Alb-Cre+/MYC+ mice are generated by crossing H11-CAG-LSL-hMYC-IRES-EGFP mice (Catalog Number: C001338), which conditionally express the human c-Myc oncogene, with Alb-Cre mice that express Cre recombinase specifically in hepatocytes under the control of the Alb promoter. The Cre-mediated recombination results in the deletion of the transcriptional stop sequence (Loxp-Stop-Loxp, LSL) in H11-CAG-LSL-hMYC-IRES-EGFP mice, leading to overexpression of the MYC oncogene in the liver and subsequent carcinogenesis. This model, therefore, spontaneously develops liver cancer with an early onset.

The Apc KO mouse is a research model constructed by using gene editing technology to knock out the sequence in the mouse Apc gene that contains the mutation cluster region (MCR), and this strain is homozygous lethal. Heterozygous Apc KO mice can spontaneously develop intestinal adenomas and exhibit significant colorectal cancer disease phenotypes in various aspects such as survival, growth, food intake, and intestinal lesions. Therefore, Apc KO mice can be used for familial adenomatous polyposis (FAP) and colorectal cancer and other tumors or tumor-related diseases, as well as the study of the regulatory mechanism of the Wnt/β-catenin signaling pathway.

The Jak2*V617F mice are generated by introducing a homologous mutation to the human JAK2 V617F into the mouse Jak2 gene via gene editing. This strain is homozygous lethal. Heterozygous Jak2*V617F mice exhibit classic MPN-like disease phenotypes such as splenomegaly and structural damage, significantly elevated red blood cell count, hemoglobin, hematocrit, white blood cell count, platelet count, marked megakaryocytic hyperplasia (with granulocytic and erythroid hyperplasia), extramedullary hematopoiesis, and congestion of splenic sinusoids. Therefore, Jak2*V617F mice can be used for studying the mechanisms of myeloproliferative neoplasms (MPNs) like polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF), as well as for evaluating therapeutic drugs.

The KS (inducible) mouse is an induced lung cancer model that is constructed by crossing LSL-K-ras G12D mice (Catalog number: C001064), a conditional over-expressing K-Ras G12D mutant gene mouse strain, and Sftpc-MerCreMer mice (Catalog number: C001501), a type II alveolar cell-specific Cre recombinase expressing mouse strain, and then inducing with tamoxifen. Tamoxifen can trigger sequence recombination between loxP sites mediated by Cre recombinase in the type II alveolar cells of the offspring mice, resulting in the specific deletion of the Loxp-Stop-Loxp (LSL) gene silencing element in the type II alveolar cells, thereby enabling the K-Ras G12D mutant gene to be selectively expressed in the lung tissue. Internal data indicates that the model may exhibit slight expression leakage in the absence of tamoxifen induction, leading to the occurrence of a small number of pulmonary adenomas.

This strain is a conditional expression model of K-ras G12C, generated by introducing the G12C point mutation into the mouse Kras gene. Under normal conditions, the expression of K-ras G12C is blocked by an upstream loxP-Stop-loxP cassette. Expression is achieved only upon crossing with Cre mice, where Cre recombinase-mediated loxP site recombination removes the blocking sequence. This enables precise temporal and spatial control of K-ras G12C expression and tumorigenesis. By mating with tissue-specific Cre mice, this model can conditionally express K-ras G12C in specific tissues, making it a valuable tool for constructing cancer models in various tissues and organs. Homozygous LSL-K-ras G12C mice are nonviable.