The deadliest trait of cancer cells is their capacity to colonize other sites of the body during a complex process called metastasis. Metastasis is the ultimate cause of death in 90% of patients with cancer, and there are still many remaining gaps in our understanding of metastasis formation. A number of studies have proposed the existence of an intricate crosstalk between primary tumors and future sites of metastases in order to transform the environment of these organs into a suitable microenvironment. This microenvironment is called the premetastatic niche, and is established to receive disseminating cancer cells, and support the growth of the metastatic colony. Melanoma is a highly metastatic cancer and preferentially establishes secondary lesions in lungs and brain. We have created a mouse model of melanoma B6(Cg)-Tg(Dct-Grm1)ESzc Tg(KRT5-rtTA)1Glk Tg(tetO-Edn3,-lacZ)Kosl or (Dct-Grm1/K5-Edn3) that spontaneously develops melanoma tumors and metastasizes to the lung. In order to describe the premetastatic niche formation in the mouse model of melanoma metastasis we monitored the appearance of bone marrow derived cells (BMDCs) clusters and metastatic cells during tumor progression by immunofluorescence and flow cytometry. We detected both BMDCs and tumors cells in the earliest stage of tumor progression suggesting that the lung melanoma metastasis in the Dct-Grm1/K5-Edn3 mouse model is independent of premetastatic niche formation. We also found tumorigenic cells staining positive for both melanocytic and hematopoietic markers in higher numbers early during primary tumor formation. The appearance of Melanoma-BMDC hybrids in the lung suggest they might be the metastasis initiating cells, which might explain why the premetastatic niche formation is not required in the Dct-Grm1/K5-Edn3 mouse model. Furthermore our findings implicate that Melanoma-BMDC hybrids are potential targets for melanoma treatment.