An Important story

This message was sent in to the website, I think it is very important I share.


Hi I just wandered if you would let your followers know that there is something else you should feel for.
I you feel a lump and you have a scan just to be told it just a cyst then beware, this is what I was told and three years later I have something called chronic prostatitis in which there is no cure.
It has wrecked my life, I can’t walk, I am in chronic pain all the time, even though I am on morphine, you cant sit down because you get a unforgiving ball up your back passage which is your prostate, when urinating its like peeing glass.
With the chronic prostatitis comes CPPS which is chronic pelvic pain and CF chronic fatigue.
Because its not known that much of you struggle to get disability living allowance which in my case is hard I have a wife and five young children to tend for.
I just think if three years ago when they said it was just a cyst they had given me a course of antibiotics then maybe just maybe I would not be in this mess.
With Cancer a least there is a course of action with CP you just get told sorry there is nothing else we can do for you.
It’s no life to lead!

Photo memories of Villa game

Please if you want any pictures from our game against Aston Villa on Sunday please visit

50% of the profit of each picture ordered is coming back to Balls to Cancer, so please get a few for yourselves

Villa team revealed

Below is the list of current Villa team players, This is pretty much the team that will be facing our boys (barring injuries)

Derek Dudley

Bryan Small

Darren Bradley

Mark Kinsella

Gareth farelly

Pat Heard

Gordon Cowans

Martin Carruthers

Mark Walters

David Norton

Neil Cox

Lee Hendrie

Dale Belford

Blood Cancer

Facts about blood cancers

Anyone can get a blood cancer at any age. Around 30,000 people, from babies to grandparents, are diagnosed with blood cancer every year in the UK.



Of the 7,600 cases of leukaemia diagnosed in the UK every year, 94% are adults.

We are leading research into tailoring treatments so that rather than a one size fits all approach, every patient in the future will receive the individual treatment they need.

Childhood leukaemia

Childhood leukaemia is the most common form of cancer in children.

In 1960 when Leukaemia & Lymphoma Research was founded, a child diagnosed with leukaemia had almost no hope of survival.

Today 9 out of 10 children survive the most common form of leukaemia thanks to our continued investment in research into better treatments.


Around 11,700 people in the UK are diagnosed with lymphoma every year. Lymphoma is challenging to treat mainly because there are so many different types (over 35) of this blood cancer.

Lymphoma is the most common blood cancer in young people aged 15 to 24.

Thanks to our pioneering research, doctors are able to diagnose lymphoma more accurately which means every lymphoma patient receives the best possible care.


Myeloma is a cancer which occurs in later life: only two percent of cases occur in people under 40.

Around 3,750 people are diagnosed with myeloma in the UK every year.

Our scientists have developed a treatment that relieves the painful symptoms of this debilitating cancer. Now they are looking for a cure.

Other disorders

Over 5,300 people are diagnosed with other blood disorders in the UK every year. These disorders are more difficult to treat because they vary so much from patient to patient.

We are integrating insights from laboratory research with information from patients on clinical trials to improve the diagnosis of these blood disorders. Accurate diagnosis will mean that patients receive better treatments.

 Number of people diagnosed in the UK

Disease Children aged 0-14 Young adults aged 15-24 Adults 25+ All ages
Acute lymphoblastic leukaemia (ALL) 370 90 290 750
Acute myeloid leukaemia (AML) 70 90 2090 2250
Chronic myeloid leukaemia (CML) 20 530 550
Chronic lymphocytic leukaemia (CLL) 3300 3300
Other leukaemias  20 10 670 700
Leukaemia (total) 460 210 6880 7600
Hodgkin lymphoma 70 250 1330 1650
Non-Hodgkin lymphoma 100 80 8820 9000
Other lymphoproliferative disorders 1050 1050
Lymphoma (total) 170 330 11200 11700
Myeloma (total)     3750 3750
Other blood cancers 10 35 45
Myelodysplastic syndromes 2000 2000
Myeloproliferative neoplasms 3300 3300
Other blood cancers (total) 10 35 5300 5345
All blood cancers (total) 640 575 27130 28345


Male Breast Cancer

What is breast cancer in men?

A breast cancer is a malignant tumor that starts from cells of the breast. A malignant tumor is a group of cancer cells that may grow into (invade) surrounding tissues or spread (metastasize) to distant areas of the body. Breast cancer occurs mainly in women, but men can get it, too. Many people do not realize that men have breast tissue and that they can develop breast cancer and need Breast Cancer Treatment Services to overcome it.

Normal breast structure

To understand breast cancer, it helps to have some basic knowledge about the normal structure of the breasts.

The breast is made up mainly of lobules (milk-producing glands in women), ducts (tiny tubes that carry the milk from the lobules to the nipple), and stroma (fatty tissue and connective tissue surrounding the ducts and lobules, blood vessels, and lymphatic vessels).

Until puberty (usually around 13 or 14), young boys and girls have a small amount of breast tissue consisting of a few ducts located under the nipple and areola (area around the nipple). At puberty, a girl’s ovaries make female hormones, causing breast ducts to grow, lobules to form at the ends of ducts, and the amount of stroma to increase. In boys, hormones made by the testicles keep breast tissue from growing much. Men’s breast tissue has ducts, but only a few if any lobules.

Like all cells of the body, a man’s breast duct cells can undergo cancerous changes. But breast cancer is less common in men because their breast duct cells are less developed than those of women and because their breast cells are not constantly exposed to the growth-promoting effects of female hormones.

diagram of the internal structure of the breast

The lymph (lymphatic) system of the breast

The lymph system is important to understand because it is one of the ways that breast cancers can spread. This system has several parts.

Lymph nodes are small, bean-shaped collections of immune system cells (cells that are important in fighting infections) that are connected by lymphatic vessels. Lymphatic vessels are like small veins, except that they carry a clear fluid called lymph (instead of blood) away from the breast. Lymph contains tissue fluid and waste products, as well as immune system cells. Breast cancer cells can enter lymphatic vessels and begin to grow in lymph nodes.

Most lymphatic vessels in the breast connect to lymph nodes under the arm (axillary nodes). Some lymphatic vessels connect to lymph nodes near the breast bone (internal mammary nodes) and either above or below the collarbone (supraclavicular or infraclavicular nodes).

diagram of the lymph nodes of the breast

It’s important to know if the cancer cells have spread to lymph nodes. If they have, there is a higher chance that the cells could have gotten into the bloodstream and spread (metastasized) to other sites in the body. This is important to know when you are choosing a treatment. The more lymph nodes with breast cancer cells (positive lymph nodes), the more likely it is that the cancer might be found in other organs as well. Still, not all men who have positive lymph nodes develop metastases, and in some cases a man can have negative lymph nodes and later develop metastases.

Benign breast conditions

Men can also have some benign (not cancerous) breast disorders.

Benign breast tumors

There are many types of benign breast tumors (abnormal lumps or masses of tissue), such as papillomas and fibroadenomas. Benign breast tumors do not spread outside the breast and are not life threatening. Benign tumors are common in women but are very rare in men.


Gynecomastia is the most common male breast disorder. It is not a tumor but rather an increase in the amount of a man’s breast tissue. Usually, men have too little breast tissue to be felt or noticed. A man with gynecomastia has a button-like or disk-like growth under his nipple and areola, which can be felt and sometimes seen. Although gynecomastia is much more common than breast cancer in men, both can be felt as a growth under the nipple, which is why it’s important to have any such lumps checked by your doctor.

Gynecomastia is common among teenage boys because the balance of hormones in the body changes during adolescence. It is also common in older men due to changes in their hormone balance.

In rare cases, gynecomastia occurs because tumors or diseases of certain endocrine (hormone-producing) glands cause a man’s body to make more estrogen (the main female hormone). Men’s glands normally make some estrogen, but it is not enough to cause breast growth. Diseases of the liver, which is an important organ in male and female hormone metabolism, can change a man’s hormone balance and lead to gynecomastia. Obesity (being extremely overweight) can also cause higher levels of estrogens in men.

Some medicines can cause gynecomastia. These include some drugs used to treat ulcers and heartburn, high blood pressure, and heart failure. Men with gynecomastia should ask their doctors if any medicines they are taking might be causing this condition.

Klinefelter syndrome, a rare genetic condition, can lead to gynecomastia as well as increase a man’s risk of developing breast cancer.

Breast cancer general terms

Here are some of the key words used to describe breast cancer.


This is a term used to describe a cancer that begins in the lining layer (epithelial cells) of organs such as the breast. Nearly all breast cancers are carcinomas (either ductal carcinomas or lobular carcinomas).


An adenocarcinoma is a type of carcinoma that starts in glandular tissue (tissue that makes and secretes a substance). The ducts and lobules of the breast are glandular tissue (they make breast milk in women), so cancers starting in these areas are sometimes called adenocarcinomas.

Carcinoma in situ

This term is used for an early stage of cancer, when it is confined to the layer of cells where it began. In breast cancer, in situmeans that the abnormal cells remain confined to ducts (ductal carcinoma in situ, or DCIS). These cells have not grown into (invaded) deeper tissues in the breast or spread to other organs in the body. Ductal carcinoma in situ of the breast is sometimes referred to as non-invasive or pre-invasive breast cancer because it may develop into an invasive breast cancer if left untreated.

When cancer cells are confined to the lobules it is called lobular carcinoma in situ. This is not actually a true pre-invasive cancer because it does not turn into an invasive cancer if left untreated.

Invasive (infiltrating) carcinoma

An invasive cancer is one that has already grown beyond the layer of cells where it started (as opposed to carcinoma in situ). Most breast cancers are invasive carcinomas, either invasive ductal carcinoma or invasive lobular carcinoma.

Types of breast cancer in men

Ductal carcinoma in situ (DCIS)

In DCIS (also known as intraductal carcinoma), cancer cells form in the breast ducts but do not grow through the walls of the ducts into the fatty tissue of the breast or spread outside the breast. DCIS accounts for about 1 in 10 cases of breast cancer in men. It is almost always curable with surgery.

Infiltrating (or invasive) ductal carcinoma (IDC)

This type of breast cancer breaks through the wall of the duct and grows through the fatty tissue of the breast. At this point, it can spread (metastasize) to other parts of the body. At least 8 out of 10 male breast cancers are IDCs (alone or mixed with other types of invasive or in situ breast cancer). Because the male breast is much smaller than the female breast, all male breast cancers start relatively close to the nipple, so they are more likely to spread to the nipple. This is different from Paget disease as described below.

Infiltrating (or invasive) lobular carcinoma (ILC)

This type of breast cancer starts in the breast lobules (collections of cells that, in women, produce breast milk) and grows into the fatty tissue of the breast. ILC is very rare in men, accounting for only about 2% of male breast cancers. This is because men do not usually have much lobular tissue.

Lobular carcinoma in situ (LCIS)

In LCIS, abnormal cells form in the lobules, but they do not grow into the fatty tissue of the breast or spread outside the breast. Although LCIS is sometimes grouped with DCIS as a type of non-invasive breast cancer, most breast specialists think it is a risk factor for developing breast cancer rather than a true non-invasive cancer. As with invasive lobular carcinoma, LCIS is very rare in men.

Paget disease of the nipple

This type of breast cancer starts in the breast ducts and spreads to the nipple. It may also spread to the areola (the dark circle around the nipple). The skin of the nipple usually appears crusted, scaly, and red, with areas of itching, oozing, burning, or bleeding. The fingertips can be used to detect a possible lump within the breast.

Paget disease may be associated with DCIS or with infiltrating ductal carcinoma. It accounts for about 1% of female breast cancers and a higher percentage of male breast cancers.

Inflammatory breast cancer

Inflammatory breast cancer is an aggressive, but rare type of breast cancer. It causes the breast to be swollen, red, warm and tender rather than forming a lump. It can be mistaken for an infection of the breast. This is very rare in men.

Debbie Knight Raises money doing the Moonlight Colourthon

One of our Twitter followers has kindly agreed to do the Moonlight Colourthon (details Below) Debbie Knight @debsknig will be doing this on the 7-7-12. If you would like to join her or sponsor her please do here

Moonlight Colourthon

This has been our flagship event but to celebrate and enhance its success this year we’re launching our brand new ‘Twilight Colourthon’ 10k walk.
The ‘Moonlight Colourthon’ is in essence a sponsored walk with a difference. Walkers walk a half marathon (13.1 miles) at night and are encouraged to dress as brightly as their imagination will allow them to! This year’s events set off from Chalkwell Park at 8pm on Saturday 7th July, 2012. It takes in the waterfront along Southend Seafront and Westcliff’s picturesque cliff tops with their brisk sea breezes, drops down overlooking the famous pleasure pier and then travels through the exclusive Chalkwell Hall Estate, past Old Leigh Village with its quaint cottages and fisherman’s sheds returning back through Leigh itself, finishing back at Chalkwell Park.

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  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

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

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


Middlesex, UB8 3PH

Tel: 01895 266293


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.




  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.