Cell cycle stage assignment of the SCLC cells from the autochthonous model.

Characterization of cell types isolated from the autochthonous scRNA-seq data.

Description of samples in the autochthonous study

Description of samples in the xenograft study

Gene module membership and expression of module 5 (related to Figure 1g)

Validation of the LBC labeling and xenograft growth.

The exponential growth of the cancer neuroscience field has shown that the host's immune, vascular, and nervous systems communicate with and influence each other in the tumor microenvironment, dictating the cancer malignant phenotype. Unraveling the nervous system's contributions toward this phenotype brings us closer to cancer cures. In this review, we summarize the peripheral nervous system's contributions to cancer. We highlight the effects of nerve recruitment and tumor innervation, the neuro-immune axis, glial cell activity, and neural regulation on cancer development and progression. We also discuss harnessing the neural control of peripheral cancers as a potential therapeutic approach in oncology. Significance: The continued and growing interest in cancer neuroscience by the scientific and medical communities reflects the rapidly accumulating interdisciplinary understanding of the nervous system's modulation of immune, vascular, and cancer cells' functions in malignancies. Understanding these regulatory functions can identify targets for intervention that may already be clinically available for other indications. This potential brings great excitement and hope for patients with cancer worldwide.

Validation of GAGE2A and PAGE5 shRNAs and overexpression vectors.

Validation of the autochthonous barcoding model.

Determining effective concentrations for treatment of SCLC cell lines with cisplatin and etoposide.

Normalized CTA expression from NCI-H209 cell, xenografts, and chemo-treated xenografts (related to Figure 5f)

Expression and validation of AP-1 family genes in late tumor development.

In silico removal and characterization of isolation of murine cells.

Normalized gene expression across NCI-H209 subclones (related to Figure 4)

Graphic displaying the sample makeup of the three NCI-H209 sample arms.

GAGE2A and PAGE5 upregulation upon treatment of cisplatin and etoposide.

Validation of GAGE2A and PAGE5 shRNAs and overexpression vectors.

Differential gene expression across NCI-H209 and NCI-H82 cluster (related to Figure 4)

SCLC Subtype-specific marker expression from the RPR2-Cas9 mouse model.

Determination of LBC counts by PCR error correction.