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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