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

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

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]
WEE1	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]
WEE1	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]
PKMYT1	Mutation	N	Biological effect or prognostic value unknown	[61]

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

ISSN: 1756-8722