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Showing results for tags 'lung cancer biomarkers'.
“Squamous cell cancer offers distinct therapeutic challenges by virtue of presentation in older patients, its physical location in the chest, pattern of metastasis and association with comorbidities that can compromise treatment delivery and exacerbate toxicity.” This quote is from the article Targeted Therapy for Advanced Squamous Cell Lung Cancer. When diagnosed, almost 13 years ago, I didn’t realize lung cancer had types. Pathologists visually classify lung cancer cells seen under a microscope as small cell and non-small cell. From this simple delineation, further classification gets complicated introducing sub-type terms of adenocarcinoma, squamous cell and large cell. Large cell as a type of non-small cell? I recall dwelling on the large cell moniker and finally concluding a non-small cell can be a large cell. I remember the emergency room physician telling me I was lucky; my form of lung cancer was treatable compared to the other type. He didn’t say small cell, but I think that is what he meant. Indeed about 15-percent of us suffer from this nasty presentation that metastasizes rapidly. Adenocarcinoma sub-subtypes have morphed into an alphanumeric soup as research at the genetic level identifies biomarker profiles, mutations in an individual’s lung cancer that can serve as attack portals into the cancer cell by targeted therapy. Now adenocarcinoma survivors use terms like ALK, KRAS, EGFR and PIK3CA to further classify their disease and new targeted treatment drugs emerge to attack, like mutant Ninja Turtles! Some of these are so effective, they’ve moved to first-line therapy. Adenocarcinoma describes a type of cancer that occurs in the mucus-secreting glands throughout the body. Lungs naturally have an abundance of these glands but so do the prostrate, pancreas, and intestines. Squamous cells derive their name from the Latin squama meaning scale like those present on a fish. We have a lot of squamous cells including skin, the lining of hollow organs, and passages of digestive and respiratory tracts. The right main stem bronchus contained my squamous cell tumor. The location is what tipped-off the emergency room physician; he didn’t realize how lucky I was given the nature of my treatment and extent of survival. Speaking of treatment, the cited article reports: “therapeutic progress in squamous cell lung cancer has been relatively slow, with relative stagnation of survival numbers….Treatment for SqCC [squamous cell cancer] of the lung remains an unmet need, and novel strategies are needed including specific targeted therapies….” That’s not good. First-line therapy for many continues to be the dual recipe of some variation of taxol and carboplatin, the same drugs I was administered from 2004 through 2007. And, survival rates have not significantly changed despite chemistry changes in platinum and taxol based agents. Thankfully, these have lowered the incidence of peripheral neuropathy and this is helpful. Second and subsequent line therapies for squamous cell have benefited somewhat from research. Immunotherapy research has yielded some success in developing drugs that enhance our immune system’s ability to recognize and attack cancer cells. The alphanumeric monikers PD-1 and PD-L1 are starting to resonate with squamous cell survivors. I do like the names of these approaches ⎯ PD meaning programmed death! The idea of programming cancer cells to die is satisfying although that is not the means of attack. Nevertheless, the scientist that named this approach deserves recognition because a scheduled execution of squamous cancer cells would be well deserved payback. All squamous lung cancer cells are programmed to die tomorrow at high noon! But, progress in the genetic arena for squamous cell cancer has been slow because it is genetically more complex compared to adenocarcinoma and mutates faster. So it is a harder target to hit. When I think of hard cancer targets, I am reminded of Siddhartha Mukherjee’s superb book The Emperor of all Maladies. He aptly describes the challenge of chemotherapy as “finding some agent that will dissolve away the left ear and leave the right ear unharmed.” He also called cancer a “clonally evolving disease.” Cancer cells grow by cloning at a rate far faster than normal cells. Every new cohort creates mutants and some of these survive the assault of chemotherapy. All that need survive is one; it will rapidly grow now immune to the drugs targeted to kill it. Mukherjee said: “the genetic instability, like a perfect madness, only provides more impetus to generate mutant clones. Cancer thus exploits the fundamental logic of evolution unlike any other illness.” Cancer is pure evolutionary nastiness! “Better things for better living through chemistry” was the tagline of the DuPont Corporation. Growing up in southeastern Pennsylvania, many neighbors were chemists commuting to the company research center, just across the Delaware state line. DuPont changed our world evolving from an 1802 gunpowder maker to inventing Nylon, Mylar, Teflon, and Nomex to name a few. Squamous cell lung cancer survivors need better chemistry. The call goes out for a biochemist to step-up and shut down the perfect madness of the clonally evolving squamous cancer cell. Stay the course.