Myeloid malignancies and acute lymphoblastic leukemia (ALL).

Deletion of 7p as the sole abnormality occurs in disorders with myelodysplastic or myeloproliferative features and acute lymphoblastic leukemia, and may therefore affect early hematopoietic progenitor cells.

Myeloproliferative disorders mainly: chronic myeloproliferative disorder in 9 (balanced sex ratio; 4 males and 5 females aged 53 to 79 years old, median age 63 years) (Bernstein et al., 1980; CML Yunis et al., 1986; Obeid et al., 1989; Palka et al., 1990; Rodjer et al., 1990; Ohyashiki et al., 1993; Pedersen-Bjergaard et al., 1993; Lezon-Geyda et al., 2001; Maciejewski et al., 2002) and AML in 10 patients (4 males and 6 females, aged 0 to 80 years, median age 0 years) (Bernstein et al., 1984; Testa et al., 1985; Mecucci et al., 1989; Abruzzo et al., 1992; Veldman et al., 1997; Chessells et al., 2002; Babicka et al., 2007; Blink et al., 2012). Male prevalence and prevalence of T-cell phenotype and in ALL (6 males and 2 females aged 3 to 50 years, median age 25 years) (Kaneko et al., 1989; Berger et al., 1990; Bernard et al., 2001; Berger et al., 2003; Douet-Guilbert et al., 2004; Mullighan et al., 2009; Russell et al., 2009; Safavi et al., 2015). 5 patients with myeloid malignancies had secondary disorders treated for a previous malignancy (Mecucci et al., 1989; Rodjer et al., 1990; Abruzzo et al., 1992; Pedersen-Bjergaard et al., 1993). Three patients were Down syndrome patients (Table 1).

Chronic myeloproliferative disorders
1	F/64	CMD	46,XX,del(7)(p11)
2	M/71	RAEB	46,XY,del(7)(p11p22)
3	F/62	CMMoL	46,XX,del(7)(p11)
4	F/68	RAEB	46,XX,del(7)(p13)
5	M/62	RA	45,XY,-10/46,XY,del(7)(p13p14)       multiple myeloma, chemotherapy
6	F	RA	46,XX,del(7)(p14)
7	F/63	MDS	46,XX,del(7)(p11) 46,XX,-7,+21       multiple myeloma, chemotherapy
8	M/76	MDS	46,XY,del(7)(p12p15)
9	M/53	RA	47,XY,del(7)(p13p22)
Acute myeloid leukemia
10	M/7	AML-M2	46,XY,del(7)(p11)
11	M/51	AML-M1	46,XY,del(7)(p1?5)
12	F/20	AML-M4	46,XX,del(7)(p14
13	M/47	AML-M2	46,XY,del(7)(p12p21)       Hodgkin disease, chemotherapy, radiotherapy
14	F/80	AML-M4	46,XX,del(7)(p12p21)       polycythemia vera, chemotherapy, radiotherapy
15	F/11	AML	46,XX,del(7)(p12)       mature B-cell neoplasm, chemotherapy
16	F/57	AML-M7	47,XX,del(7)(p?),+21c
17	F/0	AML-M7	46,XX,del(7)(p15)
18	M/55	AML-M0	46,XY,del(7)(p12)/46,idem,t(2;2)(q31;q35)
19	F/1	AML	47,XX,del(7)(p11),+21c
Acute lymphoblastic leukemia
20	M/14	T-ALL	46,XY,del(7)(p15)
21	M/25	T-ALL	46,XY,del(7)(p13p15)
22	M/25	T-ALL	46,XY,del(7)(p13)
23	M/29	T-ALL	46,XY,del(7)(p11p15)
24	M/50	T-ALL	46,XY,del(7)(p12)
25	F	ALL	47,XX,del(7)(p13p15),+21c
26	F/3	B-ALL	47-48,XX,+17,del(20),+21,inc/46,XX,del(7)(p11)
27	M/30	T-ALL	46,XY,del(7)(p13)

Abbreviations: M, male; F, female; CMD, chronic myeloproliferative disorder; RAEB, refractory anemia with excess of blasts; MDS, myelodysplastic syndrome; CMMoL, chronic myelomonocytic leukemia; RA, refractory anemia; AML-M2, acute myeloblastic leukemia with maturation; AML-M1, acute myeloblastic leukemia without maturation; AML-M4, acute myelomonocytic leukemia; AML, acute myeloid leukemia; AML-M7, acute megakaryoblastic leukemia; AML-M5, acute monoblastic leukemia; AML-M0, acute myeloblastic leukemia with minimal differentiation, ALL, acute lymphoblastic leukemia/lymphoblastic lymphoma.
1. Bernstein et al., 1980; 2. Yunis et al., 1986; 3. Obeid et al., 1989; 4. Palka et al., 1990. 5. Rodjer et al., 1990; 6. Ohyashiki et al., 1993; 7. Pedersen-Bjergaard et al., 1993; 8. Lezon et al., 2001; 9. Maciejewski et al., 2002; 10. Bernstein et al., 1984; 11. Testa et al., 1985; 12-14. Mecucci et al., 1989; 15. Abruzzo et al., 1992; 16. Veldman et al., 1997; 17. Chessells et al., 2002; 18. Babicka et al., 2007; 19. Blink et al., 2012; 20. Kaneko et al., 1989; 21. Berger et al., 1990; 22. Bernard et al., 2001; 23. Berger et al., 2003; 24. Douet-Guilbert et al., 2004; 25. Mullighan et al., 2009; 26. Russell et al., 2009; 27. Safavi et al., 2015.

Represents as interstitial (9 cases) or terminal deletion (18 patients) with various breakpoints.

Deletion of 7p, appears to confer increased risk of treatment failure and inferior outcome, same as it observed with monosomy 7 in myeloid malignancies. Similarly, event-free survival and survival for patients with monosomy 7 or del(7p), but not of patients with del(7q), were significantly worse in ALL patients than those lacking these abnormalities suggesting the critical region of loss may be on the p-arm (Mecucci et al., 1989; Heerema et al. 2004).

Chromosome 7p deletion is a recurrent cytogenetic abnormality that may be observed at initial presentation or may emerge during disease progression. Terminal or interstitial 7p deletions result in loss of the deleted material, supporting the existence of tumor-suppressor genes in that region. While no consistent region of loss was identified, these chromosomal deletions may contain areas harboring multiple functionally linked genes whose loss of function is thought to be the major event in disease initiation or progression. Most 7p losses involve large chromosomal regions, therefore it is likely that a cluster of cooperating tumor-suppressor genes collectively promote oncogenesis in dosage-dependent manner.

T-ALL