TABLE 1.

Incidence, mutational landscape, precursor lesions, chemotherapy response, and prognoses of the five major subtypes of EOC.

	HGSOC	CCOC	ENOC	MOC	LGSOC	References
Incidence	70%	10%	10%	3%	<5%	Prat et al. (2018)
Commonly mutated genes	Near-ubiquitous TP53 mutations	ARID1A most frequently mutated (50%–60% of cases)	ARID1A mutated in up to 30% of cases	KRAS and NRAS frequently mutated	BRAF, KRAS and NRAS commonly mutated	Shaw et al. (2002), Risch et al.(2006), Jones et al. (2010), The Cancer Genome Atlas Research Network, (2011), McAlpine et al. (2012), Emmanuel et al. (2014), Kanchi et al. (2014), Hunter et al. (2015), Friedlander et al. (2016), Itamochi et al. (2017), Maru et al. (2017), Murakami et al. (2017), Kim et al. (2018), Shibuya et al. (2018), Cybulska et al. (2019), Cheasley et al. (2019), Morice, et al. (2019), Gorringe et al. (2020), Pierson et al. (2020), Cheasley et al. (2022)
	BRCA1/2 germline mutations or inactivation	PIK3CA, KRAS, PTEN, SMARCA4 also mutated	PIK3CA, KRAS, PTEN, CTNNB1 also mutated	Mutations in ARID1A and PIK3CA	TP53 mutations rare
		TP53 mutations in up to 20% of cases	TP53 mutations in ∼17% of cases	Amplification of ERBB2 and copy number loss of CDKN2A
				TP53 mutations in up to 64% of cases, often confined to later stages
Precursor lesions	Serous tubal intraepithelial carcinoma (STIC) lesions in the fallopian tube	Endometriosis and retrograde menstruation, adenofibroma	Endometriosis and retrograde menstruation, adenofibroma	Mucinous benign cystadenomas and mucinous borderline ovarian tumors (MBTs)	Serous borderline tumors (SBTs) in 60%–80% of cases	Lee et al. (2007), Medeiros et al. (2006), Kurman and Shih, (2010), Wiegand et al. (2010), Erickson et al. (2013), Ahn et al. (2016), Prat et al. (2018), Cheasley et al. (2019), Shih et al. (2021)
Response to chemotherapy	Initially responsive (80%) but 20%–30% of tumors relapse 6 months after treatment and can develop resistance	Poor response (15%) and resistance to platinum chemotherapy noted	High grade ENOCs initially sensitive to platinum chemotherapy	Intermediate response (15%–60%) and resistance to platinum chemotherapy noted	Poor response (26%–28%)	Sugiyama et al. (2000), Gershenson et al. (2009), Alexandre et al. (2010), Berns and Bowtell, (2012), Kim et al. (2012), Prat et al. (2018), Lheureux et al. (2019a), Morice et al. (2019)
Clinical outcome	Poor survival rates due to overall later stage diagnosis and recurrent tumors after chemotherapy	Intermediate, with a greater risk of venous thromboembolism than other subtypes. Late stage CCOC has a poorer prognosis than late stage HGSOC	Low grade ENOC more prevalent and favourable, poorer outcomes in high grade ENOC cases	As 65%–80% are diagnosed at an early stage, survival is favourable, later stages have a poorer prognosis than late stage HGSOC	Most favourable outcomes of all subtypes, along with low-grade endometrioid carcinoma	Mackay et al. (2010), Berns and Bowtell, (2012), Peres et al. (2018), Prat et al. (2018), Ricciardi et al. (2018), Soyama et al. (2018), Morice et al. (2019)