Dr Momna Hejmadi

Dr Momna Hejmadi

A member of University of Bath’s cancer research group, Dr Momna Hejmadi has also received awards for excellence in teaching and has carried out work in open education resources.

Location Bath


  • I use it for my first year classes to Patricia - I absolutely agree - its a great website for beginners

  • Cancer cells 'release' factors (typically proteins such as Vascular Endothelial Growth Factor) that stimulate blood vessels to divide and expand the network of blood vessels inside the tumour.

  • Genomic imprinting is one mechanism in which epigenetic marks are inherited through one of the parental copies. Prof. Andrew Ward researches on genomic imprinting and its impact on development and disease https://researchportal.bath.ac.uk/en/persons/andrew-ward

  • thats correct, they do code for RNAs Reuben. Traditionally, coding typically refers to proteins (and for the purpose of this course)

  • you should have access to all 4 weeks Patricia, from what I understand. Please email the Futurelearn team if you dont get access to all 4 weeks.

  • Hi Phil. Introns are excised out and it is the exons that are spliced together that are then translated to make proteins. If the DNA (i.e. exons) have a mutation, it can change the type of protein made, which in turn MAY lead to abnormal proliferation.

  • many thanks for pointing this out Lily. The link is updated now.

  • Good to see the lively discussion here, and why it is indeed a case of natural selection. Interestingly, while the phenomenon was discovered a while ago, the gene mutation (gene called 'cortex') responsible was only discovered in 2016 by Illik Saccheri's group in Liverpool. It also has an unusual event that gave rise to the mutation. The original paper is here...

  • Hi Joseph. Certainly, the implication, if any, was unintentional.

  • they could still breed since the two colours of mice belong to the same species. Speciation occurs when breeding does not happen. If the two strains of mice breed, then the fur colour would vary depending on whether the offspring inherited the mutation that causes the change in colour. The human equivalent of the same gene, Mc1r, is the one that is linked to...

  • apologies about the volume, will try to re-record this for next time. However, the subtitle and video transcripts may help for this one

  • to add to Laurence's point, somatic cells have a higher mutation rate but cells also have very effective DNA repair mechanisms that usually 'fix' most mutations that arise through metabolic or replication errors.

  • but we do know Hind, each rung is a complete A=T or a C=G link. The Human Genome Project in 2000 mapped precisely that, and we know that within each nucleus of a typical human cell, there is 323,000,000,000 base pairs of DNA (or 'rungs' of the ladder)

  • certainly John. What would you suggest we could include in the future?

  • that is absolutely correct Steven

  • thank you very much for this feedback Kelly. I shall certainly be forwarding your comments on to our staff. I am also slightly surprised by this because we have a history of having mature students on our courses, many of whom have won prizes and gone on to do PhDs. Once again, thank you for your honest feedback, this really helps!

  • I am really sorry to hear that you are undergoing treatment for kidney cancer and I hope the treatment works. Unfortunately, kidney cancer is also called a 'silent' cancer because the symptoms -typically back ache and fever (which in the vast majority of people are not cancer-related) - usually occur only after the tumour has grown quite large and spread. You...

  • http://go.nature.com/2FsOnhL
    This Nature Community Hub blog post explores how host genetics, microbiome and environmental factors can influence a person's cancer-immune setpoint.

  • I will reply in the video Mari

  • The 2 processes may work in parallel, not necessarily in a linear order Kelly. E.g. in certain leukaemias, we now know that alterations in stem cell reprogramming (i.e. transcription factors) are key to the formation of aberrant blood stem cells. In other cases, such as colon cancers, this is less well documented, although we are now discovering mutations in...

  • The hallmark of EMT is the loss of epithelial surface markers, most notably E-cadherin, and the acquisition of mesenchymal markers including vimentin and N-cadherin. This is very well documented in the literature, Khem. Here is a link to one of them https://www.ncbi.nlm.nih.gov/pubmed/26905733

  • I was referring to chemotherapy Susan.

  • There are various classes of chemo drugs, each working in a different way. They do not trigger metastasis on their own.

  • its the tumour cells usually that secrete VEGF which binds to VEGF receptors found on the endothelial cells, which stimulates the endothelial cells to divide and form new vascular structures

  • Interesting point Karen. We do know that normal vascularisation is not evenly distributed in all organs equally though. For instance, kidneys, liver, colon are very highly vascularised (as you would expect for its function) but the brain has a protective blood brain barrier. Secondly, tumour vascularisation is highly disorganised and uneven, compared to normal...

  • my apologies, it is remnant from an earlier version of the course (which was longer). Do ignore the comment 'last week' - the narrative is still correct in that cell growth and division is part of normal function. Thanks for pointing this out

  • the organisation of a plant cell (thicker walls) is very different to an animal cell (thinner walls). Supply of oxygen and nutrients is via circulatory system in animals but through xylem / Phloem in plants. You might find this link below useful

  • Hi Khem and Kelly. You have picked up on a relatively poorly understood cancer group, leukaemias. ALL (acute lymphocytic Leukaemia) is relatively rare compared to the chronic version (CLL). ALL progresses much more rapid than CLL and is the most common type of leukaemias in children. CLL on the other hand, is more common in 60+ age group, and it progresses...

  • Thanks for pointing out the glossary issue everyone, we will try to fix it as soon as possible

  • Plant cells also develop tumours but are less frequent and less lethal than animal cells because of the typical plant cell wall structure. This is also the reason why metastasis (spread) does not occur in plants because plant cells do not tend to move around.

  • Hi Nicky
    I am not a clinical oncologist so I cannot comment on how human tumours look like, but have seen a lot of mouse tumours. It will depend on the type of tumour. For example - a melanoma on the skin shows up as a change in size, shape and colouration of a mole or wart. With internal tumours, such as colon carcinoma, it usually starts as polyps or a...

  • One can only REDUCE the RISK of developing cancer, not prevent it really. As I mentioned, one of the biggest risk factors is age, but diet and lifestyle can play a big part in reducing the risk. There are many public awareness campaigns in the UK (mainly through charities such as Cancer Research UK) which aim to inform the public of these risks.

  • Hi Linda
    One of your co-learners, Stephanie McLeod has provided a very useful link https://www.varian.com/en-gb/oncology/solutions/radiotherapy
    In brief, radiation can be given from sources outside the body as beams (External Beam radiotherapy) or inside the body through tiny radiation-emitting beads/seeds (brachytherapy). The choice depends on the tumour...

  • I would advise people to view websites promoting products that prevent cancer with the healthy criticality it deserves. Our diet and lifestyle can play a big part in REDUCING THE RISK but not preventing cancer development. The

  • that is correct Nicky, that cancer stem cells tend to be resistant to chemotherapy. This resistance also depends on the type of cancer stem cell (progenitor, pluripotent or multipotent) and also the tumour microenvironment which can protect the cancer stem cells from chemotherapeutic drugs. Here is a link you may find interesting to...

  • The normal job of a tumour suppressor gene product (i.e the protein) is to prevent cell division in times of DNA damage or stress to the cell (so that the cell has time to repair or fix this damage first before continuing through to division). Therefore the normal functioning tumour suppressor suppresses abnormal cell division (i.e. cancer). However, when the...

  • thats correct Janet, mutations or epigenetic changes alter the cell behaviour to make them either more likely to detach and spread through the blood and/or lymphatic systems.
    Interesting question about benign tumours. If a tumour is benign, these cells are no longer dividing (hence no increase in size or growth), then it is very unlikely that they will...

  • Hi Lyall
    The presence of stem cells or stem cell-like cells are now being discovered in more and more tissues of the human body. The normal role of stem cells is to either self-renew or progress into a differentiated cell type. As you mentioned the HSC (haematopoietic stem cells) in the bone marrow enable formation of different NORMAL blood cell types. What...

  • Hi Janet
    Almost all cells have the capacity to respond to various chemical signals. e.g. endocrine cells send hormones as chemical messengers (e.g. ovarian sex hormones such as estrogen) which can be picked up by target cells which express receptors for these hormones (such as estrogen receptors in the breast cells).

  • this is a really interesting question Karen, and an area on ongoing research. There are several models proposed, but one prevailing hypothesis is that cancer cells undergo at least two rounds of transitional cell type changes. Typically, if the cancer cells originate in epithelial tissues (as most common cancers are), they transform into mesenchymal cell...

  • i've answered this question that you posted in the earlier sections Gilberte :)

  • thats right, necrosis could be stress induced. E.g tissue injury due to frostbite

  • drugs ending in 'mab' means that these are 'Monoclonal AntiBodies - antibody based therapies which target specific proteins, as opposed drugs ending in 'ib' which are essentially drugs that are 'inhibitors'

  • Hi Sally
    As your colleagues have rightly pointed out, there are a range of histopathological and mutational screening analysis that are done using both biopsy samples and blood. If you are interested in finding out more, there is a free course on the classification system below

  • Here are some links on histones and chromatin
    1. This one is a short youtube video https://www.youtube.com/watch?v=eYrQ0EhVCYA
    2. Animation using structural information showing how it works https://www.youtube.com/watch?v=gbSIBhFwQ4s

  • Hi everyone
    Please don’t worry about the access to this just yet. At the end of every week, I record a brief ‘wrap-up’ video, which will then become available to you around Mon or Tue. The idea is to answer/highlight/summarise some of the key points or questions from your learning in each week. Best wishes, Momna

  • Hi Lindsay. It certainly is very likely. There are so many unique species out there and that is where the challenge lies. Identifying the traits and researching on them all is a very expensive (not to mention the ethics of working on endangered wild species)

  • Hi Alex
    In answer to your questions (not sure I follow your train of thought though? are the 3 points linked in any way?)
    1. The hyaluronan is a unique version is the NMR called HMM (high molecular mass hyaluronan), making it particularly thick. http://www.nature.com/nature/journal/vaop/ncurrent/fig_tab/nature12234_F3.html
    2. Yes it does, perhaps you may...

  • Hi Tamara
    Our immune systems are quite complex, but I will attempt to simplify it further. Immunotherapy, in the context that Tania referred to, is about using a tumour-specific antigen to target it for destruction. So in this case, an antibody (drug) acts like a homing missile. In terms of cancer metastasis, there seems to be dual roles for certain immune...

  • Good question Rob. The ex-vivo method that you describe has being used since 1996, but in a slightly different way. Essentially, it is used to load a target antigen in a petridish, using a patients immature dendritic cells (a type of immune cell), which is then injected back into the patient.
    Here is an article that may...

  • Fred is absolutely right Brid. Most of us are researchers, working in labs. We have contributions from clinical medical oncologists on week 5, but it is much better to talk to your oncologist, who knows your case history best, and is in the best position to offer you sound advice.

  • Hi everyone. Thanks to an update from one our learners based in Canada on a sabbatical, I have been told that it is possible to listen to BBC Radio4 outside the UK (but unlike the IK, its not free). The link she used was EasyLoad (I think?), but I am sure there may be others.

  • thanks Kim. I have used this activity very successfully with schools outreach, even down to primary school level sometimes. I also like your idea of the sweets (you may have seen another use of sweets at the end of week 1, when I explain clonality of cancer mutations)

  • almost all cells contain DNA because some specialised cells like our erythrocytes (mature red blood cells) don’t contain DNA.

  • Good idea Bronwen. I shall pass it on to our e-learning team to see if thats possible. Thanks

  • Hi everyone and welcome to the course.
    To download the book, you can tick any box, as suggested by Fred Robinson below, and you should have access. I look forward having you all on the course.

  • Thank you very much for supporting research into cancer Sue. It really is invaluable for those of us, working away in the labs!

  • HeLa cells are an example of the usefulness of cell lines as a quick first screen of targets in vitro. Usually, a range of cell lines in addition to HeLa are used, ideally closest to the tissue type. However, the second round of screening would most likely use in vivo models, like mice.

  • Hi Elaine. I must confess I have not come across any peer-reviewed scientific papers that suggest a link between the two! And it is very, very unlikely, because if it were the case, incidences of lymphoma would be much higher in bed-bug infested regions. Secondly, one of the symptoms of NHL can be itching and rashes, which is similar to bedbug bites, so its...

  • To add to Dr. Caunt’s links below, here is a paper giving the global cancer statistics

  • thank you Jenny. I must say that this is the third run of the course and the first time that we have noticed some people misinterpreting what the course is about.

  • HI William. Leaky as in gaps in the vessel wall. So if there is a dense layers of tumour cells, there is more likelihood of the odd cells sloughing off into the bloodstream. I think I showed an Transmission Electron Microscopic image in my slides somewhere.
    You may find this paper useful

  • Hi Willie. There should be a full stop in the transcript between the two (hypoxia and acidity). Leaky capillaries create stagnant and acidic micro environments (mainly due to poor drainage through vessels and lymphatic systems). Hypoxic cells on the other hand, are found within the tumour tissue and not within the blood vessels. Maybe this review might...

  • Hi John. The timescale for the angiogenic ‘switch’ (stimulating division of the tumour vasculature) can take anywhere from weeks to years. Aggressive cancers such as pancreatic cancers make the switch early (primarily due to mutations which confer this - e.g. increased expression of angiogenic factors like VEGF) whereas in others they can be years (certain...

  • Hi Linda. I must say that ontology is not something I know much about but perhaps you may find this link to the thesaurus at the National Cancer Institute useful?
    It gives you a list of all the terms, including ‘cancerous’; metastasis and malignant.
    Hope this helps

  • Hi Sharon. It is very unlikely that this would increase a risk of cancer. The reason is that the cues for switching on apoptosis in developmental stages are very different to adult tissues. Thanks for sharing!

  • Hi everyone - its a transcript error - it should read 'BRake' as in car barke. proteins that inhibit cells from dividing.

  • Hi Beverly - Good thinking! That is absolutely the point! This experiment is about being able to see DNA. DNA is a polymer and each cell has 3 billion base pairs. Its the salt that enables the DNA to clump together (Na+ in salt neutralise the negative phosphates in DNA to do this) and the ethanol then helps precipitate it out!

  • Hi Nana. It is vital to chew gently for at least 1 min (but may be difficult if you have braces etc.). Alternative is a clean toothbrush - scrape gently and then mix in water)

  • Hi Claire. Resistance to treatment is one of the many possible outcomes. We will be covering chemoreistance is greater detail at the end of week 5 when we discuss treatments.

  • Hi Willie. Red blood cells (erythrocytes) are an example cells without DNA. The nucleus (containing the genomic DNA) is removed during maturation. The reason is so that these cells can carry more oxygen-carrying Haemoglobin and. These cells typically last 120 days and are replenished by the bone marrow.

  • thats right James

  • It is great to see you asking the right sort of questions. We will be covering almost all of these in the subsequent weeks (genes, proteins and epigenetics in week 2; apoptosis and other cancer hallmarks in weeks 3 & 4). In the meantime, if you would like to find out more on genes and proteins, you may find this link useful...

  • you touch upon a fascinating area of biology Beverly. Years of research have revealed a lot about protein synthesis and almost all bioscience textbooks cover this in detail. We will touch upon this in week 2 but in the meantime, you may find this link useful to understand how genes are translated into...

  • my apologies Luke, I did not think of this. It was an unconsciously random colour choice (maybe because of the Indian and Irish flag colours! - lived in these countries for a while)

  • Good question Alan. There are several theories and some experimental evidence to indicate why this is so. One of the most interesting is that molerats have a special type of thick, gelatinous substance called High Molecular Mass Hyaluronans (HMM-HA), which helps cells stick together. This special type of HMM-HA is one of the reasons for cancer resistance....

  • Hi Matthias - long lifespans is simply how long one lives (e.g. 85 years old). Hormonal exposure refers to the length of exposure to our male or female hormaones like progesteron and oestrogen respectively. The hormonal changes in post-menopausal females can also increase the risk of developing certain types of cancer (e.g. breast cancer)

  • Hi David. 5-FU typically leads to cell cycle arrest (either in the G2 / S / G2 phase depending on the dose and tissue type). This results in cell death, mainly due to apoptosis. Proteins that inhibit cell cycle division are increased, and cell cycle arrest can activate caspases, the key enzymes that trigger apoptotic cell death.

  • Hi Elllie. Interesting point and Isabel is correct that the HeLa cells are unusual even among cancer cell lines. In practice, the more cells divide, the higher the risk of genetic drift. Even HeLa cells are very unlikely to be anything like the original cells genotypical.

  • Hi Ika. A good point. Radiotherapy is typically non-specific (affects normal and cancer cells) and the free radicals generated by the radiolysis of water cause significant damage to DNA in the form of double strand breaks. Usually the damage is a lot more than a single mutation, and hence it leads to cell death, rather than mutations alone. However, it is...

  • Hi Madeleine. You make a very good point. There is now increasing research and support on ‘survivorship’ - such as the National cancer survivorship initiative http://www.ncsi.org.uk

  • Its known to be important for certain leukaemia’s too. There has been a resurgent interest in the use of thalidomide (which caused abnormal limb development) for treating some leukaemia’s, with one of the mechanisms identified as angiogenesis. Here is a useful review

  • Useful point David. See my comment above to Laura’s question. Research into angiogenesis turns out to be more fascinating and complex than we first expected!

  • You have made a good point Laura. Removing vasculature can be tricky for several reasons. First, normal vasculature in other healthy tissues can be affected (tissue specificity is one of the biggest challenges). Second, and interestingly, some drugs that were supposed to destroy vasculature actually helped to repair them for a short time. So some researchers...

  • Hi Anetta and Peter. The blood vessels in most major tissues exist as capillaries (very thin, usually 1 endothelial cell in thickness). And tissues have extracellular spaces too. So when a mass of cells starts to grow and release (or secrete) VEGF, these VEGF proteins which are usually in the extracellular spaces initially, latch on to the receptor for VEGF...

  • Hi Rhonaliza. Good to see to stayed with the course and took up the challenge and sent the assignment.

  • Hi Debra. I did think of leaving the choice of cancer type to learners (as we did in the first run of this MOOC). But some learners found it difficult to pick and wanted more specific direction. Also, it would help with the peer review. However, you can choose Lung cancer too, there may be others out there who may share your interest and offer to review.

  • Hi everyone. Our course has a diversity of learners, with diverse backgrounds and motivations for learning. So please do not feel intimidated by sharing your assignments or your ideas. As I keep repeating, it genuinely is a wonderful thing to see the energy and motivation for learning from you all. I can only reiterate Peter Crilly’s comments below (thanks...

  • Hi Liz. It would be wonderful if you could try it like an academic essay, but only if you want to. It may be very useful learning tool for any of your fellow learners attempting an academic essay for the first time.

  • Ray is right - its two targets in total, one for each cancer type

  • Hi everyone. Over the next 2 weeks, we will explore some of the cellular and molecular details on how cancers develop and spread. I would like to reassure everyone that you can write as much or as little as you like on the assignment AFTER two weeks (not before!!).
    This may also be an excellent opportunity for the advanced learners to support the biology...

  • HI Anne. Don’t worry about it just yet. Over the next 2 weeks you will find out that there are a number of potentially useful cellular genes and proteins that can be targeted against cancer.

  • the rate (or speed ) of cell division is not affected Harry. Its simply the number of mutations (or mutation frequency) increases with increasing numbers of cell division. You are also correct that the cell checks that the DNA is replicated correctly (done by a subunit of the DNA polymerase enzyme). But like most other things, its is not always 100% correct...

  • Thanks for this Alice. The point about using dogs to detect certain cancers is interesting but still controversial. Here is a recent article on some of the problems http://www.biomedcentral.com/content/pdf/1471-2490-14-22.pdf
    We will try to signpost any relevant Open Access research articles wherever we can, but most mainstream research articles are only...

  • I agree! It is rather difficult to track questions among all the lovely feedback too. FL have created this ’Feedback’ section (to the left) which I presume is mainly for comments. I shall certainly pass on your suggestions to FL and our e-learning team. Thank you.

  • Hi Myer. This is a very good point. The figure is based on evidence from multiple sources including
    1. Cancer registry–based incidence patterns,
    2. Population behavioural risk-factor survey data
    3. Systematic reviews of epidemiological studies.
    All of these form the basis for estimates of relative risk, the prevalence of exposures to various lifestyle...

  • Hi Phil. You are right in that when any cell divides to form two daughter cells (mitosis), both of which are healthy young cells. The new cells inherit one old and one new copy of the DNA strand. But did you know that every time DNA is replicated, it also gets shorter by a few nucleotides? This eventually leads to cell death in normal cells. Some cancer cells...

  • As you will see in the next week Robert, evolution is not bad at all, in fact it is necessary for species diversity.

  • Thanks for raising the point Ken. Contagious cancers are extremely rare because the body's adaptive immune system usually destroys any cancer cell from another body. The Devil facial tumor disease (DFTD) in tasmanian devils is one of the two known cases. One of the reasons why a bite from one animal to another tasmanian devil results in DFTD is because of...

  • That is an interesting point. However, they tend to be the exceptions rather than the norm. The overwhelming epidemiological evidence is that increased exposure to carcinogens increases the risk of certain cancers.