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PathY5 > Gynae Path 2 > Flashcards

Gynae Path 2 Flashcards

1
Q

What’s the distinction between high and low grade gynae cancers?

A

Surgical operation may differ​:
Omentectomy​
Lymphadenectomy​

​Adjuvant therapy may differ​

​Prognosis: ​
Recurrence free survival
grade 1, 95% ​
grade 2, 82% ​grade 3, 68%

Overall survival​
grade 1, 89%
grade 2, 84%
grade 3, 63%

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2
Q

What is a Stage I Tumour confined to the corpus uteri​?

A

IA No or less than half myometrial invasion​

IB Invasion equal to or more than half of the myometrium

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3
Q

What is a stage 2 tumour?

A

Stage II Tumour invades cervical stroma

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4
Q

What is a Stage III Local and/or regional spread of the tumour?

A

IIIA Tumour invades the serosa of the corpus uteri and/or adnexa​

IIIB Vaginal and/or parametrial involvement​

IIIC Metastases to pelvic and/or para-aortic lymph nodes​

IIIC1 Positive pelvic nodes​

IIIC2 Positive para-aortic lymph nodes with or without positive pelvic lymph nodes

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5
Q

What is a Stage IV Tumour invades bladder and/or bowel mucosa, and/or distant metastases?

A

IVA Tumour invasion of bladder and/or bowel mucosa​

IVB Distant metastases, including intra-abdominal metastases and/or inguinal lymph nodes

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6
Q

What is the TCGA classification?

A

Group 1: EEC with mutations in POLE (Polymerase E- ultramutated) ​

​Group 2: EEC with MSI (hypermutated)​

​Group 3: EEC with low copy number alterations​

Group 4: (serous-like) tumours show TP53 mutations

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7
Q

What are POLE mutant tumours?

A

​These tumours often appear to be high-grade. ​

In the absence of the knowledge of their POLE gene mutation status, they would be mistakenly included into a category of tumours with bad prognosis. ​

POLE gene mutation confers a quite better prognosis. ​

So, the identification of this mutated subgroup is essential for better personalised treatment and prognosis analysis.

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8
Q

A fundamental cellular mechanism for preventing DNA alteration that are created largely during DNA replication

A

A fundamental cellular mechanism for preventing DNA alteration that are created largely during DNA replication

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9
Q

What is the Mismatch repair system?

A

Mutations or silencing by hypermethylation of one of the DNA mismatch repair genes results in MSI​

​

Microsatellite instability (MSI): Alterations in the length of short, repetitive DNA sequences called microsatellites.​

​

This results in an increase of the rate of mutations contributing to tumorigenesis, again with a high mutation burden.​

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10
Q

What shows strong nuclear expression in tumour cells of endometrioid carcinoma.​?

A

HMLH1 (A), PMS2 (B), MSH2 (C) and MH6 (D) show strong nuclear expression in tumour cells of endometrioid carcinoma.

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11
Q

What are hypersensitive to the immune checkpoint inhibitor, anti-PD-1, monotherapy?

A

EECs exhibiting POLE mutations and MSI are hypersensitive to the immune checkpoint inhibitor, anti-PD-1, monotherapy because,​

these tumours are characterised by a high mutation load which produces more neo-antigens. ​

they have a higher number of tumour infiltrating lymphocytes.

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12
Q

What are Gp 4 tumours?

A

​Composed mostly of SCs, but also include some EEC; many grade 3 but also some grades 1 and 2

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13
Q

What are the 4 patterns of p53 staining?

A

There are 4 main patterns of p53 staining:​

Normal/wild-type​

Complete absence​

Overexpression​

Cytoplasmic

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14
Q

What are leiomyomas?

A

Smooth muscle tumour of myometrium​

Commonest uterine tumour​

20% of women >35yrs​

Lay term is fibroid​

Usually multiple​

May be intramural, submucosal or ​

subserosal
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15
Q

What are leiosarcomas?

A

Malignant counterpart of leiomyoma - rare​

Usually solitary​

Usually postmenopausal​

Local invasion and blood stream spread​

5yr survival 20-30%

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16
Q

What are endometrial stromal sarcomas?

A

Low grade, high grade and other ​Tumour types

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17
Q

What is endometriosis?

A

Presence of endometrial glands and stroma outside the uterus​

​

Common – 10% of premenopausal women​

​

Origin:​

Metaplasia of pelvic peritoneum​

Implantation of endometrium, retrograde menstruation​

​

Ectopic endometrial tissue is functional and bleeds at time of menstruation > pain, scarring and infertility​

​

Can develop hyperplasia and malignancy

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18
Q

What are the types of ovarian cysts?

A

Non neoplastic cysts:​

Follicular and luteal cysts ​

Polycystic ovarian disease: ​

3-6% of reproductive age women​

patients have persistent anovulation​

obesity and hirsutism / virilism​

​

Endometrioitc cyst

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19
Q

What is the classification of ovarian tumours?

A

Primary tumours​

​

Epithelial tumours​

​

Sex cord-stromal tumours​

​

Germ cell tumours​

​

Miscellaneous tumours​

​

Secondary tumours

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20
Q

What is the Incidence and age of onset of epithelial tumours?

A

make up 65% of all ovarian tumours & 95% of malignant ovarian tumours​

​

50% found in 45-65 age group

21
Q

What is the Incidence and age of onset of germ cell tumours?

A

have bimodal distribution; one peak 15-21 year olds and one peak at 65-69

22
Q

What is the Incidence and age of onset of sex cord stromal tumours?

A

most commonly seen in post-menopausal women but some sub-types peak in 25-30 year age group

23
Q

What is the WHO classification of serous, mucinous and endometroid tumours?

A

Serous tumours​

Benign: cystadenoma and adenofibroma​

Borderline ​

Malignant:​

Low-grade serous carcinoma​

High-grade serous carcinoma​

​

Mucinous tumours​

Benign: cystadenoma and adenofibroma​

Borderline​

Malignant​

Mucinous carcinoma​

​

Endometrioid tumours​

Benign: Endometriotic cyst, cystadenoma and adenofibroma​

Borderline ​

Malignant​

Endometrioid carcinoma

24
Q

What is the WHO classification of clear cell, Brenner and seromucinous tumours?

A

Clear cell tumours​

Benign: cystadenoma and adenofibroma ​

Borderline​

Malignant​

Clear cell carcinoma​

​

​

Brenner tumours​

Benign​

Borderline​

Malignant​

Malignant Brenner tumour​

​

Seromucinous tumours​

Benign: cystadenoma and adenofibroma​

Borderline​

Malignant​

Seroumucinous carcinoma

25
Q

What are the benign epithelial tumours?

A

​Serous Cystadenomas​

Cystadenofibromas​

Mucinous cystadenomas​

Brenner tumour

26
Q

What are benign epithelial tumours?

A

Tumours whose biologic behaviour cannot be predicted on histologic grounds ​

​

Tumours that have very low but definite metastatic potential​

​

Morphologically similar tumours may behave differently ​

​

To date, there are no reliable histological or molecular predictive markers for the behaviour of these tumours

27
Q

What is the epidemiology of malignant epithelial tumours?

A

Worldwide is the 6th most common cancer in women​

​

2nd commonest female cancer causing death in women​

Difficult to diagnosis at an early stage​

Develops resistance to therapeutic agents

28
Q

What are the RFs of malignant epithelial tumours?

A

Nulliparity, infertility, early menarche, late menopause.​

​

Genetic predisposition: Family history of ovarian and breast cancers

29
Q

Describe hereditary ovarian cancer

A

Up to 10% of epithelial ovarian cancer cases are familial​

​

​

3 familial syndromes: All are transmitted in an autosomal dominant fashion​

familial breast-ovarian cancer syndrome​

site-specific ovarian cancer​

cancer family syndrome (Lynch type II)​

​

Familial breast-ovarian cancer and site-specific ovarian cancer syndromes​

Associated with mutations of the BRCA1 and BRCA2; account for 90% of familial ovarian cancers​

​

Hereditary ovarian cancer occurs at a younger age than sporadic​

​

Carriers have 15 fold increase risk of ovarian carcinoma to non-carriers ​

​

> 90% cancers are of serous: ovarian, peritoneal, fallopian tube.

30
Q

What is Lynch syndrome?

A

HNPCC is responsible for 3% of ovarian carcinomas​

​

Ovarian cancers associated are mainly of the endometrioid and clear cell types​

​

31
Q

What has Molecular analysis has shown?

A

Molecular analysis has shown that different patterns of genetic aberrations underlie the development of the different histologic subtypes.

PTEN beta catenin
KRAS
TP53/ Rb
PIK3CA
BRAF
32
Q

Describe High Grade Serous Carcinoma​

A

Most common type of malignant tumours (80%)​

​

Aggressive​

​

Alteration in P53, in virtually all​

​

BRCA1 or BRCA2 abnormalities (germline and somatic mutations; BRCA1 promoter methylation) ​

These genes encode proteins that play important roles in DNA repair (homologous recombination).

33
Q

What is the Significance of Homologous Recombination Deficiency Testing​?

A

Identification of hereditary cases.​

Current data suggests that BRCA2 mutations confer an overall survival advantage compared with either being BRCA-negative or having a BRCA1 mutation in high-grade serous ovarian cancer. ​

BRCA mutation status has a major influence on response to chemotherapy. ​

Patients can benefit from targeted therapy by PARP inhibitors.

34
Q

What are low grade serous carcinomas?

A

Distinct pathogenesis from high grade serous carcinoma.​

​

Low grade, relatively indolent, arise de novo or from borderline ovarian tumours. ​

​

Mutations in KRAS, BRAF. ​

​

No association with BRCA mutations.

35
Q

What are mucinous tumours?

A

Morphological features similar to mucinous tumours of the gastrointestinal tract.​

KRAS mutations.

36
Q

What are secondary ovarian tumours?

A

​Metastatic colorectal carcinoma: ​

Ovaries, an anatomic site prone to involvement by metastatic colorectal adenocarcinoma.​

4-10% of CRC go to ovary.​

Ovarian lesions are identified prior to the primary tumor in 14-32% of cases.​

​

Krukenberg tumours: ​

Bilateral metastases composed of mucin producing signet ring cells.​

Most often of gastric origin or breast.

37
Q

What are endometrial carcinomas?

A

10-20% associated with endometriosis, but most others thought to be derived from surface epithelium​

​

Co-existence with endometrioid carcinoma in uterus common

38
Q

Which mutations are associated with endometrial carcinomas?

A

CTNNB1 (38%-50%) ​

PTEN (15-20%)​

KRAS and BRAF (4%-36%)​

MSI (8-38%)​

PIK3Ca in (20%)​

P53 >60% and usually in high Endometriosis is a precursor

39
Q

What is associated with Clear cell carcinoma?

A

Strong association with endometriosis​

​

Molecular changes:​

MSI (6-21%)​

PTEN (6%)​

P53 (8.3%)​

BRAF (6.3%)​

PIK3Ca (20-25%)​

B-catenin (3%)

40
Q

What are the sex cord stromal tumours?

A

Pure stromal tumours: ​
e.g. Fibroma, Thecoma, microcystic stromal tumour​

Pure sex cord cells: ​
e.g. Adult type and juvenile granulosa cell tumour​

Mixed sex cord-stromal tumours:​
e.g. Sertoli Leydig cell tumour

Fibroblasts: Fibromas: ​benign, no endocrine production​

Granulosa cells: Granulosa cell tumor variable behaviour, may produce estrogen​

Thecal cells: Thecoma:​ benign, may secrete oestrogen, or rarely androgens​
​
Sertoli-Leydig cells: Sertoli-Leydig cell tumor​ variable behaviour, may be androgenic

41
Q

What are the Molecular Changes in Sex Cord-Stromal Tumours​?

A

Adult type granulosa cell tumour (GCT):​

97% of adult GCT show somatic mutation of the Forkhead transcription factor FOXL2, is a master transcription factor that regulates cell proliferation and apoptosis.​

​
Microcystic stromal tumour:​
FOXL2 mutation can be done in AGCT to confirm the diagnosis in cases where the diagnosis is in question.​

Mutation in CTNNB1

42
Q

What is Peutz Jeghers syndrome?

A

Peutz Jeghers syndrome:​

Germline mutations of STK11 ​

​

Sex cord stromal tumour with annular tubules​

​

Cases occurring in PJS usually show indolent behaviour.​

43
Q

What is DICER1 syndrome?

A

DICER1 Syndrome​

Germline mutation in DICER1, a gene encoding an RNAse III endoribonuclease.​

​

Familial multinodular goitre with sertoli / leydig cell tumour, and tumour susceptibility includes pleuropulonry blastoma in childhood.​

​

Found in up to 60% of seroli-Leydig cell tumours.

44
Q

What are germ cell tumours in?

A

20% of ovarian tumours​

95% benign​

predominantly occur in first or second decade

45
Q

What are dermoid tumours?

A

Benign ​

Solid or cystic ​

May show many lines of differentiation but all mature adult type tissues​

Teeth and hair very common

46
Q

What are immature teratomas?

A

Indicates presence of embryonic elements​

Neural tissue particularly conspicuous​

A malignant neoplasm that grows rapidly, penetrates the capsule and forms adhesions to the surrounding structures​

Spreads in the peritoneal cavity by implantation​

Metastasis to lymph nodes, lung, liver and other organs​

Three tier grading system according to amount of primitive elements

47
Q

What are Mature cystic teratoma with malignant transformation​?

A

​

Malignant transformation is rare occurring in 2% of cases, usually in post menopausal women​

​

Most frequently squamous cell carcinoma​

​

Also carcinoid, thyroid carcinoma, basal cell carcinoma, malignant melanoma, intestinal adenocarcinoma, leiomyosarcoma, chondrosarcoma and angiosarcoma

48
Q

What are Prognostic Factors in ovarian malignancies?

A

Stage of Disease​

Tumour type​

Tumor grade​

Size of residual disease ​

Tumor response to therapy

PathY5 (98 decks)

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