Tandom Parachute Jump 9-9-12

We have arranged a day of Tandom Parachute jumps to help raise funds. Anyone wanting to take part need to be 16 + and no heavier than 16 stones (with clothes)

We will be jumping in Cirencester and we hope for good weather.

We will be asking for £300 for each jumper. That covers the cost of the dive( £220)  and a donation to the Charity obviously if you raise more than that, that will be fantastic but you will need to raise that prior to the jump.

I suggest any participants set up a just giving page http://www.justgiving.com/bye-to-cancer  as they make things a lot easier for you (I can post you a sponsorship form if you would prefer)

So good luck if you want to be added to the list and meet the above criteria then email me your contact details and I will add you to the list mark@ballstocancer.com

By the way we can jump 60 in a day…. so no excuses 🙂

The Jumpers…. (if you are not on this list and want to jump I haven’t got a completed form)

Kate Bayliss

Kieran Langan

Georgia Gibson

Matt Watson

Lee Hatton

Chris Gilbert

Daniel Soskic

Danny Moloney

Adriano Di Maria

Lor Hunter

Samantha Kennell

Adam Freeman

Georgia Downie

James Holton

Adam Watson

Kieran Newey

Lauren Watson

Louis Perry

Alison Nolett

Matt Kelly

Dayle Hallard

Scott Hallard

Steven Nollett

Nicola Morrisey

Guv Rai

Anna Aloia

David Miles

They will be jumping from 13,000 ft here…..

Duke of Gloucester Barracks
South Cerney Airfield
Cirencester
Gloucestershire
GL7 5RD

Our First Research project

Using DNA Repair Biomarkers to Predict the Response of Cancer Patients to Anticancer Therapy.

 

Dr. Christopher N. Parris

Senior Lecturer

Brunel Institute of Cancer Genetics and Pharmacogenomics

Division of Biosciences

Brunel University

Kingston Lane

Uxbridge

Middlesex, UB8 3PH

Tel: 01895 266293

christopher.parris@brunel.ac.uk

 

Cytotoxic (cell killing) therapy (chemotherapy and radiotherapy) are the main methods of anticancer therapy for the treatment of early stage (primary) cancers or those that have spread (metastasised) to other sites in the body. The effectiveness of anticancer therapy can be limited by the extent and severity of painful side-effects which are caused by the administration of the treatment. The painful side-effects associated with anticancer therapy can decrease patient welfare, leave the patient with persistent or permanent disabilities and increase patient care cost to the NHS.

            Cytotoxic anticancer therapy works by damaging and ultimately destroying the DNA within cancer cells. However, normal non-cancer cells within the body are also destroyed by the treatment and it is the extent of normal cell damage that will govern the level of side-effects experienced by the patient.

Most human cells have number of cellular DNA repair mechanisms that can reverse the effects of DNA damage and return the cell back to its normal condition. Therefore the efficiency of DNA repair in cancer and normal cells will play an important role in:

  1. Controlling tumour response and determining the clinical outcome (cure or non-cure of the cancer) by the anticancer therapy.

  2. Determining the severity of side-effects experienced by the patient.

Interestingly, some individuals are afflicted by inherited conditions where they have an inborn inability to repair certain types of DNA damage. Such individuals would be at extreme risk of life-threatening side-effects if they were treated with normal anticancer therapy. An example of such a disease is Ataxia Telangiectasia (A-T), in which there is an inability to repair DNA strand breaks caused by radiation exposure. These patients also have an elevated risk of cancer as a result of the disease but it would be lethal to the patient if their cancers were treated with radiotherapy and consequently other treatment options would have to be considered.

            While A-T is an extreme case, there is good evidence to suggest that cancer patients with more mild and previously undiagnosed defects in DNA repair mechanisms are also at risk of dramatic and painful side-effects during therapy. In fact our research group recently demonstrated in a patient whom experienced drastic side-effects to radiotherapy (eventually leading to death), a previously un-described defect in a gene controlling the repair of radiotherapy induced DNA damage (Abbaszadeh et al, 2010). Therefore a pre-treatment diagnostic test to determine how cancer patients respond to therapy is likely to prevent such occurrences in the future.

For many years, clinicians and scientists have looked to develop experimental methods that could be used to predict how cancer patients are likely to respond to anticancer therapy. All of these tests rely on taking a sample of tissue (normally a skin biopsy) from the cancer patient. These cells are then grown in culture and exposed to the very same drugs and/or radiation that a patient might receive during the course of the anticancer treatment. The response of the patient’s cells is compared to cells from a normal individual, and if the cancer patient’s cells are abnormally sensitive then it is likely that the patient may experience a high level of painful side-effects. Some of these methods can reliably predict how a patient might respond to therapy, however, the tests take many weeks to perform and therefore cannot provide a result within a useful timescale, since it is imperative to commence therapy as soon as possible following diagnosis. Thus there is a need to develop a simple diagnostic test that will provide useful information to the consulting oncologist within days rather than weeks enabling the design of an effective treatment protocol without delay.

            To address this problem our research group has been employing a new method as a predictive test. This method is called the gamma-H2AX assay. When cells are exposed to radiotherapy or anticancer drugs, a break (damage) in the DNA occurs. The cell responds to this damage by activating (phosphorylating) a protein bound to the DNA called H2A. Once this protein is activated it is now called gamma-H2AX and it acts as a “beacon” (foci) to attract the appropriate DNA repair protein to repair the DNA break. If the DNA damage is successfully repaired, the gamma-H2AX foci will disappear within a few hours. If there is a failure to repair (as would be expected in a patient with severe side-effects) then the gamma-H2AX foci will persist. It is possible to measure and quantify the level of gamma-H2AX foci within both cancer and normal cells from patients and this test can be performed within 24 hours.

How the test is performed

  1. 10 ml of blood is taken from the patient and delivered to the laboratory.
  2. The white (lymphocyte) cells are purified from whole blood.
  3. The lymphocytes are treated with radiotherapy or chemotherapeutic drugs to cause DNA damage.
  4. The measurement of gamma-H2AX foci is performed over the period of one day.
  5. Results are returned to the oncologist for consideration in designing an appropriate treatment schedule for the patient.

In collaboration with Dr Nick Plowman (Head of Radiotherapy Department) of St. Bartholomew’s Hospital, London, UK, we have recently demonstrated that a group of patients who had earlier experienced severe radiotherapy induced side-effects (including severe nerve damage, deep skin destruction and severe ulceration) during routine treatment were unable to repair radiotherapy-induced DNA damage. Lymphocyte cells were exposed to radiotherapy and failed to repair DNA strand breaks measured by gamma-H2AX levels. Therefore, we have preliminary exciting data using a rapid and convenient assay which suggests we can successfully predict how individual patients might respond to anticancer radiotherapy within the clinical setting.

 Experimental Plan

To fully exploit the potential of our diagnostic test we wish to extend these findings to:

  1. Analyse gamma-H2AX induction in human cells using a panel of cancer chemotherapeutic drugs with different mechanisms of action.
  2. Exploit our diagnostic test (gamma-H2AX assay) within the clinic to pre-determine painful side-effects in patients with genetic conditions which may leave them at risk of extreme toxicity to radiotherapy and/or chemotherapy.

We have demonstrated that we can use the gamma-H2AX test to predict how patients are likely to respond to radiotherapy. It is now important to take this technology to the next stage and place it within the clinical setting. Initially we aim to test specific groups of cancer patients with:

  • A strong family history of cancer, especially breast cancer, as evidence suggests that such patients might be hypersensitive to both radiotherapy and chemotherapy (Moule et al., 2009).
  • Potential DNA repair defects which may leave them at extreme risk during radiotherapy.
  • Unusual tumours or case histories where the consulting oncologist suspects that there may be an over-reaction to the treatment.

The long-term goal of this research is to provide a mechanism whereby anticancer therapy can be designed for each patient based upon our diagnostic test. Therapy can then be individualised and made more effective and tolerable for each patient.

In conclusion, we have good experimental evidence that using our DNA repair based test, we can identify patients at risk of severe side-effects during therapy. This data has been based upon retrospective studies. However, now we need to move the test forward into a clinical setting. We appreciate that this will take a few years to fully exploit the technology for patient benefit but require funding to perform further experiments towards this goal.

 

 

References

  1. Abbaszadeh F, Clingen PH, Arlett CF, Plowman PN, Bourton EC, Themis M, Makarov EM,  Newbold RF, Green MHL, Parris CN. A novel splice variant of the DNA-PKcs gene is associated with clinical and cellular radiosensitivity in a xeroderma pigmentosum patient. J.Med Genet. 2010, 47(3):176-181.
  2. Bourton EC, Plowman PN, Smith D, Arlett CF, Parris CN. Prolonged expression of the g-H2AX DNA repair biomarker correlates with excess acute and chronic toxicity from radiotherapy treatment. Int. J. Cancer 2011;129(12):2928-34.
  3. Bourton EC, Plowman PN, Adam Zahir S, Senguloglu GU, Serria H, Bottley G, Parris CN. Multispectral Imaging Flow Cytometry Reveals Distinct Frequencies of g-H2AX Foci in DNA Double Strand Break Repair Defective Human Cell Lines. Cytometry Part A, 2011, Dec 13. doi: 10.1002/cyto.a.21171. [Epub ahead of print].

Coventry’s Male mile.

Coventry City footballs club have organised a Male Mile at their Ricoh football Stadium for their Mens Health week. They have kindly offered to raise funds for us at the event and many of #teamnuts will be there to collect and offer morale support.

If you live in or near Coventry why not enter as a warm up to the Fathers day 5K event.

Competition winner!

Please meet our competition winner Donna Klander on our new poster. Donna entered our competition to send in a picture with a ball or balls covering you bits and pieces. Donna’s poster will be used nationwide to help raise awareness.

Thank you Donna and Congratulations!

Liam’s Story

Liam is a chap I have been speaking to for sometime on Twitter and he is a brilliantly strong and kind person, this is his story……..

Hi, my names Liam, I’m 14 years old and my grandad recently passed away from cancer. My grandad has always been a father figure to me as my real dad was never around. I’ve always been close to him, and in April 2009 I had a huge argument with my mum which forced me to move in with my nan and grandad who were kind enough to take me in despite them both suffering from health problems. My grandad has beat one type of cancer, two heart attacks and lived through a near fatal anuerysm, he had 25% kidney function for much of his later life. Then in September 2010 he was diagnosed with upper GI cancer which is for those of you who don’t know is cancer of the Esophagus which limited his ability to eat and drink even simple things such as; mousses, soft sponge cake etc. After Christmas of 2011 his health started to deterioate, in January his mobility was gone and he had to stay in bed so instead of him being upstairs all the time on his own we got a hospital bed put in downstairs so he could be with the family. A few days after my birthday which was on March the 3rd I was told by some family members that my grandad had 1-2 weeks to live, however a few days later he passed away on the 17th of March. I’ve never done anything harder than watching him die as it wasn’t just a grandad I was losing it was a dad, a bestfriend and most of all someone I could trust with anything. His funeral was on the 5th of April and luckily I had my best friend Louis there who was kind enough to come to support me, he also knew him. Well thats my story, hopefully nobody else has to die of this sick, sick disease.

Jack Thompson!!!!

UPDATE 19-5-12 Jack has successfully completed his jump and has raised a magnificent £370.00 for the charity.

“I would personally like to thank him on behalf of the charity. Thank you Jack you are a star” (Mark Bates Founder)

_______________________________________

21 year old Jack Thompson has decided to do a Parachute jump for us, Jack from Gornal in Dudley (a former pupil of Ellowes Hall) is now working as an engineer in Netherton.

Jack said “I hope to raise lots of money for the charity”  So if you want to support Jack and sponsor him, please get in touch through the website and we will pass your details on to him.

Jack will be doing his jump on Saturday the 3rd March at Hinton Skydiving

We wish Jack all the best and thank him for doing it for us.

We’re Registered!!

We are very proud to announce that we are now a fully registered Charity. After long hard weeks we managed to get through the process and we are very happy.

We would like to thank everyone associated with the very first race we had back in October who have worked so hard to raise the lions share for the £5000 needed to be able to register our charity. So lad’s you know who you are thank you!!!

We would also like to thank each and every one of #teamnuts who have bought a wristband, Pen, Trolley coin, Tee shirt or calendar because every penny counts and your contribution is as important as any other.

Please keep buying, keep fundraising and keep running for us!! We LOVE you all!!

Charity Number 1146185

Male Cancer incidence and Mortality rates

Below is a list of Male Cancer Incidence (shown as I) (recorded in 2008) and Mortality rate (Shown as M) (recorded in 2009). This is the reason we need your help. The incidence continues to grow as does the Mortality rate.

We need to put a stop to this and beat Cancer! Please do whatever you can to help or donate.

 

Bladder (I)7,390 (M) 3,352
Bone and Connective Tissue (I)1,281 (M) 549
Brain and Central Nervous System, Malignant and NonMalignant
(I) 4,602  (M) 2,621
Brain and Central Nervous System, Malignant  (I)2,062  (M) 2,179
Brain and Central Nervous System, Non-Malignant
(I) 1,879 (M) 442
Breast (I) 341  (M)77
Cancer of Unknown Primary (I) 5,028 (M) 4,962
Colorectum (includes Anus)(I) 22,097 (M) 8,600
Colon  (I)13,359  (M) 5,076
Rectum, Rectosigmoid Junction and Anus  (I) 8,738  (M) 3,524
Hodgkin Lymphoma (I) 948 (M) 171
Kidney (I) 5,377 (M) 2,296
Larynx (I) 1,890 (M) 650
Leukaemia (I) 4,463 (M)2,557
Acute Lymphoblastic Leukaemia (I) 369  (M)129 1
Acute Myeloid Leukaemia  (I) 1,303  (M)1,311
Chronic Lymphocytic Leukaemia  (I) 1,703  (M) 669
Chronic Myeloid Leukaemia (I) 339  (M) 111
Liver  (I) 2,286  (M) 2,159
Lung  (I) 22,846 (M) 19,724
Malignant Melanoma  (I) 5,584 (M) 1,159
Mesothelioma (I) 1,967  (M) 1,913
Multiple Myeloma (I)  2,480  (M) 1,367
Non-Hodgkin Lymphoma  (I) 6,343  (M) 2,423
Oesophagus (I) 5,461 (M) 5,097
Oral  (I) 3,824  (M)1,273
Other Digestive Organs (I) 362(M) 1,518
Pancreas (I) 4,001 (M) 3,881
Penis (I)  488 (M) 118
Prostate (I) 37,051 (M) 10,382
Small Intestine  (I) 576 (M) 213
Stomach (I)  4,923  (M) 3,167
Testis (I) 2,138 (M) 69
Thyroid  (I) 558 (M) 137

Spend Save Support!!

Spend Save and Support

We have teamed up with www.easyfundraising.org.uk so now you can save money shopping online and earn money for the charity.  There is no cost to you or the charity.

Easyfundraising is FREE to join and there are no subscription charges.  The website is an online shopping portal with access to 000’s of retailers offering discount codes, cashback and cash incentives.

Sign up at http://www.easyfundraising.org.uk/causes/ballstocancer/?t=Easyfundraising-lo&v=a&=  and start saving.