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Table 1 WEE1 and PKMYT1 molecular alterations in hematological and solid tumors according to literature

From: A WEE1 family business: regulation of mitosis, cancer progression, and therapeutic target

Gene Genetic alteration Disease Effect/prognostic value Reference
Hematological tumors
WEE1 Over-expression ALL; AML; MM; CML; CLL; DLBCL Crucial for cell viability of cancer cells (experimentally proven). [35,36,37,38,39,40, 43, 54]
Copy number Gain AML Biological effect or prognostic value unknown [55]
PKMYT1 Over-expression ALL; MM Crucial for cell viability of cancer cells (experimentally proven). [35, 44]
Solid tumors
WEE1 Over-expression GC; MaM; GL; OC; CC Associated with lymph node involvement, induction of metastasis, increased biomarkers of proliferation (CCND1, Ki67 or CCNA1), resistance to treatment and poor overall survival. [48,49,50,51, 56,57,58,59,60]
Mutation PA Insertion causing decrease WEE1 expression upon DNA damage [33]
PKMYT1 Over-expression HC; CC; GLB; NSCLC; N; GS Associated with tumor progression, aggressive disease and poor overall survival. [31, 32, 45,46,47]
Mutation N Biological effect or prognostic value unknown [61]
  1. ALL acute lymphoblastic leukemia, AML acute myeloid leukemia, MM multiple myeloma, CML chronic myeloid leukemia, CLL chronic lymphocyte leukemia, DLBCL diffuse large B cell lymphoma, GC gastric cancer, MaM malignant melanoma, GL gliomas, OC ovarian cancer, CC colorectal cancer, PA pancreatic adenocarcinoma, HC hepatocellular carcinoma, GLB glioblastoma, NSCLC non-small-cell lung cancer, N neuroblastoma