The public generally believes that cancer is not contagious, so the tragic characters in romantic movies and TV dramas will suffer from various types of leukemia, stomach cancer and brain tumors, not swine flu, which is a powerful and rustic infectious disease. Relatives and friends did not give up and did not wear masks, hugged and kissed with patients and ate kimchi together, not worried that the plot would go to Train to Busan.
So, is cancer really not contagious?
Movies are right.
…unless the tragic protagonists are long-lost siblings. That involves extreme cases.
It is true that healthy people do not easily “infect” cancer from cancer patients, but, in extreme cases, it is possible for cancer to be passed from one person to another and continue to grow and develop in the new body.
In some special cases, cancer cells can indeed enter another individual to make waves
one transplant,
Four patients ‘infected’ with breast cancer
A 53-year-old female organ donor donated kidneys, lungs, livers and hearts for transplants after she died in 2007 of a stroke (aka “stroke”). After 16 months, the woman with the lung transplant found herself with a tumor that had spread to the lungs, bones and mediastinal lymph nodes. She died a year later. Analysis of specific DNA sequences revealed that these metastatic cancer cells came from the original donor.
The medical staff was surprised.
According to regulations, people with aggressive and active malignant cancer are not allowed to donate organs. The donor has no detectable cancer and no cancerous tissue is found in a comprehensive physical examination, which includes a general physical examination, laboratory Laboratory tests, abdominal and cardiac ultrasounds, chest X-rays, and bronchoscopy. But the medical staff did not know at the time that there were undetectable cancer cells hidden in the donated organs.
They contacted other transplant recipients who were still alive for tests. The results were very unfortunate: two women who had their left kidney and liver transplanted were also diagnosed with cancer in their bodies, and died of cancer a few years later. A 32-year-old male patient who received a right kidney transplant also had metastatic breast cancer cells detected in his body in 2011, and received a series of treatments for it. As of follow-up in April 2017, the patient was alive and awaiting another kidney transplant.
This extreme case is the first to be reported in a 2018 paper published in the American Journal of Organ Transplant (Am J Transplant) in which multiple recipients develop tumors from a single donor.
In this case, the cancer cells were able to evade inspection at the time of transplantation, probably because the cancer tissue in the donor was too small to be detected by conventional means, but had already metastasized and was hiding in the transplanted organ waiting for an opportunity.
Such free tumor cells are not uncommon. In stage 1 breast cancer, there may already be circulating tumor cells that travel with the bloodstream, and some cancer screenings that use blood rather than tissue biopsies are based on this.
When the immune system is suppressed,
Cancer has an opportunity
Under normal circumstances, the chance of a solid tumor (compared to “liquid tumors” of blood and bone marrow cancers) due to transplantation is 0.01% to 0.05%, that is, no more than 5 in 10,000, which means that at the time of organ transplantation The preventive inspection methods are basically effective. Several studies in the UK have shown that hundreds of organs donated by cancer patients did not bring cancer to recipient patients, which means that some organs from cancer patients may also be used for transplantation, so there is the potential to expand the organ resource.
More than 1.5 million people are waiting for an organ transplant in China, and more than 100,000 people are on the waiting list in the United States. According to the statistics of the World Health Organization (WHO), the ratio of patients who need organ transplants to donated organs is 20:1, and there is still a huge gap. So, if the cancer isn’t contagious, it’s very meaningful news for patients waiting for a transplant.
However, the cancers in the donors in these studies in the UK are mainly primary brain tumors, which are not likely to metastasize to other organs, so patients with cancers in other tissues will still be limited in donating organs.
Less likely to get cancer from transplant, but still be very cautious about donating organs
But in those cases that did develop cancer from the transplant, why didn’t the cancer cells thrive in the donor’s body until they were transplanted? A very important reason is that there is no immune system monitoring at this time – recipients who receive transplants need to use immunosuppressive drugs to suppress their immune rejection.
The immune system is the body’s built-in defense system that recognizes and defends against foreign substances – such as viruses and bacteria. For something like a transplanted organ, the immune system does not know that it is here to save lives, and it will recognize it as a foreign substance to attack, resulting in transplant rejection. To help the body accept a transplanted organ, the patient’s own immune system needs to be suppressed, often with drugs and sometimes surgery.
The internal defenses are suppressed, and it is the right place for cancer cells to take advantage of the opportunity.
In addition to immunosuppressed patients, there are also some groups of people who are at higher risk of being “infected”, including immunocompromised infants and young children, or people with immune deficiencies (such as AIDS patients).
Thanks to the immune system,
Talents are not easily defeated by cancer cells
Since the discovery of proto-oncogenes in the 1970s, the understanding of the biomolecular roots of cancer has advanced by leaps and bounds. Cancer is essentially caused by genetic abnormalities. A healthy adult has millions of cells being replaced every minute. With such a large number of replications and divisions, it is normal for some genes to go wrong during the replication process.
There are many factors that can cause genetic problems and eventually lead to cancer. Basically, they are the things that make the fat house happy… Including excessive sun exposure (skin cancer), smoking (lung cancer), drinking (liver cancer), masturbation (stomach cancer and bowel cancer), drinking milk tea (diabetes and pancreatic cancer), and getting older (various types of cell division errors accumulating cancer).
Why is the world so dangerous, yet we are not covered with tumors like Rei Kawakubo’s “Lump” series? Because the immune system can not only recognize bacteria and viruses and the kidney of the king next door, but also recognize the “non-self” in the body – such as cancer cells.
The “Lump” series is the work of Japanese fashion designer Rei Kawakubo in 1997.
Irregular stuffing in different parts of
The human immune system is divided into innate immunity and adaptive immunity. Innate immunity is fast and ferocious, and can directly recognize and destroy pathogens, including bacteria, viruses, fungi, parasites, and abnormal cells. Cancer cells are quite abnormal. Cells like NK cells (natural killer cells) can kill cancer cells. The adaptive immune system, on the other hand, recognizes objects through the response of antigens and receptors. Killer T cells are a type of T cells that kill cancer cells, virus-infected cells, and other damaged cells.
But many people who seem to be in good health and have no immune system deficiencies also develop cancer.
Why can’t the immune system completely destroy its own cancer cells?
One possibility is that cancer cells originate within themselves, and that cells that regulate immune responses may identify themselves as “self” and prevent killer T cells from attacking them, avoiding the abuse of police power against civilians.
Another possibility is that cancer cells falsify their identities so that the immune system does not recognize them. Each cell has its ID card (specific protein antigen on the surface), those without ID cards will be cleared by NK cells, and those without ID cards will be cleared by T cells. Scientists have found that cancer cells can downregulate surface antigens, blur the photos on ID cards, and become uncharacteristic Internet celebrities, which can sometimes escape the siege of NK cells and T cells.
Another reason is that cancer cells have evolved special means to suppress the killing of the immune system. The human body itself has a reverse regulation mechanism for the immune system, that is, “brakes” such as immune checkpoints. If the brakes on T cells are pressed, the activity of the immune system can be suppressed. Cancer cells take advantage of this by expressing proteins that put the brakes on to evade T-cell clearance. After scientists discovered this, they used drugs to prevent cancer cells from stepping on the brakes, so that T cells could be unrestrained and have an attack power of +999, which brought great clinical benefits and long survival to cancer patients. “Cancer therapy by modulating immune checkpoints”, Bell Prize in Physiology or Medicine.
Fights spread cancer cells
Can cancer be transmitted under any circumstances other than transplantation? Technically, there are, and there are two other routes of infection, but the mechanisms are very different.
The first is that the cancer itself is transmitted among individuals with very similar immune backgrounds. Scientists have discovered this phenomenon in devils.
The Tasmanian devil is a marsupial carnivore that is now only distributed in Tasmania, Australia, so it is also commonly known as the “Tasmanian Devil”. They look like a cross between a mouse and a bear. They are not big and temperamental. They hunt for food, occupy land, and even mate.
Tasmanian devils are grumpy animals
Tasmania’s devils existed 14,000 years ago, isolated on isolated islands because of rising sea levels, so the kinship of extant devils is a bit muddled. More than a decade ago, spot monitoring found that tens of thousands of Tasmanian devils were suffering from facial tumors (DFTD), which are distributed in the face, head and neck, and mouth of the devil, making it difficult for them to eat. Affected devils mostly die within 12 to 18 months, reducing their numbers by an estimated 80%, reaching a staggering 90% in some areas!
Ten rooms and nine empty spaces, this is very scary, is this cancer contagious? Scientists sampled and studied and found that the facial tumors of these devils have the same genetic characteristics-the characteristic of cancer cells is that they are unruly. The tumors of all have the same karyotype, indicating that it is likely to originate from the same devil. Subsequent DNA analysis and others have supported this speculation.
Scientists speculate that it may be because these tumor cells are not tightly combined, they fell into each other’s facial wounds during the daily tearing of the Tasmanian badgers, and took root and grew on the faces of the Tasmanian badgers, making the whole group look like Very hardcore. No matter how you look at it, this is the “contagion” behavior of cancer cells to achieve the achievement of Shattering the Void and spread from one individual to the next.
This type of tumor (DFT1) originated in the neurites of a female devil’s devil and spread across the island. A second type of Tasmanian devil facial tumor (DFT2) that was later discovered originated in male devils and was mainly confined to the southeastern region of the island.
More than 350 papers have been published on Tasmanian facial tumors since they were reported in 1996. Interestingly, while the karyotype of cancer cells is often unstable, the genome of DFT1 achieves a certain homeostasis that allows it to maintain its identity during long-term dissemination. This homeostasis is absent in most tumors.
Most devils affected by facial tumors die within a year or so.
In addition to Tasmanian devils, scientists have found contagious cancers in two other animals, a canine transmissible venereal tumor in dogs and an artificial tumor spread in laboratory hamsters. The former, similar to the Tasmanian devil’s DFT1, also showed some kind of chromosomal stability in the transmission of more than 10,000 years, which shows that even for the tattered tumor genome, the evolutionary survival pressure can be screened out. The most important survival gene.
But don’t panic. Cancer cells are actually very fragile things outside the body. Individual cells are fragile outside the body and are too easy to kill. The transmission route of Tasmanian Facial Tumors requires a large number of cancer cells to be exchanged, and then surviving cancer cells enter the wound of the infected target. Most importantly, the genotype of the recipient must be sufficiently similar to that of the donor—for example, isolation Inbreeding on isolated islands for thousands of years – allowing cancer cells to take root and grow in new environments.
XKCD’s comic “Bullet has the best anti-cancer effect” brilliantly describes why means that have anti-cancer activity/killing cancer cells in vitro are not necessarily clinically useful.
For humans, it is unlikely that cancer will be transmitted from passers-by. Even if there are close relatives of siblings who have cancer, as long as they don’t play fight club with them, it should be said that there is almost no possibility of infection – unless there is a scientist doing something. .
Doctors at Northwestern University in Chicago have been documented to have transplanted a 50-year-old woman’s melanoma into her 80-year-old mother “for the sake of science”…
It was a dark age when biomedical ethics had not yet been fully developed, and there was a lack of supervision on human experiments. At that time, it was also the era of rapid development of organ transplantation. In 1954, the first successful living-donor kidney transplant was performed, and the first heart transplant was performed in 1967. . The experiment, conducted in 1961, was also intended to understand the effects of cancer at different stages on transplantation. Sadly, the daughter died of intestinal perforation a day later. The mother also died 15 months later, and the melanoma had ravaged her body and had metastasized to the lungs, ribs, lymph nodes and diaphragm.
In this case, the daughter and mother were genotypes similar enough to allow for the tumor, and the mother was old enough to survive. This kind of experiment should never happen again.
Viruses can also be the culprits of cancer
The second way of “infection” of cancer is more indirect, that is, through the transmission of cancer-causing viruses. But if you want to pick words, it’s just carcinogens spreading here, and the cancers they cause are not contagious themselves.
In 1909, Peyton Rous, who was working at the Rockefeller Institute in New York, USA, studied a reed chicken that has been famous in history. He removed tumors from chickens, injected tumor filtrate into other hens, and found that he induced tumors in healthy hens. It was later found that the tumor was caused by a retrovirus called Rous sarcoma virus (RSV), and it was the first time in human history that cancer could be transmitted by viral infection.
Subsequent studies found that RSV can cause cancer because it contains a sequence stolen from the genome of chicken cells. This sequence, originally responsible for regulating cell growth and proliferation, was stolen and turned into an oncogene. When RSV replicates in the host, it can integrate its own genetic information into the host’s genome. At this time, it is like a random connection. In many cases, this road is blocked, so it is harmless, but sometimes it just places the oncogene in a strong Under the switch, the cells grow out of control, which may eventually form cancerous tissue.
Studies have shown that retroviruses can cause a wide range of cancers in chickens, mice, cats, monkeys and other vertebrates. Humans are not immune. There have been reports that two viruses are associated with a certain human lymphoma and prostate cancer, but the chances of infection are very low.
Compared with these two retroviruses, one virus has a clearer relationship with cancer, that is, human papillomavirus (HPV), which can induce cervical cancer.
According to WHO statistics, cervical cancer is the second most common cancer in women worldwide. While most HPV infections do not cause any symptoms, persistent HPV infection can lead to abnormal cervical cell production, which in a certain percentage has the potential to develop into cervical cancer. It is estimated that 99% of cervical cancers are associated with HPV infection. HPV is mainly spread by contact, and in addition to cervical cancer, it can also cause other types of cancer in both men and women, including anal, genital, head and neck cancers, and genital warts. Therefore, regardless of gender, HPV vaccination before having sex for the first time is effective in preventing these cancers—not the cancer itself, but the viral infection that causes the cancer.
However, some preclinical cancer vaccine studies have shown extremely encouraging results, and in a few years, some cancers themselves may be vaccine-preventable.
All in all, cancer is not transmitted to healthy people with large individual differences, and immunocompromised people are at certain risk. Certain infectious viruses may cause cancer, but the cancer itself is not infectious. If regenerative medicine is further developed and the source of organs is further expanded, “cancer due to organ transplantation” will become a thing of the past.
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