ONE-ONE-ONZE

Are antiprotons a viable alternative

for proton therapy in cancer
treatment?

Viability analysis in antiproton therapy for treating cancer

Radu Bolborea1, Andrei Borcoman 2, Luciana Murăreanu3, Matei Pleșcan4,

Ioana Popa2, Iancu Scurtu5, Andrei Știrbu 6
1
Colegiul Național „Ion Minulescu” Slatina, 2Colegiul Național „Andrei Șaguna” Brașov, 3Liceul
„Regina Maria” Dorohoi, 4Colegiul Național Iași, 5Colegiul Național „Petru Rareș” Piatra Neamț,
6
Colegiul Național „Vasile Lucaciu” Baia Mare

Special thanks to our professors and our coach:

Cătălin Agheorghiesei 7, Daniel Radu7, Alexandra Ioana Popa7
7
Universitatea „Alexandru Ioan Cuza” din Iași

1
Contents:
1. Introduction 3
1.1 About us and why we want to come to CERN 3
2. Experiment idea 3
2.1. Our idea 3
2.2. Theoretical background 3
2.2.1. Bragg Peak 3
2.2.2. Why antiprotons? 3
2.3. The target and our simulations 5
2.4. Experimental setup 6
3. Challenges for antiproton therapy 6
4. Conclusions 7
5. References 7

2
1. Introduction
1.1 About us and why we want to come to CERN
We are a group of seven high-school students living in different cities from all of Romania. What
brings us together? Our shared love for science! After meeting at the RO-HSSIP 2021, we reunited
willing to take on another challenge: the BL4S competition.

Although coming from different backgrounds, all of us are passionate about the way different
scientific areas combine in order to solve real-life problems. Therefore, we were all thrilled to
discover radiotherapy as the bridge between anatomy, particle physics and engineering. After
researching proton therapy, we wondered if we could find a more viable approach for cancer treatment
and came across antiprotons. By implementing our experiment at CERN we want to test the feasibility
of our idea, while getting to learn from experienced scientists.

2. Experiment idea

2.1. Our idea

We are going to shoot a beam of antiprotons at a simulated tumor, hoping that when coming in contact
with the tumor, they will disintegrate each other. Moreover, the energy released by the particles will
damage the surviving cancerous cells, rendering them nonfunctional and potentially dead. We aim to
compare the energy release of antiprotons at their Bragg Peak with that of protons and other particles.
If the deposited dose is bigger, the potential of the beam killing the cancerous cells is higher.

2.2. Theoretical background

2.2.1. Bragg Peak

When fast charged particles move through matter, they deposit energy along the path. Just before the
particles come to a complete stop, a peak with maximum energy deposition occurs. This is called the
Bragg Peak.

2.2.2. Why antiprotons?

Just like protons and heavy ions, antiprotons can be used to deliver radiation to the human body in a
controlled way for therapeutic purposes. Although antiprotons travel through human tissue in a similar
manner to protons, when reaching their Bragg Peak they annihilate and deposit twice the dose of
energy of protons (Figure 1). Therefore, the effectiveness might be increased by using antiprotons
instead of protons.

3
Antiprotons behave like protons on their way to the tumor, creating free electrons and free radicals
that are distributed thinly along the track, posing a low risk to the cells on the path [1]. In the tumor,
however, antiprotons create DNA damage, leading to the permanent deactivation of the cell. At
annihilation, an antiproton leads to the emission of 3-5 pions (Figure 2) that share its annihilation
energy, and if one or more of these pions enter the nucleus of the target cell, an intracellular collision
cascade would occur, leading to the emission of many heavy ions. Fortunately, however, due to the
low energy emitted by these secondary ions, the damage created by them stays within the “endpoint
voxel” [1].

According to the ACE experiment [1], the biologically effective dose ratio of antiprotons is 3.75 ±
0.50 larger than the one of protons. This factor is truly significant: increasing the dose administered to
prostate cancer by a factor of 1.5 increases the tumor control probability from 15% to 95%.

4
2.3. The target and our simulations
In our experiment, we chose to use epoxy resin as the target for the antiproton beam since it simulates
well biological tissue if mixed with the proper chemicals (phenolic microspheres, calcium carbonate,
and pulverized bull bone) [6].

We decided either to place a metallic shield [5] before the target or to use the Antiproton Decelerator
at CERN [8], in order to reduce the high energy of the beam (0.5 GeV) so the Bragg Peak won’t occur
outside the so-called “human body”.

We performed simulations using SRIM to determine the necessary width of the metallic shield so the
Bragg Peak occurs at a depth of 10 - 15 cm inside the epoxy-resin target (approximate depth of a
tumor inside a patient). Due to the lack of antimatter particles in the software, we used protons for this
calculation, since protons and antiprotons share the depth of their Bragg Peak for a given energy [7]
[8].

As can be seen from Figure 3, a layer of 32 cm of Titanium or a layer of 47 cm of Aluminum leads to

a Bragg Peak at a depth of approx. 12 cm inside the epoxy-resin target [5]. As shown in Figure 4, the
results obtained for epoxy resin are comparable with the ones for a simulated stomach tissue.

5
2.4. Experimental setup
Our experiment will consist of an analysis of the Bragg Peak (using dosimetry methods), measured in
our probe for different energies of the antiprotons. Next, we will analyze antiproton annihilations
using the calorimeters and other trackers which surround the target. With this information, we will be
able to quantify the advantages and disadvantages of our method, in order to respond to our question:
is antiproton therapy viable?

Except for the fixed setup, we will use:

● MRPC for ToF measurements (to determine the velocity and energy of exiting antiprotons)
● Metallic shield
● Our probe
● A set of calorimeters and other available trackers around the probe
● MicroMegas detector for tracking remaining particles
● Calorimeter

3. Challenges for antiproton therapy

When traversing tissue, some
particles are “removed from the
beam” either due to elastic or
inelastic scattering on target
nuclei or due to electronic
stopping. From Figure 6 [2], the
loss of antiprotons when passing
through water (a good mimic of
living tissue) is smaller than the
loss of 12C and 20Ne ions, but
bigger than the loss of protons.

6
4. Conclusions

Even though we were not able to come up with answers for all of our questions while writing our
proposal, we hope to test our hypotheses at CERN and to discover whether antiproton therapy really
has the potential to revolutionize the field of cancer treatment. We are confident that our method of
analysis will provide a concrete answer to the question with which we started our journey: are
antiprotons a viable alternative to proton therapy in cancer treatment?

5. References

[1] - Antiproton therapy - ScienceDirect

[2] - Cancer Therapy with Antiprotons
[3] - Antiproton induced DNA damage: proton like in flight, carbon-ion like near rest - J. N. Cavanagh
et al
[4] - Bragg Peak - a Harvard study
[5] - Nuclear stopping power of antiprotons - Kai Nordlund et al.
[6] - Construction and characterization of materials equivalent to the tissues and organs of the human
body for radiotherapy - Yemby Huamani T. et.al.
[7] - A systematic review of antiproton radiotherapy - Martin-Immanuel Bittner et. al.
[8] - Physics at CERN’s Antiproton Decelerator - M.Hori et. al.
[9] - Positron annihilation in aluminum at low and superlow temperatures - Troyo Dimov Troev
[10] - SRIM - Lessons and Tutorials