<\/span><\/h2>\nEpidermal<\/span> growth factor<\/span> receiver<\/span> (EGFR) inhibitors are a new group of drugs developed to treat a wide range of cancers. EGFR overexpression in approximately 30% of cancers is one reason for their cell excess proliferation<\/span> and tumor<\/span> increase.<\/p>\nAlthough effective in treating many types of cancer, EGFR inhibitors often result in Adverse reactions<\/span> on the skin, which occurs in at least half of treated patients.<\/p>\nSide effects are helping scientists learn more about skin disorders. In some cases, the presence of an adverse skin reaction indicates that the drug is effective in treating the tumor.<\/p>\n
People can be treated with these drugs for long periods and will have to weigh the benefits against the side effects.<\/p>\n
<\/span>What are protein kinase inhibitors?<\/span><\/h2>\nProtein kinases are enzymes<\/span> inside the cell resulting in cellular<\/span> proliferation. Protein kinase inhibitors reduce cell proliferation. point to amino acids<\/span> tyrosine, threonine and serine. Some EGFR inhibitors are also protein kinase inhibitors.<\/p>\n\n
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<\/span>How do these inhibitors work?<\/span><\/h2>\nEGFR inhibitors are specifically directed against EGFR on the outside of the cell. Protein kinase inhibitors target protein kinases inside the cell. The specific receptors found in the Cancer<\/span> determine which medication is likely to be beneficial.<\/p>\n\n- EGFR is found in the cell membrane. By binding with an epidermal growth factor ligand outside the cell, they activate a protein kinase inside the cell.<\/li>\n
- Protein kinase prevents the phosphorylation of the specific protein. amino acids<\/span>like tyrosine.<\/li>\n<\/ul>\n
EGFR and kinase inhibitors may be particularly useful in cancer therapy as they are less toxic<\/span> than more traditional chemotherapies. Specific drugs target different types of cells and can be monoclonal<\/span> antibodies<\/span> with the suffix -mab or small molecules<\/span> with the suffix -nib.<\/p>\n\n\n\n| drug name<\/th>\n | \nMolecular<\/span> objective<\/th>\n | Indication<\/th>\n<\/tr>\n |
\nMonoclonal antibody<\/span>\n<\/td>\n<\/tr>\n\n| Cetuximab<\/td>\n | KRAS<\/td>\n | colorectal cancer
Scaly<\/span> head and neck cell carcinomas<\/td>\n<\/tr>\n\n| Panitumumab<\/td>\n | KRAS<\/td>\n | colorectal cancer<\/td>\n<\/tr>\n | \nLittle molecule<\/span>\n<\/td>\n<\/tr>\n\n| Imatinib<\/td>\n | BCR-ABL, PDGFR and c-KIT<\/td>\n | \nChronic<\/span> myeloid<\/span> Leukemia<\/span> (CML)
Gastrointestinal stromal tumor.<\/td>\n<\/tr>\n\n| Gefitinib<\/td>\n | EGFR, HER1<\/td>\n | Non-small cell lung cancer (NSCLC).<\/td>\n<\/tr>\n | \n| erlotinib<\/td>\n | EGFR<\/td>\n | \nMetastatic<\/span> NSCLC
Pancreatic cancer.<\/td>\n<\/tr>\n\n| Lapatinib<\/td>\n | EGFR, HER2\/neu<\/td>\n | Breast cancer<\/td>\n<\/tr>\n | \n| Osimertinib<\/td>\n | EGFR, T790M\/neu<\/td>\n | Non-small cell lung cancer<\/td>\n<\/tr>\n | \n| Vandetanib<\/td>\n | EGFR, VEGFR, RET tyrosine kinase<\/span>\n<\/td>\n | thyroid tumor<\/td>\n<\/tr>\n | \n| Sorafenib<\/td>\n | VEGFR, PDGFR, RAF<\/td>\n | \nRenal<\/span> cell carcinoma<\/span>
hepatocellular carcinoma<\/td>\n<\/tr>\n\n| Sunitinib<\/td>\n | PDGFR, VEGFR, KIT and others<\/td>\n | Renal cell carcinoma
Gastrointestinal stromal tumors
Neuroendocrine<\/span> pancreatic tumors<\/td>\n<\/tr>\n<\/tbody>\nSome of the EGFR inhibitors available<\/caption>\n<\/table>\nEGFR = epidermal growth factor receptor; PDGFR = platelet<\/span>derived growth factor receptor; VEGFR = vascular<\/span> endothelial<\/span> growth factor receptor<\/p>\nThere is currently great interest in the small molecule mutated B-RAF inhibitors, vemurafenib and dabrafenib, which are effective in the treatment of B-RAF-positive metastases. melanoma<\/span>. B-RAF is a specific protein threonine kinase.<\/p>\nMany more EGFR and protein kinase inhibitors are in development.<\/p>\n <\/span>Which are the cutaneous<\/span> side effects of EGFR monoclonal antibody inhibitors?<\/span><\/h2>\nThe most common skin side effects of EGFR monoclonal antibody inhibitors are:<\/p>\n <\/span>Folliculitis<\/span><\/h3>\nFolliculitis (inflamed hair<\/span> follicles<\/span>) occurs in up to 40-85% of patients. It is an early event, usually seen within the first ten days of treatment. Sterile inflammatory<\/span> papules<\/span> and pustules<\/span> seen predominantly in the T-zone of the face, but can be more extended<\/span> involving the chest and back. Occasionally the scalp and pubic regions are involved or rarely the entire body.<\/p>\nFolliculitis is especially common and often severe with cetuximab. The intensity of folliculitis can fluctuate even when you continue to take the drug.<\/p>\n Folliculitis is often managed with:<\/p>\n \n- camouflage cosmetics<\/li>\n
- Current<\/span> antibiotics<\/li>\n
- Oral antibiotics<\/li>\n
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Topical steroids<\/li>\n<\/ul>\n If the folliculitis is severe, the medication may need to be stopped and it will resolve. The iIncidence and severity of inhibitor-induced EGFR follicular<\/span> Reactions are halved by pretreatment with doxycycline or minocycline. These tetracycline medications may also be prescribed once you eruption<\/span> has occurred allowing continued treatment with the EGFR inhibitor drug.<\/span><\/p>\n\n<\/span>Protein kinase inhibitor folliculitis<\/span><\/h5>\n<\/section>\n\n\n \n  \n<\/div>\n Vemurafenib folliculitis<\/p>\n<\/p><\/div>\n<\/section>\n <\/div>\n <\/span>\nAlopecia<\/span> and trichomegaly<\/span><\/h3>\nDrug-induced alopecia (hair loss) is less common than folliculitis and tends to occur later, usually by 2-3 months. Patients may find that their hair becomes fine and brittle. They may experience frontal-temporary<\/span> hair loss similar to male pattern baldness. This may or may not improve if the drug is stopped.<\/p>\n\n<\/span>Protein kinase inhibitor alopecia<\/span><\/h5>\n<\/section>\n\n\n \n  \n<\/div>\n Vemurafenib alopecia<\/p>\n<\/p><\/div>\n<\/section>\n <\/div>\n In contrast, patients often experience excessive growth of facial hair and eyelashes (hypertrichosis<\/span>, trichomegaly).<\/p>\n<\/span>Dry Skin (xerosis<\/span><\/span>pulpitis)<\/span><\/h3>\ndry skin is predominant<\/span> and handled with emollients<\/span>. These drugs can cause pulpitis with pain fissures<\/span> at the fingertips.<\/p>\nDry skin sometimes seems seborrheic<\/span> dermatitis<\/span>.<\/p>\n\n<\/span>Dry skin and keratoderma due to protein kinase inhibitor.<\/span><\/h5>\n<\/section>\n\n\n \n  \n<\/div>\n Keratoderma due to vemurafenib<\/p>\n \n  \n<\/div>\n Dry skin due to vemurafenib<\/p>\n<\/p><\/div>\n<\/section>\n <\/div>\n <\/span>Paronychia<\/span><\/span><\/h3>\nParonychia refers to painful inflammation<\/span> of the nail folds. The fingers are affected more often than the toes. Paronychia can sometimes resolve on its own even with continued use of the drug, but it quickly disappears on discontinuation.<\/p>\nTreatment involves avoiding trauma<\/span> such as tight shoes, avoiding excessive trimming or nail biting, and wearing appropriate footwear. Topical steroids and antiseptics can help. It is essential to treat the secondary. bacterial<\/span> and mushrooms infection<\/span>.<\/p>\n<\/span>Skin cancer<\/span><\/h3>\nSquamous cell carcinomas and multiple keratoacanthomas have been reported to arise in patients treated with sorafenib and other EGFR inhibitors.<\/p>\n <\/span>What are the side effects of small molecule tyrosine kinase inhibitors?<\/span><\/h2>\nSmall molecule kinase inhibitors often block multiple enzymes, which means there is crossover in the actions and side effects of these drugs.<\/p>\n The most common side effects are:<\/p>\n \n- nonspecific rashes<\/li>\n
- Newspaper edema<\/span>\n<\/li>\n
- \nAcral<\/span> erythema<\/span>\n<\/li>\n
- Splinter hemorrhage<\/span><\/li>\n
- \nPigmentation<\/span> changes<\/li>\n
- Photosensitivity<\/span><\/li>\n<\/ul>\n
the same side effects can also arise <\/span>with monoclonal antibodies.<\/p>\n<\/span>nonspecific rashes<\/span><\/h3>\nImatinib induces a rash in one third of patients who start taking it, but this rash is usually self-limiting. Imatinib has rarely been associated with vasculitis<\/span>Steven Johnson | | | | | | |