Cutaneous Toxicities of Small Molecules in Targeted Cancer Therapy Part I - Mechanisms of Toxicity

Ian Nykaza1, Bernice Kwong2, Allison Gordon1

  • 1Memorial Sloan Kettering Cancer Center, Department of Medicine, Dermatology Service, New York, NY, USA; Weill Cornell Medicine, New York, NY USA.

Keywords:
AKTAcneiform dermatitisAcneiform eruptionActinic keratosesBRAFBurton’s tyrosine kinase (BTK)CDK4/6CSF1REGFR (epidermal growth factor receptor)ERKEZH2FGFRFLT3HH (Hedgehog) pathwayJAK inhibitorsJAK/STAT pathwayKITMAPK/ERK pathwayMEKMETNotch signalingPARPPDGFRPI3KPI3K/AKT/mTOR pathwayRASRAS/MAPK pathwayRETSMO inhibitionSRC kinase familyStevens-Johnson syndrome (SJS)TRKVEGFRXPO1alopeciaaphthous ulcersatypical nevib-cell lymphoma-2 (BCL-2)basal cell carcinoma (BCC)breakpoint cluster region-Abelson murine leukemia (BCR-ABL)bullous pemphigoid (BP)cheilitiscutaneous epithelial proliferations (CEP)drug-induced hypersensitivity syndrome (DIHS/DRESS)eczematous dermatitisepidermal hyperplasiaepidermal necrolysis (TEN)epidermoid cystsepigenetic inhibitorsepigenetic regulationeruptive nevifolliculocentric eruptionshair changeshair depigmentationhand-foot skin reaction (HFSR)hirsutismhistone deacetylase (HDAC)hyperkeratosishyperpigmentationhypopigmentationhypoxia inducible factor (HIF)ichthyosiform eruptioninterface dermatitisisocitrate dehydrogenase (IDH1/2)keratoacanthomaskeratosis pilaris-like eruptionslichenoid eruptionmTORmaculopapular rashmelanocytic lesionsmelanomamelanonychiamucositismultikinase inhibitorsnail brittlenessnail dystrophynail pigment changesnon-kinase inhibitorsnon-receptor tyrosine kinase inhibitors (NRTKIs)oral lichenoid lesionspalmoplantar erythrodysesthesia (PPE)palmoplantar keratoderma (PPK)papulopustularparonychiaphotosensitivitypigmentary changesproteasomepsoriasiform eruptionreceptor tyrosine kinase inhibitors (RTKIs)sebaceous gland dysfunctionseborrheic keratosesserine/threonine kinase inhibitorssmall molecule inhibitors (SMIs)spongiotic dermatitissquamous cell carcinoma (SCC)stomatitistrichomegalytyrosinase inhibitionvitiligoxerosisxerostomiay-secretase

Related Concept Videos

Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
8.9K
Toxic Reactions: Overview01:26

Toxic Reactions: Overview

When toxic substances penetrate the human body, they disseminate to various tissues, undergoing metabolic changes. This process yields reactive metabolites that may covalently bind with specific target molecules, resulting in toxicity.
Toxicity falls into two primary categories: local and systemic.
Local toxicity appears at the exposure site, such as protein denaturation caused by caustic substances.
In contrast, systemic toxicity requires the toxic agent's absorption and distribution,...
2.0K
Cancer Therapies02:49

Cancer Therapies

Cancer therapies are various modes of treatment, such as surgery, radiation therapy, and chemotherapy that are administered to cancer patients.
However, cancer treatments can pose several challenges, as therapies used to kill cancer cells are generally also toxic to normal cells. Moreover, cancer cells mutate rapidly and can develop resistance to chemical agents or radiation therapy. Besides, all types of cancer cells may not respond to the same therapy. Some cancer cells respond to one...
10.2K
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
7.1K
Mechanisms of Retrovirus-induced Cancers01:51

Mechanisms of Retrovirus-induced Cancers

Retroviruses are RNA viruses that have been shown to cause cancers in diverse species, including chickens, mice, cats, and monkeys. The RNA genomes of these viruses are first reverse-transcribed into single and then double-stranded DNA (dsDNA) copies. This dsDNA called proviral DNA then integrates into the host genome. Subsequently, the host cell transcribes the proviral DNA in concert with the chromosomal DNA. This leads to the production of viral RNA and proteins that assemble at the host...
7.0K