How does x ray kill cancer cells

Less often, a source of radiation may be put right into your body. It might be radioactive seeds or tubes that are put right into or as close to the cancer as possible.

Sometimes a radioactive medicine is swallowed ingested or put into your blood through a vein injected intravenously or IV. For instance:. Radioactive medicines can be injected into your blood to travel around your body and attach to and kill bone or liver cancer cells. An applicator that holds the radiation can be put next to a tumor through a body opening, like into the vagina to treat cervix or uterus cancer.

Internal radiation can be used to give a higher dose of radiation over a shorter time. And the radiation only travels a short distance, so it kills the cancer cells with little damage to nearby tissues. Some sources of the radiation stay in the body for only a short time.

Others, like seeds and radioactive medicines stay in the body forever. But the radiation gets weaker and is used up over time. Internal radiation does make you radioactive for a short time. You may have to stay in the hospital during treatment, or you may go home. Either way, you'll need to protect the people around you. Talk with your healthcare provider about the safety steps you need to take when getting this treatment.

To plan your treatment, you'll meet with a team of cancer specialists. This team might include a surgeon, radiation oncologist, and medical oncologist. A healthcare provider who specializes in treating cancer with radiation is called a radiation oncologist. This provider works with you and your cancer care team to decide how radiation will be used. External radiation is aimed as precisely at the tumor as possible. This is important to help keep nearby normal tissues from getting too much radiation.

You may also need the services of a dietitian, physical therapist, social worker, dentist or dental oncologist, pharmacist, or other health care providers. It has long been known that radiation therapy can slightly raise the risk of getting another cancer.

For the most part, the risk of a second cancer from these treatments is small and is outweighed by the benefit of treating the cancer, but the risk is not zero.

This is one of the many reasons each case is different and each person must be part of deciding which kind of treatment is right for them.

The risk is different depending on where the radiation treatment will be in the body. Still, this is your decision to make. Knowing as much as you can about the possible benefits and risks can help you be sure that radiation therapy is best for you.

If the area getting radiation in your body includes the ovaries, it is possible that the dose of radiation can cause the ovaries to no longer work sterility , and that you would be unable to have children. If you are thinking about radiation therapy that will affect the ovaries, talk to your doctor about how this might affect having children in the future. Because of this, doctors often advise men to not get a woman pregnant during and for some weeks after treatment.

Talk to your doctor to find out more about this. If the area getting radiation includes the testicles, it is possible that the dose of radiation can cause the testicles to no longer work sterility and that you would be unable to have children. It is important to know the risk of this possibility in advance of receiving radiation therapy. There is no clear research about how sperm that is exposed to radiation affects future children made from that sperm.

If you are thinking about radiation therapy that will affect the testicles, talk to your doctor about how this might affect having children in the future.

An element called gadolinium delivered into cancer cells releases killer electrons when hit by specially tuned X-rays. The approach, published in the journal Scientific Reports , could pave the way towards a new cancer radiation therapy. Conventional radiation therapies employ polychromatic X-rays, consisting of various energy levels, with low-energy X-rays failing to penetrate the body's surface.

Monochromatic X-rays, on the other hand, have the same precisely tuned energy level. If they could be aimed at electron-releasing chemical elements inside tumours, they could be damaging. To achieve this, the researchers used specially designed silica nanoparticles that were loaded with the chemical element gadolinium. The cancer cells in a 3D tumour culture effectively consumed the particles after one day of incubation. The particles specifically located just outside tumour cell nuclei, where their most critical machinery is found.

However, DNA damage response mechanisms represent a vital line of defense against exogenous and endogenous damage caused by radiation and promote two distinct outcomes: survival and the maintenance of genomic stability.

Radiation mainly acts in two ways. Multiple pathways are involved in the genome maintenance of a cell after its exposure to ionizing radiation. Radiation therapy like the most anticancer treatments achieves its therapeutic effect by inducing DNA damage and thereafter cell death Baskar et al. Several experiments were performed indicating that the DNA of cancer cells repair more slowly and also produce more DNA breaks single strand break and double strand breaks than the normal cells Parshad et al.

Therefore, ionizing radiation as applied in the cancer treatment induces a complex response in the cells. Some processes aim to repair the radiation induced damage of the normal cells, whereas others counteract the damage or induce cancer cell death. Growing evidence suggests that various signaling pathways including the DNA repair response pathways shows redundancy in normal cells Moding et al. Since cancer cells have various mutations that cause the loss of this redundancy and therefore targeting the DNA damage response pathways in the cancer cells can induce cell death.

Radiation damages the genetic material DNA causing single strand breaks SSB or double strand breaks DSB in the cells, thus blocking their ability to divide and proliferate further. Mechanisms involved in the decrease of radiosensitivity of the fast doubling cancer cells, while increasing radioresistant of the slow doubling normal cells benefits the cancer patients. However, whether p53 induces apoptosis or cell cycle arrest for the DNA damage repair is a complex process and partly depends on the abundance of the p53 protein low protein levels lead to cell cycle arrest and high protein levels lead to apoptosis Lai et al.

However, various DNA repair mechanisms within the tumor cells interfere with the radiation induced damage and further increase the radioresistance of cancer cells Jorgensen, Besides the DNA repair pathways, ionizing radiation also triggers cancer cells adaptive cellular responses. Various treatment resistant signal transduction pathways are activated and the resistance can be either intrinsic or an acquired resistance during the fractionated radiation treatment Toulany and Rodemann, Signaling pathways that provide cancer cells with a proliferative advantage or allow them to evade the cell death remains a major clinical problem.

One of the molecular events by which tumors can become radioresistant is through the ligand-independent activation of signal transduction pathways such as those regulated by membrane-bound receptor tyrosine kinases RTKs. These pathways control the most hallmarks of cancer, including cell cycle, survival, metabolism, invasion, angiogenesis, and genomic instability Datta et al. Among the prosurvival pathways activated by RTKs, PI3K-AKT-mTOR signaling pathway is frequently upregulated in human tumors and regarded as one of the most challenging prosurvival pathways involved in the resistance to cancer treatment Engelman, ; Liu et al.

Furthermore, improvement in preclinical methods for the biological mechanisms involved in signaling pathway s for the treatment resistance, cell cycle checkpoints, DNA damage and repair, anti-angiogenesis could increase the therapeutic response of tumor microenvironment, while sparing the surrounding normal tissues.

Furthermore, inhibition of the cancer cell survival could also affect the radiosensitivity of normal tissues as well, thus decreasing the overall therapeutic index of radiation.

Therefore, strategies to improve radiation therapy to increase the effect on tumor while less toxicity on the normal tissues should be achieved without sensitizing the normal tissues and also without protecting the tumors to the radiation treatment. Cancer therapy usually involves exposing the body to agents that kill cancer cells more efficiently than the normal cells.

Recent advances in radiation biology and oncology have demonstrated that the radiation is an effective tool to control the localized tumors. Ionizing radiation induces DNA damage in the form chromosomal aberrations were first reported not only in the directly exposed cells but also in their neighboring non-irradiated cells, termed as radiation-induced bystander effect RIBE Nagasawa and Little, Therefore, the discovery of non-targeted responses to radiation, such as the bystander response, has called the direct radiation effect paradigm into question.

Various biological effects of ionizing radiation are not restricted to only the directly irradiated cells targeted effects , but are also observed in the progeny of non-irradiated cells non-targeted effects Bensimon et al. RIBE has been demonstrated in numerous in vitro and in vivo studies using a variety of biological endpoints.

These effects include various molecular and genomic instabilities as seen in the targeted cells. Bystander effects has been extensively studied in the past two decades and reported cell death Seymour and Mothersill, , induction of sister chromatid exchanges Nagasawa and Little, ; Deshpande et al.

Schematic representation of bystander effects induced by radiation to the adjacent cells and distanced organs. Radiation can cause chromosomal aberrations arising de novo in the cell progeny, several generations after irradiation.

Delayed genomic instability has been observed in many types of mammalian cells Ponnaiya et al. Therefore, communication between cells and their microenvironment is critical for both normal tissue homeostasis and tumor growth. RIBE has important implication in tumor control and in radiation therapy, wherein the targeted directly irradiated cells transmit the damaging signals to the non-irradiated normal cells, thereby inducing a response similar to that of directly irradiated cells Mothersill and Seymour, ; Shao et al.

Two major mechanisms mediate RIBE. Recently, Jiang et al. RIBE has an important implication in radiation therapy and its impact in radiation oncology is gradually beginning Munro, RIBE is also reported using mouse model, the bystander responses of internal tumor cells or tissues were also confirmed in vivo , further cancer-associated events such as p53 alteration, MMPs Matrix metalloproteinases activity and epigenetic changes were reported in the RIBE Camphausen et al. BE can be mediated through an increase in genomic instability, cell cycle delay, cell death apoptosis , formation of micronucleus, mutations, changes in proteins gene expression, and further by malignant transformation Nagasawa and Little, ; Hickman et al.

However, the components released from the irradiated cells and further the communication signals involved between the irradiated and non-irradiated cells are still not well known. Recently, Bensimon et al. Recently Aravindan et al. However, little is known about the type of DNA damage of the bystander cells, its radiation resistance and further damage of non-targeted normal cells contributing to tumorigenesis and how this damage can be repaired by designing novel therapeutic approaches to cancer treatment paves a way for an effective strategy to compact the disease.

Though tremendous progress has been made toward understanding the hallmarks of cancer, cancer is responsible for one in eight deaths worldwide Garcia et al. Despite the use of chemotherapy, radiation therapy and surgery, the overall outcome for cancer cure continues to be disappointing. Radiation therapy offers an effective treatment for advanced cancer and the prime goal of radiation treatment is to inhibit the cancer cells multiplication potential and eventually kill the cells.

Certain tumors are intrinsically radioresistant, while others acquire radioresistance during the treatment Seiwert et al. To overcome the tumor cell radioresistance, it will be a challenging one to identify tumor specific pathways and inhibitors. In the past few years, enormous progress has been made in radiation therapy leading to the possibility of depositing more radiation energy proton beam radiation therapy, e.

We do not have a comprehensive answer about the molecular mechanisms involved in the initiation of cancer, developing resistance to treatment and further individual variations in treatment susceptibility, especially of therapy-related beneficial or detrimental effects. In a microenvironment, cancer cells are influenced by various growth signaling pathways to resist the radiation effects and further modify the adjacent normal tissues to impede tumor recurrence or metastasis.

Overall, small increase in radioresistance will lead to a large number of cancer cell survivals and further the proliferation forms cancer mass and with a logarithmic decrease in cancer cell death after radiation treatment. Therefore, in the coming years more thrust should be given on the cancer cells radioresistance, e. Furthermore, with a greater understanding of the tumor biology, evolution of radiation therapy will continue with the improvements in imaging, computing and engineering advancements, and potentially decimate the cancer cells with fewer side effects.

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. I am indebted to Dr. Kothandharaman Subramanian for his critical editorial comments and help in the preparation of this manuscript.

National Center for Biotechnology Information , U. Journal List Front Mol Biosci v. Front Mol Biosci. Published online Nov Author information Article notes Copyright and License information Disclaimer. Louis, USA. This article was submitted to Cellular Biochemistry, a section of the journal Frontiers in Molecular Biosciences. Received Jul 11; Accepted Oct The use, distribution or reproduction in other forums is permitted, provided the original author s or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice.

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