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Oncogene is a gene which in certain circumstances can transform a cell into a tumour cell.
Everything we have has reason and meaning. Or there was some use in past.
What's the reason for we have oncogenes?
A proto -oncogene is a normal gene that could become an oncogene due to mutations or increased expression. The resultant protein encoded by an oncogene is termed oncoprotein. Proto - oncogenes code for proteins that help to regulate cell growth and differentiation.
So, we actually do not have oncogenes. Instead we have proto-oncogenes. Due to mutation or virus, these are converted into oncogenes.
Since, proto-oncogenes are required for normal cell division and differentiation, they are necessary. Also, these can change to oncogenes any time. So, we always have to live with probability of this conversion.
Hisashi Tatebe , Kazuhiro Shiozaki , in Handbook of Cell Signaling (Second Edition) , 2010
Dephosphorylation of the Cyclin-Dependent Kinase (Cdk)
Cdk is the master regulator driving the eukaryotic cell cycle at critical steps. During cell cycle progression, Cdk is regulated by interaction with cyclin subunits and by the inhibitory tyrosine phosphorylation. In addition, like MAPKs, activation of Cdk requires threonine phosphorylation in the T-loop, which is carried out by the Cdk-activating kinase (CAK). In budding yeast, Ptc2 and Ptc3 PP2Cs efficiently dephosphorylate this phosphorylated threonine in the Cdc28 Cdk both in vivo and in vitro  . In humans, the corresponding threonine residue in Cdk2 and Cdk6 is dephosphorylated by PP2Cα and PP2Cβ2  . Binding of cyclin to Cdk inhibits dephosphorylation by PP2C in both organisms, indicating that PP2C dephosphorylates only monomeric Cdk.
There are different categories of cancer cell, defined according to the cell type from which they originate. 
- , the majority of cancer cells are epithelial in origin, beginning in the membranous tissues that line the surfaces of the body. , originate in the tissues responsible for producing new blood cells, most commonly in the bone marrow. and myeloma, derived from cells of the immune system. , originating in connective tissue, including fat, muscle and bone. , derived from cells of the brain and spinal cord. , originating in the mesothelium the lining of body cavities.
Cancer cells have distinguishing histological features visible under the microscope. The nucleus is often large and irregular, and the cytoplasm may also display abnormalities. 
The shape, size, protein composition, and texture of the nucleus are often altered in malignant cells. The nucleus may acquire grooves, folds or indentations, chromatin may aggregate or disperse, and the nucleolus can become enlarged. In normal cells, the nucleus is often round or solid in shape, but in cancer cells the outline is often irregular. Different combinations of abnormalities are characteristic of different cancer types, to the extent that nuclear appearance can be used as a marker in cancer diagnostics and staging. 
Life cycle of a cancer cell.
Cancer cells are created when the genes responsible for regulating cell division are damaged. Carcinogenesis is caused by mutation and epimutation of the genetic material of normal cells, which upsets the normal balance between proliferation and cell death. This results in uncontrolled cell division in the body. The uncontrolled and often rapid proliferation of cells can lead to benign or malignant tumours (cancer). Benign tumors do not spread to other parts of the body or invade other tissues. Malignant tumors can invade other organs, spread to distant locations (metastasis) and become life-threatening.
More than one mutation is necessary for carcinogenesis. In fact, a series of several mutations to certain classes of genes is usually required before a normal cell will transform into a cancer cell. 
Damage to DNA can be caused by exposure to radiation, chemicals, and other environmental sources, but mutations also accumulate naturally over time through uncorrected errors in DNA transcription, making age another risk factor. Oncoviruses can cause certain types of cancer, and genetics are also known to play a role. 
Stem cell research suggests that excess SP2 protein may turn stem cells into cancer cells.  However, a lack of particular co-stimulated molecules that aid in the way antigens react with lymphocytes can impair the natural killer cells' function, ultimately leading to cancer.  [ failed verification ]
Cells playing roles in the immune system, such as T-cells, are thought to use a dual receptor system when they determine whether or not to kill sick or damaged human cells. If a cell is under stress, turning into tumors, or infected, molecules including MIC-A and MIC-B are produced so that they can attach to the surface of the cell.  These work to help macrophages detect and kill cancer cells. 
Early evidence of human cancer can be interpreted from Egyptian papers (1538 BCE) and mummified remains.  In 2016, a 1.7 million year old osteosarcoma was reported by Edward John Odes (a doctoral student in Anatomical Sciences from Witwatersrand Medical School, South Africa) and colleagues, representing the oldest documented malignant hominin cancer. 
The understanding of cancer was significantly advanced during the Renaissance period and in to the Age of Discovery. Sir Rudolf Virchow, a German biologist and politician, studied microscopic pathology, and linked his observations to illness. He is described as "the founder of cellular pathology".  In 1845, Virchow and John Hughes Bennett independently observed abnormal increase in white blood cells in patients. Virchow correctly identified the condition as blood disease, and named it leukämie in 1847 (later anglicised to leukemia).    In 1857, he was the first to describe a type of tumour called chordoma that originated from the clivus (at the base of the skull).  
Cancer cells have unique features that make them "immortal" according to some researchers. The enzyme telomerase is used to extend the cancer cell's life span. While the telomeres of most cells shorten after each division, eventually causing the cell to die, telomerase extends the cell's telomeres. This is a major reason that cancer cells can accumulate over time, creating tumors.
Scientists have discovered a molecule on the surface of tumors that appears to promote drug resistance—by converting the tumor cells back into a stem cell-like state.
When the tumor cells began to exhibit drug resistance, the cells were simultaneously transforming into a stem cell-like state, which made them impervious to the drugs. It appeared that the treatment itself was driving this transformation by activating a specific molecular pathway. Luckily, several existing drugs, such as Bortezomib for example, can attack this pathway and reverse the cellular transformation, thus ‘re-sensitizing’ the tumor to treatment.   
In February 2019, medical scientists announced that iridium attached to albumin, creating a photosensitized molecule, can penetrate cancer cells and, after being irradiated with light (a process called photodynamic therapy), destroy the cancer cells.  
Apoptosis: why and how does it occur in biology?
The literature on apoptosis has grown tremendously in recent years, and the mechanisms that are involved in this programmed cell death pathway have been enlightened. It is now known that apoptosis takes place starting from early development to adult stage for the homeostasis of multicellular organisms, during disease development and in response to different stimuli in many different systems. In this review, we attempted to summarize the current knowledge on the circumstances and the mechanisms that lead to induction of apoptosis, while going over the molecular details of the modulator and mediators of apoptosis as well as drawing the lines between programmed and non-programmed cell death pathways. The review will particularly focus on Bcl-2 family proteins, the role of different caspases in the process of apoptosis, and their inhibitors as well as the importance of apoptosis during different disease states. Understanding the molecular mechanisms involved in apoptosis better will make a big impact on human diseases, particularly cancer, and its management in the clinics.
Could we cut out cancer genes using CRISPR gene editing?Credit: Samantha Lee/Business Insider
An oncogene is a gene that has the potential to cause cancer. Fusion oncogenes are cancer-causing genes that are made when two separate genes are fused together to make a new gene. Data from The Cancer Genome Atlas has found that fusion oncogenes cause more than 16% of cancers in humans.
Finding a way to stop and fix fusion oncogenes could be an important tool to stop these cancers. Scientists think genome editing may be the answer. But how can scientists edit these fusion oncogenes? They use a laboratory technique involving the CRISPR/Cas9 system.
[An earlier] study used CRISPR to target fusion oncogenes , but it was considered potentially expensive and inefficient to do clinically because the therapy would have to be personalized to each patient. Because of this, they wanted to do it in a way that isn’t patient-specific.
A sequence of misperceptions in biology
The resolution of the controversy about theories of carcinogenesis is not an inconsequential “academic” pursuit but directly impacts glaring inconsistencies that arise when interpreting data generated under the premises of the SMT. More significantly, resolving this controversy will help correct misunderstandings about basic biological phenomena such as the default state of cells and causality among levels of biological organization. In addition, the resolution of this controversy will provide guidance in medically related issues such as cancer diagnosis and treatment .
Adoption of the cell-centered theory of carcinogenesis, i.e., the SMT and its variants, has led to several misconceptions. According to the SMT, somatic DNA mutations in cancer cells induce them to proliferate incessantly this is not supported by evidence given that those cells can either proliferate or be dormant [77,78]. Moreover, they do not proliferate autonomously, as exemplified by their fate in hormone-dependent cancers . The implicit premise that the constitutive (default) state of cells in multicellular organisms is quiescence generated the search, identification, and characterization of putative growth factors  and oncogenes [81–85]. Paradoxically, however, conclusions that those putative growth factors and oncogenes are indeed direct stimulators of cell proliferation have been duly contradicted by evidence and acknowledged even by those who originated this significant misperception [6,80–87]. Given that proliferation is considered the noncontroversial default state of unicellular organisms [54, 88], a switch from proliferation as the default state in unicellular organisms to quiescence in multicellular ones is an evolutionary novelty that should have been noted, highlighted, and explained. Curiously, notwithstanding, the current dominant perception in the field of biology at large that the proliferation of cells in multicellular organisms depends on being directly stimulated by “growth factors” and/or “oncogenes” remains practically unaltered. A clarification of this basic biological principle is highly overdue through a rigorous analysis of the published record. Next, the subsequent adoption of evolutionarily relevant premises that replace the unreliable ones should be implemented (proliferation as the default state of all cells and a search and characterization of inhibitors of cell proliferation), as we have argued previously [6,28,89–91]. Altogether, the unchallenged adoption of the misleading premises of the SMT gave way to the primacy of a strict reductionist approach to the subject of carcinogenesis.
For decades, the management of clinical cancers has been based on the premises of the SMT that, in short, meant to kill the allegedly immortalized, mutated “cancer cells.” This approach ignores evidence that the carcinogenic process is reversible, as repeatedly proven both experimentally [92–95] and clinically [14,16,38,96]. Regardless of these damning conclusions, the SMT and its variants have maintained their hegemony in academic circles, in the hospital ward, in BigPharma, in the specialized and lay media at large, and, equally important, in study sections of funding agencies, in which short- and long-term future trends in cancer research are decided.
Are There Improved Treatment Options for Attacking Cancer Cells Today?
Dr. Baljevic: So over the years, as we learned more and more about cells and what makes them, what drives them, and how their living cycle is controlled, we have also learned about many other genes, many other proteins. And in examples of some cancers, we have learned a limited number of these places or genes really almost control the entire process sometimes. So a good example for something like that is chronic myelogenous leukemia, for example, which has this protein BCR-ABL, that is an abnormal protein that normally doesn't exist in our cells. And with reshuffling of our genes, it is artificially created and then leads to a situation of continuous signal sending and continuous drive for multiplying, for increasing, etc.
So that's how cancer, for example, in that case starts. And we found a way to interrupt that specific protein and it's functioning with what we call molecularly designed or molecularly driven drug. And so that was sort of a poster child of that type of approach for many years. And of course, since then we have advanced in many different ways. And our understanding has increased to a point that we now have many different examples of these so-called molecularly driven cancers and molecularly specific therapies for them. Of course, as you mentioned, the name of the game these days is really tailored, specific therapy for every specific patient.
Andrew Schorr: Dr. Shah, I wonder if you could explain something to me because we patients have been hearing a lot about next generation sequencing. So we've heard a little bit about cancer genes that may be driving cancer. And then also, Dr. Baljevic was just talking about proteins. So could you help differentiate a little bit between oncogenes that have gone awry and proteins.
How ecDNAs Might Support Cancerous Growth
The circular nature of ecDNAs can enable gene interactions that may support the increased transcription of oncogenes, as genetic elements normally found in distant parts of the genome may come together to interact. While insulators in the chromosomal DNA sit at the stem of a loop structure and ensure that regulatory sequences such as enhancers work only on their nearby target genes, the circular shape of ecDNA generates new interactions with additional regulatory sequences that would not normally occur on chromosomal DNA.
Additionally, ecDNAs tend to have a more-open chromatin structure than chromosomes that promotes increased gene expression. DNA is wound around histone cores into units of organization called nucleosomes. On chromosomes, some regions can become highly compacted, rendering the DNA inaccessible to the transcriptional machinery, but ecDNAs have an altered chromatin structure in which the nucleosomes do not compact, resulting in highly accessible DNA that is primed for transcription. Moreover, ecDNAs are loaded with active histone marks but have a paucity of repressive histone marks, promoting high levels of transcription.
We also found that ecDNA is loaded with chromatin modifications that promote transcription and has a paucity of repressive chromatin marks, suggesting that it is poised for high levels of gene expression. Further, we found that ecDNA chromatin is well organized into loops that are normally an important part of gene regulation, but with a three-dimensional topology that is distinct from that of chromosomal DNA. As the DNA segment becomes circular, in a process that is still incompletely understood, distal DNA elements are brought into proximity, enabling ultra-long-range chromatin interaction that cannot be achieved by chromosomal DNA. This could potentially form new gene regulatory circuits, including new active contacts that drive oncogenic transcription. Consistent with these findings, we found that oncogenes residing on ecDNA are in the top 1 percent of the most-transcribed genes in cancer cells that have them.
We published these results in Nature in November 2019, and the paper was highlighted in a story by Carl Zimmer in The New York Times. Very shortly thereafter, two other groups—one led by Peter Scacheri of the Cleveland Clinic and Case Western Reserve University and Jeremy Rich of the University of California, San Diego, and another by Anton Henssen of Charité Hospital in Berlin and Richard Koche of Memorial Sloan Kettering Cancer Center—added further evidence that ecDNAs may play a pivotal role in reorganizing the transcriptional control of cancer genomes by bringing regulatory elements encoded on ecDNA into contact with genes with which they would never interact in chromosomes.
Recent work from Chang, in collaboration with myself, Bafna, and Henssen, has begun to suggest a very exciting new way that these circular pieces of DNA, instead of acting alone, often organize themselves into nuclear bodies called ecDNA hubs. These hubs are tethered by proteins and appear to provide a platform for cooperative transcription, in which ecDNAs work together to drive the expression of cancer-promoting genes.
The question then became, how do we capitalize on this new understanding of ecDNA to improve patient outcomes? In 2018, Chang, Bafna, and I, with other scientists, cofounded Boundless Bio, where several staff scientists now seek the answer to that question.
Short H2A histones, part II: a natural-born oncogene lurking in our genomes
The story of cancer is, largely, one of broken genes. The valiant tumor suppressor, defender of cellular integrity, maimed and enfeebled. The conniving oncogene, hyper-activated, allowed to run wild and sow chaos within the cell. These genes are many, and they act on an array of cellular processes. Cell growth. Cell death. Cell motility. Genome integrity. Impairment of this last process is particularly frightening in that it can, in one fell swoop, disrupt a whole suite of cancer-related genes throughout the genome, and ensure that many more will fall in quick succession. Among the defenders of genome integrity are the histones – small protein complexes that wrap DNA strands into orderly bundles. The resulting DNA-histone structure, collectively called chromatin, regulates DNA stability and gene expression. It is not surprising, therefore, that histone function is highly regulated, nor that mutated histones (called oncohistones) with disrupted DNA wrapping characteristics are found in many cancers. There is one type of histone protein, though, that in its native state appears ready-made to cause cancer. A new paper in Nature Communications - a collaborative effort between the labs of Drs. Steve Henikoff, Harmit Malik, and Robert Bradley in the Basic Sciences and Public Health Sciences Divisions and the lab of Dr. Marie Bleakley in the Clinical Research Division at Fred Hutch, led by Dr. Guo-Liang “Chewie” Chew in conjunction with Drs. Antoine Molaro and Jay Sarthy – revealed the role of this unusual histone variant in cancer.
Histones normally wrap DNA tightly and stably around themselves into structures called nucleosomes. Mutations that destabilize nucleosomes are disruptive to genome integrity and, therefore, oncogenic. While most histones are composed of a common set of proteins – called H2A, H2B, H3, and H4 – the mammalian genome contains another class of histones, called the short H2A variants (short H2As). Normally expressed in sperm, short H2As possess a unique characteristic – they destabilize nucleosomes. In other words, exactly what you seemingly don’t want a histone to do. While this doesn’t appear to be a problem for the sperm, (more on that below), these histones would likely be quite problematic if they showed up in another cell type. In fact, by looking more closely at the sequences of the short H2A genes, the authors made an astonishing discovery: “many of the most common cancer-associated mutations in canonical H2A are already present in all wild-type [short H2A] sequences.” Surprisingly, though, these genes had not been identified as cancer-causing agents. “Though a role for [short H2As] in cancer has yet to be determined, the emerging literature on nucleosome instability as cancer driver, along with [short H2As’] potent ability to destabilize nucleosomes prompted us to investigate whether [short H2As] may contribute to cancer”, said the authors of their motivation for the work.
To determine whether short H2As do, as they hypothesized, contribute to cancer, the group examined large cancer gene expression databases and found that one class of these genes, H2A.Bs, are indeed frequently turned on in many cancers, including half of diffuse large B-cell lymphomas as well as a smaller number of endometrial, bladder, and cervical carcinomas. Interestingly, while carcinomas were previously shown to have histone mutations, lymphomas were not. Therefore, H2A.B expression may be another way for cancers to acquire unstable nucleosomes. The cause of activation of the H2A.B in these cancers was unclear, although the authors note that they tended to be co-activated with several other testis-related genes. The consequence of their activation was more evident. H2A.B had been previously observed to interact with splicing factors. Examining H2A.B-reactivated tumors, “we uncovered thousands of altered splicing events…with reductions in alternative exon and [alternative polyadenylation] usage”, they reflected. This genome-wide splicing dysregulation could very well contribute to carcinogenesis, although the authors observe that it is still unclear which particular genes that are dysregulated by H2A.B contribute to cancer.
Oncohistones remain a relatively poorly understood cancer driver. The current work suggests a need to focus not only on mutations to the canonical histone genes, but also on the activities of short H2As. Looking forward, Dr. Chew is excited about the questions raised by this work: “Much remains to be explored, including why so many lymphomas reactivate H2A.B, how H2A.B promotes cancer, and whether we can take advantage of H2A.B-driven gene/splicing dysregulation to treat such cancer patients.”
Short H2A histones represent a clear and present danger: ready-made oncogenes with a natural ability to destabilize nucleosomes, lurking in our genomes, seemingly just waiting to be released in the wrong place and wreak havoc on chromatin. Which begs the question, why do we have them at all? For an answer to this question, check out the other article in this month’s 2-part series on short H2A genes in development and disease, about the important role of these genes in embryonic development, and the processes underlying their evolution.
This work was supported by The Damon Runyon Cancer Research Foundation, the Alex’s Lemonade Stand Foundation, Northwestern Mutual/ALSF, the National Institutes of Health, Stand Up To Cancer, and the Howard Hughes Medical Institute.
Fred Hutch/UW Cancer Consortium members Harmit Malik, Steven Henikoff, Robert Bradley, and Marie Bleakley contributed to this work
Chew GL, Bleakley M, Bradley RK, Malik HS, Henikoff S, Molaro A, Sarthy J. (2021) Short H2A histone variants are expressed in cancer. Nature Communications 12, 490.
Chins are a bit useless so why do we have them?
There are plenty of theories to explain why we have chins, but none of them stands up to scrutiny. Will we ever solve the mystery?
Chins: we all have them, sitting a bit uselessly at the bottom of our faces. Some people have strong chins, others are said to have weaker chins. But if you were pushed to explain what chins are actually for, would you have a good answer? Nobody seems to use their chin for anything useful.
Nobody had put forward a good idea about why humans would be the only animals with chins
It becomes even stranger when you consider that among the all primates &ndash including our extinct relatives &ndash only we have chins. Nobody seems to know why &ndash although over the last century several theories as to its purpose have been offered.
A review of all the previous literature now seeks to put some of these assertions straight. "They [chins] are really strange, and that kind of drew my attention," says James Pampush of Duke University in Durham, North Carolina, who has been studying our humble chin for several years. "Nobody had put forward a good idea about why humans would be the only animals with chins," so he set out to to untangle the enduring puzzle of the human chin in a recent review.
We all have a pretty good idea what a chin is, but it&rsquos useful to define it nonetheless. Put simply, our chin is the protrusion of the bone that appears below the front wall of the human mandible (lower jaw). No other animals have chins &ndash chimpanzee and ape jaws slant inwards for instance. Even our closest extinct relatives such as Neanderthals did not have them.
Nobody can quite agree why the chin exists
In fact, one of the ways that scientists differentiate between an anatomically modern human and a Neanderthal skull is by looking to see if it has a chin. "That is what makes the appearance of chins in anatomically modern humans so interesting. It implies that there was some sort of behavioural or dietary shift between Neanderthals and anatomically modern humans that caused the chin to form," says Zaneta Thayer of the University of Colorado, Denver, another researcher who has studied the human chin.
Although nobody can quite agree why the chin exists, there are three prominent theories that have been around for decades.
To start with it has long been proposed that our chin may help us chew food. The theory goes that we need the extra bone to deal with the stresses involved with chewing. However, this idea falls flat when you compare us to other great apes with similar-shaped jaws.
When we chew, our jaw gets pulled apart a bit like a wishbone and the further apart our jaws are the weaker the bones are. If we were to protect ourselves from the stresses of chewing we would need more bone on the inner wall of the jaw near the tongue, not beneath our jaw.
We don't have a very tough time chewing
That's exactly what you see in chimpanzees and macaques. They have extra bone on the tongue-ward side of their lower jaw, called a "simian shelf", which we do not have. The added bone that forms our chin is not very useful for additional chewing strength.
Another point Pampush is keen to make is that we don't have a very tough time chewing in the first place. Much of the food we eat is soft, especially cooked food. "That's why the chin is not an adaptation for chewing,&rdquo he says.
Flora Groening at the University of Aberdeen in the UK, agrees. Five years ago she used a computer model to look at the mechanical load on the mouth with and without a chin. "There wasn&rsquot clear evidence to support the claim that the human chin is a result of a mechanical adaptation," she says.
Others have argued that our chin helps us to speak, that our tongue needs reinforcements from extra bone below our jaw. We are the primates with the most extensive speech repertoire after all.
The issue here is that we don't need much force to speak, so it&rsquos not at all obvious why we would need extra bone to help with the process. And if we did need any extra bone, just like for chewing it would be far more useful to add it to the inside of our jaw, closer to our tongue, rather than tagging it onto the bottom of our jaw.
If it&rsquos an adaptation for sexual selection then we are the only mammal that has the same in both sexes
The third idea is that the chin doesn't have an immediate function, but that it has been chosen by sexual selection. It is our equivalent of large-flanged orangutan faces or a male elk's large antlers. These are traits that have both been selected for when the opposite sex is considering a mate. This ensures they live on in future generations even if they have no direct benefit or use.
Again there is a problem here, Pampush says. In all other mammals only one sex will have a sexually selected trait. Chins on the other hand are found on men and women. "If it&rsquos an adaptation for sexual selection then we are the only mammal that has the same in both sexes," he says.
The three hypotheses mentioned all therefore fall flat, says Pampush. In fact, he argues that nobody can know why we truly have a chin at all. "Anyone who tells you that they know [why] is lying." Many of the ideas proposed so far have not stood up to scrutiny, he says, while others are untestable.
Unfortunately, then, we are no closer to explaining why we have a chin. But if we look at it another way it might become more apparent how it came to sit on our faces so prominently, despite having no functional use.
Spandrels are a by-product of a change happening elsewhere
It could simply be what's called a "non-adaptive trait" that arises as a by-product of something else. This is an idea that was suggested in 1979 by the biologists Stephen J. Gould and Richard Lewontin. The chin, they said, is a "spandrel". This is the name given to an architectural feature below some church domes that is often so ornate it looks as if it was the starting point for the building&rsquos design. In reality, spandrels only exist because they help support the dome above them. In other words, spandrels &ndash both biological and architectural &ndash are a by-product of a change happening elsewhere.
Our faces getting smaller may be what caused this particular spandrel to show, according to Nathan Holton of the University of Iowa. He says the chin may simply be a by-product of the reduction of the human skull. Our mandibles, for instance, are less robust than those of our extinct hominin relatives. As our ancestors developed and used fire to cook their food, they no longer needed such strong jaws to chew. This means the overall strength of the jaw in turn became reduced.
The appearance of a chin could have helped to maintain some of the strength our lower jaws once had
Other features changed too. We lack a prominent brow bridge and we have a hollow point below our cheek bones (technically called the "canine fossa"). These have also been linked to our smaller faces, Holton says. "The presence of a chin is probably part of this trend as well. In this sense, understanding why we have chins is really about explaining why human faces became smaller."
Groening also favours this idea, and says that the appearance of a chin could have helped to maintain some of the strength our lower jaws once had. "Neanderthals and Homo erectus had such robust mandibles, they didn&rsquot need an extra thickening of the bone in the chin region, they already had strong jaws and robust bone," she says. Modern humans in contrast have very graceful bones. "A chin might help to provide a bit of extra resistance to maintain a certain mechanical strength, but doesn&rsquot really increase the [overall] strength."
On the other hand, a spandrel could also have been caused by a random event or accident, rather than as a by-product of useful adaptations elsewhere in our faces.
"I am doubtful that it's an adaptation," says Pampush, but the problem is that for now nobody can prove it is an accident either. "We don&rsquot have the tools to do so right now."
The chin literally sticks out
So if none of the proposed theories fit the bill, and we cannot prove the spandrel hypothesis, you might wonder why Pampush has spent so long researching the human chin.
It makes more sense when you consider that, although chins are pretty weird, studying them helps pinpoint the evolutionary processes that make us who we are today. It also exposes that evolution works in many ways.
Perhaps surprisingly, it's also rare to find a trait that is uniquely human. Many traits that humans have, other animals do too. The chin on the other hand, literally sticks out, and looking at how it did so may help us understand another step in the process that led to us.