individuals. We then expand these matches using dynamic programming to identify long, nearly identical segmental sharing that is indicative of relatedness. We use GERMLINE to comprehensively survey hidden relatedness both in the HapMap as well as in a densely typed island population of 3000 individuals. We verify that GERMLINE is in concordance with other methods when they can process the data, and also facilitates analysis of larger scale studies.

Is Genetic Evolution Predictable?
Ever since the integration of Mendelian genetics into evolutionary biology in the early 20th century, evolutionary geneticists have for the most part treated genes and mutations as generic entities. However, recent observations indicate that all genes are not equal in the eyes of evolution. Evolutionarily relevant mutations tend to accumulate in hotspot genes and at specific positions within genes. Genetic evolution is constrained by gene function, the structure of genetic networks, and population biology. The genetic basis of evolution may be predictable to some extent, and further understanding of this predictability requires incorporation of the specific functions and characteristics of genes into evolutionary theory. 10.1126/science.1158997

University of Cambridge; School of Biological Sciences; Department of Zoology; Butterfly Genetics Group
Research Themes - Introduction

What are the origins of biodiversity? There is much we still don’t understand about the evolution of new biological species and races. Our research focuses on new world tropical butterflies as a model to understand evolution at the population and species level.

In particular, we are interested in the predictability of evolution - to what extent do different populations follow the same evolutionary trajectories. Convergent evolution, such as mimicry, offers the opportunity to as whether the same genes, or the same kinds of genetic changes are involved repeatedly. Current topics of argument in evolutionary biology include the importance of cis-regulatory versus structural protein evolution in generating novel forms. The huge diversity of divergent populations and species in Heliconius offers a wealth of opportunities to answer these questions.

The Institute of Evolution at the University of Haifa has strong research and teaching programs.
The understanding of evolutionary biology today is founded on Darwinian Evolutionary Theory and the dramatic discoveries in the 20th century in the cosmological, geological, and biological sciences.
The latter comprise insights into the genome, molecular biology, chromosomal, cellular, sex, recombination, organismal biology, and biotic communities, including the morphological, physiological, and behavioral sociobiological and perspectives, under spatiotemporally environmental diversity, stress, and change.

The discoveries in the 20th century, across the physical and biological sciences, shed new light on the origins and evolution of life and humans, behavior, and culture.
This is especially true in this age of deciphering genetic codes of entire prokaryotic (viruses, bacteria, chloroplasts, and mitochondria) and eukaryotic (yeast, worms, flies, rice, mice, and humans) genomes. Evolutionary theory outlines the processes creating genetic diversity (mutation and recombination) and maintaining it through the process of natural selection at the molecular, chromosomal, and cellular levels, and its interface with the organismal phenome and coenotic evolution level (morphology, physiology, and behavior).
Moreover, evolutionary biology constitutes the theoretical and applied basis for future development of agricultural, medical, and industrial biotechnology.

Comparative sequence analysis of primate subtelomeres originating from a chromosome fission event
Subtelomeres are concentrations of interchromosomal segmental duplications capped by telomeric repeats at the ends of chromosomes. The nature of the segments shared by different sets of human subtelomeres reflects their high rate of recent interchromosomal exchange. Here, we characterize the rearrangements incurred by the 15q subtelomere after it arose from a chromosome fission event in the common ancestor of great apes. We used FISH, sequencing of genomic clones, and PCR to map the breakpoint of this fission and track the fate of flanking sequence in human, chimpanzee, gorilla, orangutan, and macaque genomes. The ancestral locus, a cluster of olfactory receptor (OR) genes, lies internally on macaque chromosome 7. Sequence originating from this fission site is split between the terminus of 15q and the pericentromere of 14q in the great apes.

Principles of transcriptional regulation and evolution of the metabolic system in E. coli
Organisms must adapt to make optimal use of the metabolic system in response to environmental changes. In the long-term, this involves evolution of the genomic repertoire of enzymes; in the short-term, transcriptional control ensures that appropriate enzymes are expressed in response to transitory extracellular conditions....

...Here, we integrate genome-scale data to investigate the evolutionary trends and transcriptional control of metabolism in Escherichia coli K12. Globally, the regulatory system is organized in a clear hierarchy of general and specific transcription factors (TFs) that control differing ranges of metabolic functions. Further, catabolic, anabolic, and central metabolic pathways are targeted by distinct combinations of these TFs. Locally, enzymes catalyzing sequential reactions in a metabolic pathway are co-regulated by the same TFs. Regulation is more complex at junctions: General TFs control the overall activity of all connecting reactions, whereas specific TFs control individual enzymes. Divergent junctions play a special role in delineating metabolic pathways and decouple the regulation of incoming and outgoing reactions. We find little evidence for differential usage of isozymes, which are generally co-expressed in similar conditions, and thus are likely to reinforce the metabolic system through redundancy. Finally, we show that enzymes controlled by the same TFs have a strong tendency to co-evolve, suggesting a significant constraint to maintain similar regulatory regimes during evolution. Catabolic, anabolic, and central energy pathways evolve differently, emphasizing the role of the environment in shaping the metabolic system. Many of the observations also occur in yeast, and our findings may apply across large evolutionary distances.
 
Pseud0-intelligent layman level here. Always happy to learn more. Thanks for the list.
 
I'm discussing once again the topic of evolution and I have to wonder sometimes if a person I am talking to really knows how advanced genetic research has come? These are skeptics who are fully convinced and knowledgeable about evolution theory, I'm not talking about people who are poorly informed about it. But I'm never sure if they really know that what is currently going on in genetic research is mind boggling.

I know there are several board members whose field this is. I am a lowly infectious disease practitioner. I don't have that background. But I read enough microbiology to know this field is incredibly advanced. The genetic coding of proteins and how they fold, all sorts of mechanisms for turning genes on and off, genomes galore decoded, genes transferred from rabbits to fruit flies and still function properly, the molecular pathways that that run from one species to another, not just how their skeletons morphed... all these things and tons more are discussed in the literature which I come across all the time.

Yet I'm not sure all the skeptics I discuss evolution with are completely aware of how advanced this research is.

So I put together a random sample of current research from university professors' pages to genetics journals to news stories just to give people a flavor of how much we really know about the genetic mechanisms of evolution work. We know a lot! There is no order here, just stuff that looked relevant to genetic science and evolution theory which came up in a Google search for, "extent genetic research evolution". The point is just to check, were you aware they were looking at genetics in this much detail? This is only a teeny tiny fraction of the research which is currently going on.

Please post any additions you come across that boggled your mind as well that we were looking at genetics at such an incredible level of understanding.

First of all, thank you for these links.

Secondly, being one of those people whose knowledge in current genetics you have come to doubt recently, I will admit that much of the exact details of what you list here was previously unknown to me (1), though in at least some cases, I have heard of similar things before. I knew, for example, that the molecular lab I work in has been able to shave off quite a bit of the sequencing costs by sending all our material to Korea instead of sequencing it locally. We don't do whole-genome sequencing in my lab, though (but that would be cool, and extremely useful!). Similarly, sequencing of extinct organisms and "accurate" placement of these in the tree of life is something I am aware of from an excellent article about Moas I read a while ago.

I work with systematics, both molecular and morphological, and as such am biased towards these subjects when it comes to what journals I browse, what articles I read, and what symposia and conferences I attend (not nearly enough of these, sadly... I blame the economy^^). Nevertheless, I spread out my interest over quite a large range of organisms.

Having studied Clitellates for my masters, I still follow that research, and having one of the leading experts in the world in Clitellate systematics on the same floor certainly helps doing that. I have developed quite a large collection of articles on evolution in asexual and/or polyploid organisms, and the implications these phenomena have both for the organisms involved, and for what sort of data we can get, and how we interpret it (2). I work with lice on birds myself, so I tend to follow research in both groups, as well as other bird parasite and other parasite groups, as it is immediately applicable to my own research. I further have a large amount of interest in several groups this forum has lead me to, such as lizards, frogs, and others, where I have been forced to read up on something to be able to participate in some discussion, and then kept the interest up. As our department is much focused on marine invertebrates, I tend to get a lot of nemertean, bryozoan, polychaete, and general high-level systematics as well. Lastly, I am very interested in the ongoing discussions on taxonomic theory, tree-building theory, and so on, as this is directly connected to my line of work.

The reason for this listing is perhaps not obvious. As we both know, there are too many articles out there for anyone to be able to be on top of everything. I would even go so far as to say that the current "politics" of how people write articles means there are too many articles out there, as it often seems to me that the amount of data used to justify an article has decreased over time. Through spreading my interest across the animal kingdom (and a bit to that of plants), I would say I get indirectly exposed to much of the new advances in cell biology as well. Even if I have never heard of something before, the extended network consisting of all the people whose articles I read may have, and if it is relevant enough, they are likely to expose me to this knowledge through their articles as well.

The result is, of course, the acquisition of a general familiarity with many new advances, even if I have no detailed knowledge of it (the exception being the areas asexuality and polyploidy, where I tend to read more exclusively cell biological and technical articles).

Am I unqualified for discussing these more basic topic due to this lack of time and, frankly, interest in cell biology? In a specific discussion on the possibility of something given the recent advances and data on cell biology, the answer is undoubtedly yes, though I am far from reluctant to educate myself if there is a need. In the present discussion (3), I would say no. The discussion we've had that has resulted in this new topic is general enough for anyone, be they scientists or laymen with an interest and some basic knowledge of scientific theory and the theory of evolution, can participate, albeit perhaps not with equal rigour in their arguments. In the present discussion, your question regarding how well acquainted people are with current developments in cell biology is unfounded.

While I of course applaud and thank you for these links, and the information they contain, I would much prefer if you went back to the other thread and made an argument for your case. I am as liable to have overlooked something fundamental flaw in my reasoning as anyone, and am willing to change my mind if you can just present arguments for your viewpoint.

---
(1) I have not yet followed any of your links, as it's weekend, and I'm planning to watch anime all evening^^.
(2) This is, I am almost ashamed to admit, the only time that my interest spills over to botany...
(3) That is, with the thread in which this discussion originated in mind.
 
(1) The links weren't meant to be followed unless something looked particularly interesting to someone. They were simply meant as examples of the level of detail genetic research had reached demonstrating evolution theory.
(2) Which for example, was an incredible discovery via genetic research, we are more closely related to plants than was thought when we only had fossils to go by.
(3) I haven't abandoned the other thread. I put this here just to give it a wider audience. I really intended this for everyone. I do sincerely believe the incredible advances in genetics are not well known to many, including skeptics and science folks from other fields.

Of course we cannot all be well informed on every topic. I like to consider myself a person who knows a lot about a little, that would be my area of practice in infectious disease; and, a little about a lot. I've always been interested in investigating a wide variety of topics and in exploring the Earth. Today I went off on a side track reading about the money supply. Wow, that was a bunch of stuff I wasn't fully aware of.

There is so much information to be had out there which interests me, I have to tear myself away from the computer. So later tonight I will go back to the other thread for more punishment from you and US.
 
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(1) The links weren't meant to be followed unless something looked particularly interesting to someone.

For a few hours that were more entertaining and interesting than any movie I've seen recently, I thank you.
 
(1) The links weren't meant to be followed unless something looked particularly interesting to someone. They were simply meant as examples of the level of detail genetic research had reached demonstrating evolution theory.

Well, several things were, indeed, not only very interesting, but also somewhat relevant to my own research. I do intend to follow up on some of them when I get back to work next week.

(3) I haven't abandoned the other thread. I put this here just to give it a wider audience. I really intended this for everyone. I do sincerely believe the incredible advances in genetics are not well known to many, including skeptics and science folks from other fields.

I gathered as much from your OP, and from the other thread. Nevertheless, whether you intended it or not, the post had a tinge of being directed towards me and US more particularly than people here in general. It appears US had the same feeling.

There is so much information to be had out there which interests me, I have to tear myself away from the computer. So later tonight I will go back to the other thread for more punishment from you and US.

If you see it as "punishment" that I try to actually engage you in the discussion by asking you for the arguments supporting your position, instead of just continuing to state your position, then you have either misunderstood the word "punishment", or have a lower threshold for what you perceive as "punishment" than most people I know.
 
Kotatsu --

I think you've been looking for a way to feel "directed towards" if you took the OP in this thread as targeting anyone. I certainly didn't, and I was (until the weekend started, anyway) following the "what would disprove evolution" thread. (You had great stuff in there, btw. Thanks.)

Just my thoughts, FWIW, Miss Kitt

PS Thanks OP for the linkies. And as an infectious disease practitioner, what do you think should--or can--be done with the mess in Zimbabwe? If interested, we can start a new thread. I just think you have the relevent background for that issue.
 
... It appears US had the same feeling....
I tired to avoid that but there was no good way to word the title which left it open to interpreting the thread either way.

Truth be known, I consider both you and US to be intelligent and knowledgeable and didn't want to make a big deal of this because you could have been in a genetics field for all I knew. And since I am not, I might have looked really stupid.

...If you see it as "punishment" that I try to actually engage you in the discussion by asking you for the arguments supporting your position, instead of just continuing to state your position, then you have either misunderstood the word "punishment", or have a lower threshold for what you perceive as "punishment" than most people I know.
Punishment is recognizing you have an underlying premise that is the basis of a disagreement of opinion while the other party continues to argue the overlying facts. I tried to point that out when sol invictus articulated it better than I had been, but it didn't seem to register. When you said I was repeating myself, it's because you were still missing the differing underlying premises.
 
I think you've been looking for a way to feel "directed towards" if you took the OP in this thread as targeting anyone.

I mean "directed towards" as in "asking for comments particularly from". I understand it could be interpreted as something more victimising, but that was not my intention.

Truth be known, I consider both you and US to be intelligent and knowledgeable and didn't want to make a big deal of this because you could have been in a genetics field for all I knew. And since I am not, I might have looked really stupid.

I have a recurring problem, pointed out at several places by all kinds of people, that not only am I much to verbose, but I also tend to adopt a veneer of what has been described as "arrogant formality", "hostile impersonality" or, more recently, "the snobbery of an early-20th century academic lecturing to a layman" (1), which, perhaps, is more apparent when I write articles and so on. This has in many cases led people to believe that I am actually angry of the person I am talking with, which is very rarely the case. It seems to happen when I write in Swedish as well, and I never notice it myself, nor does it seem possible for me to change it. So if I have given this impression, I apologise; it is unintentional, and would never happen if we were talking face to face.

Punishment is recognizing you have an underlying premise that is the basis of a disagreement of opinion while the other party continues to argue the overlying facts. I tried to point that out when sol invictus articulated it better than I had been, but it didn't seem to register. When you said I was repeating myself, it's because you were still missing the differing underlying premises.

Having reread Sol Invictus' post, I believe I might understand your position a bit better, but I do not agree with Sol Invictus' division, nor with his choice of words. I have no time at the moment to elaborate, but will do so later tonight or tomorrow, and thus pull this part of the discussion back to the other thread, so this one can be more focused on what you intended it treat.

---
(1) Somewhat paraphrased.
 
.... This has in many cases led people to believe that I am actually angry of the person I am talking with, which is very rarely the case. It seems to happen when I write in Swedish as well, and I never notice it myself, nor does it seem possible for me to change it. So if I have given this impression, I apologise; it is unintentional, and would never happen if we were talking face to face.
Hey, no worries. I get accused of being condescending all the time. From where I'm sitting, I'm just not as concerned about adding the social buffers when I express my opinions as some people are. I admire Linda (fls) for her ability to disagree nicely, but I'm just not going to berate myself for not having been born with that skill. I know I am a nice person. I know I don't dislike anyone just for having another opinion.

Of course, how they express that opinion is another story. But I'm pretty sure except for one comment about my repeating my argument (and hey, so what?) that we've been having a satisfactory debate. Unrepentant Sinner, OTOH, expressed a bit too much anger that I didn't see the world through his tunnel. But I'm sure my lack of social buffering in my posts didn't help matters.

.... Having reread Sol Invictus' post, I believe I might understand your position a bit better, but I do not agree with Sol Invictus' division, nor with his choice of words. I have no time at the moment to elaborate, but will do so later tonight or tomorrow, and thus pull this part of the discussion back to the other thread, so this one can be more focused on what you intended it treat....
When you have time. I posted a bit more trying to get at this underlying issue in the other thread.
 
Kotatsu --

I think you've been looking for a way to feel "directed towards" if you took the OP in this thread as targeting anyone. I certainly didn't, and I was (until the weekend started, anyway) following the "what would disprove evolution" thread. (You had great stuff in there, btw. Thanks.)

Just my thoughts, FWIW, Miss Kitt

PS Thanks OP for the linkies. And as an infectious disease practitioner, what do you think should--or can--be done with the mess in Zimbabwe? If interested, we can start a new thread. I just think you have the relevent background for that issue.
You're welcome. I often find myself declaring, "genetic science is sooo advanced", and I thought it might be helpful to post examples. Not everyone reads materials in every field.

Interesting. I think my son said he had to write a paper on the economic problems in Zimbabwe last weekend for one of his college classes. Are you referring to the cholera epidemic? The really sad thing is a small amount of bleach or iodine, maybe some water filtering where it is particularly turbid, along with a bit of education, and they could prevent almost all those cases.

I started a related thread on the cholera. The incredible gap in world healthcare. Feel free to discuss anything you want about it there.
 
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There was some sort of symposium locally just lately. UCSD?

The newspaper gave some examples of cancer drugs that cost $100,000/year, but only work on 40% of patients. Pharma knows the genes involved, but the insurance companies can't/won't use genetics to decide treatment options. Takes six months to tell if the drug works, so $50,000 wasted, as well as six months of an at risk patients life, before moving to a better treatment.

So far as " the insurance companies can't/won't use genetics to decide treatment options", Is it their image? They don't want to be seen as withholding treatment from a certain class of patient? Or is it some legalities? Is this a case of laws needing to catch up with progress in science? Is PC costing peoples lives, by requiring the wrong treatment, allowing the cancer to further progress?
 
This looks interesting: Scientists remove cancer genes from stem cells.

It sounds like we are on the brink of designer stem cells. That means growing any organ or bone marrow is possible. 'Brink' still means years off for a usable human product, but if we live long enough to see it, it could extend our lives in a way that antibiotics did in the 50s, maybe even doubling people's lives.
 
Thanks for the links Skeptigirl. I'll give them a better look during the weekend. Somewhat goofy of me but I'm always relieved when I encounter a thread discussing genetic research. It's one of the few topics I understand well enough to no be confused by the arguments. Well, most of the time anyway. :)
 
Nice summery, skeptigirl.

I forget how quickly one can fall behind when they are out of the field for a year. I try to keep tabs on the most recent research (although I focus on population genetics rather than the other fields of genetic research), but it's hard when I no longer have access to the bigger journals.

I do recommend taking a look at the PLoS journals for those who are interested. There is some good stuff published there freely viewable. I'm pretty sure pubmed includes searches from there too, whch is handy.
 
This looks interesting: Scientists remove cancer genes from stem cells.

It sounds like we are on the brink of designer stem cells. That means growing any organ or bone marrow is possible. 'Brink' still means years off for a usable human product, but if we live long enough to see it, it could extend our lives in a way that antibiotics did in the 50s, maybe even doubling people's lives.

After digging, I found a better article here.
 
From the article:
the cells, derived from patients with sporadic Parkinson's disease, remained pluripotent and revealed a gene-expression profile that more closely resembled human embryonic stem cells than human iPS cells still carrying the reprogramming factors.

The development is noteworthy because the use of lentiviral vectors, though a very efficient way to infect cells, can cause cellular transformation and tumor formation, said Whitehead postdoc Dirk Hockemeyer. Excising the viral reprogramming factors would reduce the risk of oncogenic transformation.
The terminology alone reveals the level of molecular detail the genetic scientist are working at.
 

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