A case of Cancer that transferred from the Patient to the Surgeon
Cancer…one of the most, if not THE MOST interesting medical conditions you can have! Dating back to ancient Egypt some 3000 years ago, cancer remains an elusive disease that spreads like…well, cancer. Before I present this case, let us remind ourselves what cancer is.
Cancer is a group of diseases involving abnormal cell growth with the potential to invade or spread to other parts of the body in a process known as metastasis.
There are a lot of types of cancer, with the most common being:
Lung, breast, prostate, colorectal, skin, pancreatic cancer, and leukemia.
Lung cancer is like that friend who always mooches your cigarettes and then blames YOU for the smoke. It's the unpaid tenant in your chest, redecorating with tumors instead of paying rent.
Breast cancer is the shady contractor who convinces you to remodel, only to tear down the whole house. It's the betrayal of your own body, turning the honka honkas against you in the worst way possible.
Prostate cancer is the prankster who keeps hitting the wrong nerve, turning every bathroom break into a twisted game of Russian roulette.
Colorectal cancer is the uninvited guest at your dinner party, spilling blood everywhere and turning your toilet into a crime scene. It's the macabre masterpiece of your digestive tract.
Melanoma is the tan that comes with a price tag, turning your beach vacation into a deadly lottery. It's like your skin decided to rebel against its sun-kissed status and go full vampire.
Pancreatic cancer is the ninja assassin of cancers, striking silently and swiftly without warning. It basically has the black belt in taking you down without you even realizing there was a fight.
Leukemia is the coup d'état of your bloodstream, overthrowing order and turning your veins into a battlefield. It's the revolution that doesn't care how many good cells it destroys in the process.
There are a couple of ways cancer can spread:
Invading nearby normal tissue like a freeloading relative who won't take a hint, going full ape shit and smashing through the walls of lymph nodes and blood vessels, hitchhiking through the lymphatic system and bloodstream like a demented road trip, stopping in small blood vessels at some poor, unsuspecting location, breaking through the vessel walls and squatting in the surrounding tissue, growing into a tiny tumor like an unwanted gremlin, and demanding new blood vessels to sustain itself, turning your body into its personal horror show amusement park.
All of these contrast with benign tumors, which do not spread. In other words, a tumor is just a clump of abnormal cells, while cancer is a clump of abnormal cells that wants you to die.
Next time someone offers you a “free” ride home for the small price of injecting you with cancer cells, politely decline the offer and spend that 20 bucks on an Uber. Those 20 American dollars are affordable since the cost of 6 months of chemotherapy averages around 27000 dollars, with prices steadily increasing.
Okay, enough with the jokes.
Case report
A 40-year-old man underwent emergency surgery to remove a malignant tumor (more specifically, fibrous histiocytoma, but we’ll get to that) from his abdomen and died shortly after that of postoperative complications.
During the operation, the 41-year-old surgeon injured the palm of his left hand while placing a drain. Even though the lesion was immediately disinfected, five months later, the surgeon consulted a hand specialist because of a hard, tumor-like swelling at the base of the middle finger, the exact place where he had been injured during the operation.
The tumor was completely excised, and histologic examination revealed that it was the same type of tumor previously found on the man- a malignant fibrous histiocytoma. Two years later, the surgeon's condition was good, and there was no evidence of recurrence or metastasis of the tumor.
The pathologist who investigated both the patient's and the surgeon's tumors raised the question of whether the tumors were identical.
An extensive examination, including laboratory and genetic tests, proved that the tumors were indeed the same, but how could this happen?
Let me explain.
Normally, when you transplant tissue from one person to another, the recipient’s immune system throws a tantrum and rejects it like a nephrology department rejects kidneys from an Albanian organ donor. In this surgeon's case, there was a dramatic inflammatory meltdown around the tumor, but instead of getting the hint and leaving, the tumor “stood on business” and grew even bigger.
The tumor might have managed this creepy feat through some sinister methods:
- Switching up its major histocompatibility complex class I molecules like a pedophile switching up when caught in the woods waiting for a date with a 13-year-old.
- Hiding its tumor antigens like a body under the floorboards or
- Skimping on antigen processing like a lazy undertaker
Loss of major histocompatibility complex 1 is a frequent occurrence in many cancers.
MHC class I molecules are one of two primary classes of major histocompatibility complex molecules (the other being MHC class II) and are found on the cell surface of all nucleated cells in the bodies of vertebrates.
Their function is to snitch peptide fragments of proteins from within the cell to cytotoxic T cells, which are a type of white blood cell that attack various foreign microorganisms. This triggers an immediate response from the immune system.
Class I MHC molecules bind peptides generated mainly from the degradation of cytosolic proteins by the proteasome, a protein complex that degrades unneeded or damaged proteins by proteolysis, which is a chemical reaction that breaks peptide bonds.
The MHC 1: peptide complex is then shot out into the external plasma membrane of the cell.
A normal cell will display peptides from normal cellular protein turnover on its class I MHC, and cytotoxic T cells will not be activated in response to them due to central and peripheral tolerance mechanisms. When a cell expresses foreign proteins, such as after viral infection, a fraction of the class I MHC will display these peptides on the cell surface. Consequently, cytotoxic T cells specific for the MHC: peptide complex will recognize and kill presenting cells, along with cancer cells with the same antigens.
Cancers that contain a lot of foreign antigens are highly immunogenic, meaning they have a high ability to activate an immune response, basically yelling that they want to be killed. However, cancers that are initially immunogenic can lose visibility to cytotoxic T cells in two general ways.
If the immunogenic antigens are non-essential for cell survival, genetically unstable cancer cells can lose expression of these antigens. After this occurs, cytotoxic T cells will be ineffective in controlling cancer because the cancer cells have lost all antigenic peptides that cytotoxic T cells can recognize. This route of immune evasion will be less likely in cancers that express many immunogenic cancer antigens because it would require the simultaneous loss of expression of many independent gene products.
The other general way that cancers can lose visibility to cytotoxic T cells is by down-regulating the MHC 1 antigen presentation pathway, which is a fancy term for lowering the number of receptors for MHC molecules.
While it was never found out how exactly the tumor on the surgeon stayed alive, we can assume it was one of those mechanisms.
Fortunately, the tumor was excised, and the surgeon made a complete recovery. Pfff, that was a lot.
At least now you know not to put your hands where they don’t belong, or at least not in another man’s cancer.
Thanks for reading.