It seems fairly intuitive that evolution can produce many things- below the species-level, novel genotypes and phenotypes, population-level phenomena like polymorphisms, and macro things like novel body plans, suites of behaviors, and more. These are all ontological... it seems like anything that is dynamic (changing/changeable) and heritable is potentially or really a product of evolution.

Whether or not some individual thing can evolve, just ask yourself, is it biological? Does it change over generational time? Are the changes heritable? By these standards, most cancers die with their hosts, so they don't pass the third test. But the tumors that say, Tasmanian devils pass to each other via physical contact seem to persist and reproduce themselves in some real sense, and the mutations they operate by would be subject to natural selection, so those just might be evolving,

Cancer is basically a the result of cells within the body experiencing chance mutations which inactivate a genes that controls the cells' growth, those cells then divide more quickly than other "normal" cells and the mutated DNA is passed on to the daughter cells. It spins out of control and the result is a tumor. So, the basic processes of the evolution on a population level and those of cell lineages are the same (variation, inheritance, selection). As to whether it could be considered a species, there are a few scientists that argue that cancers are seperate species (however, one of the main proponents of this hypothesis is a guy called Duesberg who doesn't believe that AIDS is caused by HIV - so be careful about what he says if you ask me). However most scientists seem to disagree that it is a species mainly for the following reason: how would cancer spread and reproduce outside of its host? If the host dies, so does the cancer and it has no means of spreading to a new host. It's like saying that a cell infected with a virus would automatically become a new species.

As an aside, there are 3 examples (I know of) of cancers that survive outside their initial host and can be passed on to other individuals: Tasmanian Devil facial tumors, Canine Venerial tumors, Syrian Hamster sarcoma. The Syrian Hamster sarcoma even survives in a third party vector (a mosquito) to be passed on from one hamster to another. I would still say that it would not constitute its own species, but the line becomes more blurry here. However for the vast majority of cancers I think it's pretty clear that conventional definitions of species are not met.

I hope this helped, let me know if anything I wrote is unclear!

The world evolution is used incorrectly in the sense you are using it.

1) cancer and genetic parasites are not things that are alive. The characteristics of living beings state that they should be able to reproduce and produce energy on their own, which cancers and genetic parasites cannot do.

2) evolution results in change in the allelic frequencies of a population. Whether that change separates them from the original species that they were (by any method of speciation as hybrid inviability, selection against immigrants, physical barriers...) is a different question on it's own, but those terms are not applicable to species that are not "living". Even in the Darwinian sense of the evolution, it was meant more specifically for sexually mating species, so no cancers and genetic parasites do not fall under these categories and do not operate under the same processes.

Elias Oziolor the concept of evolution doesn't have that restriction. Before the discovery of the viral order Megavirales, the majority of scientifics didn't believe viruses were alive, however anybody refused they evolve.

Joseph the grand majority of the examples shown by you like products of evolution, i think all are changes in certain properties; but there are examples of something bigger (macroevolution?), i mean, we can say, the evolutionary process can produce, by the usual mechanism, new levels, e.g create a genuine multicellular organism starting whith an unicellular organism? (The diachronic question in terms of Samir Okasha and the Major evolutionary transitions)

Fabian Rudin thanks for the inherited cancer examples. I think the concept of species and the conventional notion of evolution, imply the unique product are the species (by modified or change the allelic frequencies of a certain gene of gene's sorts in a population), and doesnt include "rare entites", that doesnt fix into the classical sort of biological diversity.

Other ways, Forterre P (http://www.nature.com/ismej/journal/v7/n2/abs/ismej2012110a.html) argument the real nature of a virus isn't the virion, contrary He thinks the virus and the cell make a new entity, the virocell.

I'm sorry for my english, i hope that you could understand me

Thanks Aimer for your challenge!

Firstly, I think that such question deserves some semiological precisions!

What is a species, since it doesn't have absolute biological sense. What is a product (of evolution)?

The particular case of parasites and cancer is that they evolve in an organism, in contrast of species that evolve in none organismic environment ("open environement"). But absolutely, I think that parasite organisms are a product of evolution as we are.

So the big problem is for cancer cells.

Cancer seems no be viewed as a species, since cells doesn't reproduce, and evolution result mitotic mutation of somatic cell.

However, evolution generally involves meiotic mutation, inter and intra chromosome recombination, and finally zygotic recombination producing an original genotype.

The big difference is that this genotype will be the target of selection (positive or negatively) in open environment. In the case of cancer, no selection act, cells developp until the environment collapse (death of the organim).

As you have just ruled out scientific evidence as inadmissible, and science is the marshalling of all defensible and replicable (i.e. real) evidence, there are no ground left upon which to discuss this topic with you. Sorry

Gamal, your statement = pics or it didn't happen!

So Gamal, God invented the cancer and any other kind of biological individuality.. didn't it?

Why he did that?

http://www.youtube.com/watch?v=gHbYJfwFgOU

I hope they don't let you teach this to anybody!

I think the question here is trying to be precise in a way that simply does not work in science and has no useful meaning in philosophy. Species are not entities. They can be defined in relation to individuals living at the same point in time but not in relation to individuals living at different times on an evolutionary scale - a bit like continents. The products of evolution include the carbon dioxide we breathe out, mammoths, toenails, cancers and viruses. The mediators of evolution probably include any biological packages that contain replicable nucleic acid but may also include prions. Tumours are now transferrable so at least in labs may be part of the story. I really do not think there is any meaning to a question as broad as this. Any answer that is then used as a premise for a new set of arguments is very likely to lead to a nonsense conclusion. To my mind the main problem with philosophy is that it concentrates on generating valid conclusions but often starting with premises taken out of context so that the conclusions are not sound. Validity without soundness is a waste of everybody's time.

I like most the answers. A species is group that can reproduce and move (evolve) through time, be virus, human, plant, or bacteria.

Cancer, however, is cells in a multicellular organism that refuse to differentiate and die off, and they keep growing. Paul Ewald believes most cancers will be found to be viral caused. We already know of 15% of all cancers are viral caused. Ok, there is a vial protein p37 that is conserved in bunch of virus, Pox family, Hepatitis family, AIDS and a bunch I'm leaving out. It up/down (I forget which, have lots journal articles on it) regulates two cellular pathways that affect cellular growth. So... IF this dis-regulation of cellular growth HELPS the virus, then any cancer/s from this dis-regulation would be an "by-product" of viral "predation". Viruses will continue to cause cancers if it helps the virus spread. At first, I thought Paul Ewald, was a "bit" off to say "most" cancers, but after reading too many abstracts of p37 and connections to cancer/virus, I'm thinking he might be right. More research will tell.

Heidi,

The majority of age-related cancers (mostly carcinomas) is not caused by viruses.

There is one important cytogenetic difference between a species and a cancer:

A diploid species is defined by two identical copies of chromosomes (except for the sex chromosomes), whereas the typical carcinoma (=epithelial cancer) is characterized by chromosomal chaos. Species karyotypes are usually stable as hell. Whereas, within an epithelial cancer tissue of one individual, almost every cancer cell has a different karyotype. You find some "marker chromosomes" (=structurally abnormal chromosomes) in most cells, but you also find new structural and numerical chromosome aberrations in almost every cell.

Clearly, a cancerous tumor is no species...based on cytogenetics and karyotype!

In cancer, replicative telomere erosion has been proposed to be the cause of chromosomal instability.

I don't think that cancer "evolves", it might just be a differentiation block of tissue stem cells. Some have speculated that cancer represents the continuous and unregulated state of tissue repair (Beachy PA, Karhadkar SS, Berman DM. Mending and malignancy. Nature 2004;431:402).

Accordingly, it has nothing to do with evolution.

Nope,  I think you misunderstood me, virus do not put in genes via cancer not in our species now.   However, the quick sharing of genes, ages ago did. I don't think we'd be such complex multicellular species without all the sharing, polyploidy, etc. 

I don't think cancers help us evolve at all, that was not my point.  My point was that we are still highly prayed upon via virus and bacteria, and selection wise, if they (virus) cause cancer/s after the "fact", via fouling up our pathways during infections it doesn't hurt their selection.  Our lifespan can be affected by cancer, hence our support of offspring.

As far as the p37, I truly believe (and wrote note last year, and earlier) its going to be implicated in a lot of cancers.  It already is.  But I think Ewald and others will be vindicated as we keep seeing many more cancers that have a strong vial causation, even if it is only a component.  Obviously I immune system and great p52 working, then p37 becomes moot.   But we age, and we get weaker and then those virus can have a heyday.

In  I bugged our lab to look at compounds that might affect p37.

"October 22, 2014 

XXXXX,

There are about 158,000 deaths from lung cancer in 2014; it is the largest killer of all cancers.  This cancer is mostly attributed to smoking.   I know I “bugged” everybody about that p37 virus when I first came here.  Also BTK drugs are effective in B-cell lymphoma, all stuff we’ve discussed at lab meeting.

Obviously smoking, radon, and asbestos are Major “causes” cause of lung cancer.  However, people don’t get lung cancer until about 20+ years of smoking (some less).  Why?  Why not sooner?  Why the time-lag??   As you age your immune function decrease, and your inflammatory responses can increase.  Testosterone protects men from many allergy responses.   Tabaco has a gallizion (38+ if remember rightly) mutagenic compounds.   Ok, if you’re a smoker, your immune system’s decreasing, inflammatory responses increasing, and you get a bad flue or pneumonia.  The p37 disrupts cellular growth with all those carcinogens.  Viola lung cancer!!   We know this p-37 is very bad in prostate cancer, breast, and other cancers too!

The p37 from mycoplasma hyorhinis promotes cancer cell invasiveness and metastasis through activation of MMP-2 and followed by phosphorylation of EGFR.  Gong et al.  But p37 is found in many virus, pox family, hepatitis, HIV, and Influenza virus.   In fact, it is highly conserved in viruses.

 I’m beginning to think that the virus p37 in conjunction with “other” factors can be a MAJOR causative agent in many cancers, not just a predictor of bad outcome." 

•Gong et al. identified a pathway by which p37 is activated:

–p37 from mycoplasma hyorhinis promotes cancer cell invasiveness and metastasis through activation of MMP-2 and followed by phosphorylation of EGFR.

•Tsai et al. published that Ras/PI3K/ERK pathway stabilizes c-Myc:

–Activation of Ras/PI3K/ERK pathway induces c-Myc stabilization to upregulate argininosuccinatesynthetase, leading to arginine deiminase resistance in melanoma cells

p37 induces tumor invasiveness

Catherine M. Ketcham,1 Satoshi Anai,3 Robbie Reutzel,1 Shijie Sheng,4 Sheldon M. Schuster,1 Ryan B. Brenes,1 Mavis Agbandje-McKenna,1 Robert McKenna,1 Charles J. Rosser,3 and Susan K. Boehlein1,2

1Department of Biochemistry and Molecular Biology and 2Shands Cancer Center, College of Medicine, University of Florida, Gainesville, Florida; 3Division of Urology, College of Medicine, University of Florida, Jacksonville, Florida; and 4Department of Pathology, Wayne State University School of Medicine, Detroit, Michigan

Abstract Previous studies have shown a statistically significant correlation between human carcinomas and monoclonal antibody detection of a Mycoplasma hyorhinis–encoded protein known as p37. A potential mechanism of p37 is that it might promote invasion and metastasis. Recombinant p37 enhanced the invasiveness of two prostate carcinoma and two melanoma cell lines in a dosedependent manner in vitro, but did not have a significant effect on tumor cell growth. Furthermore, the increased binding to cell surfaces and the enhanced invasive potential of cancer cells from exposure to p37 could be completely reversed by preincubation of the cancer cells with an anti-p37 monoclonal antibody. Sequence comparisons, followed by three-dimensional molecular modeling, revealed a region of similarity between p37 and influenza hemagglutinin A, a sialic acid–binding protein that plays a critical role in viral entry. Binding of p37 to prostate carcinoma cells was found to be at least partially sialic acid dependent because neuraminidase treatment decreased this binding. Taken together, these observations suggest that M. hyorhinis can infect humans and may facilitate tumor invasiveness via p37. These results further suggest that p37 may be a molecular target for cancer therapy. [Mol Cancer Ther 2005;4(7):1031–8]

A New Player in Oncogenesis: AUF1/hnRNPD Overexpression Leads to Tumorigenesis in Transgenic Mice1

Agne`s Gouble, Sole`ne Grazide, Fabienne Meggetto, Pascale Mercier, Georges Delsol, and Dominique Morello2

Centre de Biologie du De´veloppement, CNRS-UMR5547, Universite´ Paul Sabatier, Baˆtiment 4R3, 31062 Toulouse, Cedex 4 [A. G., D. M.]; Institut Claudius Re´gaud, INSERM E9910, 20 rue du Pont Saint Pierre, 31052 Toulouse [S. G.]; UPR CNRS 2163 and Service d’Anatomie et de Cytologie Pathologiques, Hoˆpital Purpan, 31059 Toulouse, Cedex [F. M., G. D.]; Institut de Pharmacologie et de Biologie Structurale, UMR 5089, 31062 Toulouse, Cedex [P. M.], France

ABSTRACT

AUF1/heterogeneous nuclear ribonucleoprotein D (hnRNPD) binds to adenylate uridylate-rich elements contained in the 3 untranslated region of many short-lived mRNAs. This binding has been shown in vitro to control the stability of adenylate uridylate-rich elementcontaining mRNAs, including mRNAs encoding proto-oncogenes, cytokines, or other signaling molecules. However, no studies have yet been undertaken to identify the mRNAs subject to AUF1-mediated regulation in vivo. The purpose of our study was to investigate the biological functions of AUF1. Thus, we derived transgenic (Tg) mice, which overexpress one isoform of AUF1, the p37AUF1. Mice of the three Tg lines analyzed exhibit altered levels of expression of several target mRNAs, such as c-myc, c-jun, c-fos, granulocyte macrophage colonystimulating factor, and tumor necrosis factor . The Tg line with the highest amount of Tg p37AUF1 protein developed sarcomas. The tumors strongly expressed AUF1 Tg protein and Cyclin D1. Taken together, our data show that: (a) AUF1 is a key regulatory factor of gene expression in vivo; and (b) the deregulation of this heterogeneous nuclear ribonucleoprotein leads to tumorigenesis.