Category Archives: Female genital pathology

Familial biparental complete hydatidiform mole (CHM)

Familial biparental complete hydatidiform mole (CHM) – An update


👪 Represents 0.6 to 2.6% of CHM.


👪 Mutations of the NLRP7 on chr 19p and KHDC3L on chr 6p.

👪 Conventional CHM are usually of paternal origin (androgenic diploidy) , in contrast to familial CHM which are biparental .


👪 Autosomal recessive inheritance


👪 Patients present with recurrent complete hydatidiform mole.(CHM)


👪 Testing for p57 is negative similar to sporadic CHM.

Update WHO 2020 FGT.

Review question

Which of the following statements is false regarding Familial biparental complete hydatidiform mole (FBCHM)?
A) This condition is inherited in an autosomal recessive manner.
B) Germline mutations in NLRP7 are common
C) Patients present with recurrent complete hydatidiform mole (CHM)
D) P57 testing by Immunohistochemistry (IHC) is positive in cytotrophoblasts unlike complete mole.

CLICK TO REVEAL ANSWER

Correct answer is D: P57 testing by Immunohistochemistry (IHC) is negative in cytotrophoblasts complete mole both familial and sporadic CHM.

You may join telegram channel for chapterwise daily mcqs – Pathology mcqs

For pathology mcqs, weekly quizzes, interesting facts and updates – Visit HOME – Pathology for all

Join the Facebook page for daily questions- Pathology mcq

Useful for NEET-SS Oncopathology, DM Histopathology, FRCPath, and Hematopathology fellowships.

Molecular pathogenesis of ovarian epithelial tumors.

Molecular progression of serous ovarian tumor. Borderline low and high grade

1.Molecular progression of low grade ovarian serous tumors.
There is data to suggest progression from serous cystadenoma / cystadenofibroma with BRAF / KRAS mutations → SBT (serous borderline tumor) → LGSC (Low grade serous carcinoma) ; however, this is still controversial

2. Molecular progression of high grade serous ovarian tumors.

TP53 alterations in nearly all cases of high grade serous carcinoma

Germline, somatic or promoter hypermethylation (inactivation) of BRCA1 and BRCA2 in ~50% of cases

Difference between PSTT ( Placental site trophoblastic tumor) and Choriocarcinoma- Vascular invasion.

Difference between PSTT ( Placental site trophoblastic tumor) and Choriocarcinoma- Vascular invasion.

Difference between PSTT ( Placental site trophoblastic tumor) and Choriocarcinoma- Vascular invasion.
🎯📟PSTT – invasion is periphery to lumen.
🎯📟Choriocarcinoma- lumen to periphery.

For more such articles click here

Liked the page? Why not leave a tip for it’s creators

Pathogenesis of type I and type II Serous Ovarian Carcinomas

Pathogenesis of Type I and Type II serous ovarian cancers are entirely different. We will discuss the differences.

Most of the human cancers have a steady and known progression curve. Low grade cancers usually progress to high grade. This is not the case in ovarian cancers, high grade and low grade serous carcinoma have different pathogenesis.

Unlike most human cancers serous ovarian cancers rarely progress from low grade to high grade

PATHOGENESIS OF TYPE I SEROUS OVARIAN CANCERS – Progression

Type I ovarian carcinoma is associated with endometriosis, it progresses to serous borderline tumor which may transform to micropapillary serous carcinoma and then into low grade serous carcinoma. Molecular progression of ovarian cancers are shown below.

1.Endometriosis

⬇

2.Serous borderline tumor

⬇

3. Micropapillary serous carcinoma

⬇

4. Low grade serous ovarian carcinoma

PATHOGENESIS OF TYPE II SEROUS OVARIAN CANCERS – Progression

Type II ovarian carcinoma is associated with simple inclusion cysts, it progresses to serous tubular intraepithelial carcinoma which may transform to high grade serous carcinoma.

  1. Simple inclusion cysts

2. STIC Lesions (Serous tubular intraepithelial lesions)

3. High grade serous ovarian carcinoma

[table id=1 /]

For summary check the post below

For similar posts click here.

Liked the page? Why not leave a tip for it’s creators